From Medscape Pediatrics
An Expert Interview With Susanna Visser, MS
Laurie Scudder, DNP, NP
Editor's Note:
The results of the second administration of the 2007 National Survey of Children's Health (NSCH) have been reported in the Morbidity and Mortality Weekly Report.[1] The report documented an almost 22% increase in the percentage of children 4-17 years of age with a parent-reported diagnosis of attention-deficit/hyperactivity disorder (ADHD).
These findings illustrate the substantial impact of ADHD on both families and pediatric providers.
Laurie Scudder, DNP, NP, of Medscape sat down with Susanna Visser, MS, Lead Epidemiologist, National Center on Birth Defects and Developmental Disabilities, US Centers for Disease Control and Prevention, Atlanta, Georgia, to discuss the report.
Medscape: Ms. Visser, can you begin by summarizing the main findings of the 2007 NSCH study?
Ms. Visser: The primary goal of this particular report was to compare the most recent parent-reported survey results from a national survey conducted by the US Centers for Disease Control and Prevention (CDC) sponsored by the Maternal and Child Health Bureau at the Health Resources and Services Administration (HRSA) with an earlier survey.
The first survey was conducted in 2003-2004 and had 102,000 respondents. It was repeated in 2007-2008 with approximately 92,000 respondents. This large sample size allowed us to drill down into issues of child health in a way that we cannot in other surveys or through other mechanisms.
The specific question presented to parents was: "Has a doctor or health professional ever told you that your child has ADD [attention-deficit disorder] or ADHD?" Extrapolating from the survey responses to the total US population, it was determined that 4.4 million children in the United States between the ages of 4 and 17 years had received a diagnosis of ADHD as reported by their parents in 2003.
By 2007, that estimate had risen to 5.4 million children. That represents an increase of 1 million children with a parent-reported diagnosis of ADHD in approximately 4 years. That is a 22% increase over that time period and, obviously, was a number that was large and surprising. We knew that the rates were probably increasing because of our previous work, but this was a jump that really caught our attention.
Medscape: Can you describe the various stakeholders in this study and the reaction of these different groups?
Ms. Visser: At the CDC, our main goal through the use of these surveys is to keep a pulse on the health of the nation, and so what we have found here suggests that there is a growing need among American families as a result of this increase in children with ADHD.
A child with ADHD may have symptoms of inattention and hyperactivity or impulsivity, or both. Regardless of the symptoms, ADHD can cause significant functional impairment problems at home, at school, or with friends.
From a public health perspective, there are implications resulting from 5.4 million American children with ADHD. As most parents can appreciate, if you have a child with a behavioral disorder, it affects everything about that family's life, from the expectations of what a typical day is going to be like, through the expectations for school achievement, to relationships with family and friends. It can pose a number of very difficult challenges for those families. Healthcare providers are going to need to help the large number of families address the concerns that are brought into the clinical setting.
Medscape: What was the reaction of the healthcare community to this finding?
Ms. Visser: I think that clinicians -- psychologists and healthcare providers who are diagnosing, treating, and managing children with ADHD -- believed that, although this is a very large number, it was consistent with their clinical experience.
Although it is surprising to think that nearly 1 in 10 children have had a diagnosis of ADHD, it is consistent with the clinical experience. They are managing a lot of children with ADHD, with 2.7 million children taking medication in 2007.
Children typically don't just come in for a diagnosis. They are starting down a treatment and management path that we hope will include a behavioral component in addition to medical management, but we are unable to determine that from these data.
To answer your question, I think that healthcare providers believed that this was clinically consistent with what they have been seeing, and that the number, although quite large, does represent the burden of ADHD that they are seeing relative to other conditions in their practices.
Medscape: You also found some very interesting subgroup findings in different demographic groups. Could you share those findings with us?
Ms. Visser: These data confirmed previous population-based studies that revealed a 2:1 or even a 3:1 ratio of boys to girls in terms of diagnostic prevalence. That consistency really gives us a validity check. In this survey, we noted a 2.3:1 ratio of boys to girls for ever having been diagnosed with ADHD on the basis of parent report; that increases slightly to 2.6:1 for a current ADHD diagnosis. That has been very consistent in the literature and suggests that these data have some face validity. We also noted that the rates of ADHD increased with age, and that makes sense because parents were asked whether they had ever been told that their children had ADHD. Thus, those percentages should trend upward with age, and that was consistent.
We saw some interesting subgroup findings that were unique. The first was with respect to age. When we looked over time, although there were significant increases in ADHD prevalence in all of the 3 age groups that we looked at (4-10, 11-14, and 15-17 years), we saw that the 15- to 17-year-olds had a disproportionately greater increase when compared with younger children. This suggests that clinicians are probably seeing more older teens for diagnosis, treatment, and management of ADHD than in the past, and we do not have a clear understanding of why.
It may be that there is a decrease in stigma around ADHD, a greater acceptance of available treatment protocols, or increasing demands on students with greater expectations to go on to college. Children who were able to adapt to the difficulties presented by their ADHD symptoms at younger ages may have a more difficult time adapting at older ages, and the availability of more flexible treatment options may increase the likelihood that these children seek diagnosis and treatment. I think that that could be behind it. However, we do not know, and we are definitely looking to the clinical community to help elucidate that finding.
We also saw some interesting patterns across ethnic groups. Historically, in the United States, rates of ADHD have been lower in Latinos compared with non-Latino groups. Although these data confirmed that lower rate, we did see a large increase, about 53%, from 2003 to 2007 among Latinos. I think that is an important finding and suggests that the cultural differences in ADHD diagnosis or treatment may be lessening. That is an important finding to keep in mind.
Medscape: The other group who experienced a significant increase were children who were reported by parents to be multiracial.
Ms. Visser: That is correct. This is a finding that we have seen over time, and I am not sure what is behind this. There is limited literature about risk factors for ADHD and behavioral disorders in multiracial children. It is likely that the rates represent the coalescing of various social and economic risk factors within these families. However, it is not clear what is driving the findings among multiracial children.
Medscape: What about regional variance? I noted that the rate of parent-reported ADHD in North Carolina was 15.6% in this survey; however, in California it was only 6.2% -- which is obviously a dramatic difference.
Ms. Visser: That is correct. We saw a good bit of geographic variation in the rates of ADHD. Although there was a significant increase over time in the Northeast, Midwest, and South, there was not a comparable increase in the West. The regional differences were apparent at the state level, as you noted. We found that the state with the largest prevalence of parent-reported ADHD was North Carolina at 15.6%, representing nearly a 63% increase in ADHD prevalence from 2003 to 2007.
We found 3 other states with rates above 14%: Alabama at 14.3%; Louisiana at 14.2%; and Delaware at 14.1%. We are very interested in these states. We want to understand what is driving the rates up in specific states and reasons for the large variance across states. Some of our western states are quite low. In California, as you mentioned, only 6.2% of children are reported to have an ADHD diagnosis. It is important to us in terms of epidemiology to understand what is predicting both higher and lower rates of diagnosis within particular states.
We know that some of that can be accounted for by demographic factors. Risk for ADHD increases as income decreases -- a situation typically associated with lesser-resourced educational services, fewer support structures available to parents, and then more behavioral problems coupled with insufficient availability of appropriate resources and services. There are issues of access to care and limited resources to support a family in a way that will optimize the child's behavior. Those all coalesce together and relate to the environmental contributors to childhood ADHD.
Additionally, there is a genetic component to ADHD. In any population there will be a core group of children genetically predisposed to ADHD regardless of environmental factors.
It is important to understand that differences in state policies, practices, and things not related to the specific environmental and demographic factors within the state predict the diagnostic rate of ADHD, too.
We have been working with several states to try to understand the reasons for the state-level variation. We suspect that there may be very aggressive quality improvement practices and protocols in place in certain states with higher prevalence rates. When you screen more children for behavioral or developmental problems, you will find more symptoms. That greater rate of symptom identification will likely translate into greater rates of diagnosis. A state that has a higher rate is not necessarily in trouble. It may be that they are doing a fantastic job of assessing and screening the behavioral needs of their children, and that will translate to a higher rate of behavioral diagnoses. States that find themselves at the top of this list should not necessarily be concerned. It does underscore the importance of unpacking these findings to identify what is really driving these factors over time
Implications of the Changing Epidemiology of ADHD
Medscape: Do these data allow you to speculate about some of the reasons for the increased prevalence overall? You have noted that stigma may have lessened. Diagnostic awareness is certainly greater. Are there other reasons that can be teased out from these data that may be contributing to this increase?
Ms. Visser: Well, these cross-sectional data certainly cannot answer those questions for us, but we have a number of hypotheses. Greater awareness and better screening efforts are our top 2 hypotheses. There has been quite a lot of education. The American Academy of Pediatrics, for example, has really focused on quality improvement for pediatric practices, and the efforts around autism and ADHD have been focused on trying to standardize our approach to screening and diagnosis for behavioral issues.
There are probably other environmental and sociopolitical issues. As I mentioned, poverty is definitely associated with behavioral problems for a variety of reasons. The stresses of that environment on young people can really affect behavior and, when added to a lack of appropriate support for parents, can have a long-term effect on the child and family dynamic.
All of those factors likely play into it. We are focused on getting answers to a number of these questions. What we have recognized is that ADHD is not the exception. Although the prevalence of ADHD has been increasing since 1996, this recent jump has raised some concern. Reflecting that same trend, we have seen the rates of autism increase as well. We think that ADHD is a piece of the entire puzzle. American families are struggling with behavioral problems and developmental disabilities, and we need to be very aggressive about how we investigate these patterns.
Medscape: The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V) is proposing diagnostic criteria for ADHD that would increase the age of onset of symptoms from the current requirement that impairment be present at or before 7 years of age to an older onset of at or before 12 years of age.[2] Do these data support that proposed change?
Ms. Visser: I think that it is going to reflect what clinicians have already been doing, which is not weighting that criteria as heavily as other criteria. The new DSM-V criteria, with respect to age of onset, will mirror more closely clinical intuition, which is to attempt to document symptoms early on in childhood but not to be confined to before 7 years of age. However, I also think that we are going to need to understand and reflect on whether the DSM-V criteria are appropriate for teens and tweens. We may have to make some adaptations to those symptom criteria to make sure that we are able to capture the manner in which these symptoms are expressed in older children, particularly if this pattern of a rising prevalence during adolescence continues.
Medscape: What are some of the limitations to this study? Can you comment on whether parent report is a valid methodology for collection of these data?
Ms. Visser: I think the major limitation of these data is the lack of clinically validated diagnostic data. We asked parents whether a healthcare professional had told them that the child has ever had ADHD. We did not go back to medical records to verify that the diagnosis was made or how rigorously diagnostic criteria were applied. Therefore, we recognize that this estimate of prevalence reflects community diagnosis, which may include less rigorous diagnostic practices for ADHD diagnosis. However, what we do know is that parent-reported data are very reliable. They trend in a very smooth fashion over time. We have been using this question in our national surveys, this and others, since 1996, and the rates trend very smoothly. There is not a lot of jumping around, and that reliability is one measure of the psychometric value of the question.
When you look at the prevalence estimates for parent-reported ADHD, they track in magnitude very similarly to the parent report of other conditions. For example, Tourette syndrome comes up at about 2 per 1000 for current diagnosis.[3] Autism comes up at 11 per 1000, and ADHD comes up at 72 per 1000 for current ADHD diagnosis.[4] That really trends in a predictable way if you ask most clinicians. You want to see those rates stacking up in that fashion and having about that distance between them in magnitude, so there is some face validity to these estimates.
We are never going to be able to say whether the rates include overdiagnosed or underdiagnosed children with these cross-sectional data. There is probably some of each in this estimate, but there is no reason to think that there would be more or less of either of those groups. This is a cross-sectional estimate of the lived experience of ADHD in American families. If parents are telling us that their children either have had a diagnosis or are currently living with ADHD, then we believe that they are experiencing the impact of that disorder in their families, and that is an important public health measure of ADHD impact.
Medscape: Can you offer some insights into where you think future research should be focused on the basis of these data?
Ms. Visser: We really need to understand the driving forces behind this increase and try to determine whether rates are increasing due to quality improvement efforts in some states. We can look at population-based studies that are in the field now and match them to the state-based estimates in this survey, see whether they track well, and look for factors that are available at the community level to better determine who is being diagnosed and why.
That is going to be important not just for ADHD, but to inform the behavioral patterns that are seen in other developmental disorders that we are tracking. It is a priority for us. Of course, this is just one way to monitor the signal for ADHD in communities. Other studies, including both clinic-based and community-based epidemiologic studies, are also important because they allow for contribution of input from both medical professionals and teachers. These 3 pieces together allow us to get a better national representation, in a cost-effective manner, of the full picture of ADHD impact in America.
Medscape: I think the most important question for our readers is the implications of these data for primary care pediatric providers who are seeing these children on a day-to-day basis. Can you provide some insights?
Ms. Visser: Well, definitely the finding of increased rates in teens is important. Our data suggest that primary care providers may be managing more older teens with ADHD than in the past. Of course, teens should be more active participants in the treatment and management of their symptoms than younger children might be.
The other issue is that we noted an increase in rates of medication among girls as they got older. In boys, rates of medication use increase throughout childhood, peaking at 11- to 14-year-olds and then declining after that. The answer to the question of why we are seeing this variance in medication use is likely to come from the clinical community.
Finally, the findings of a significant increase in ADHD among Latino children is important. What we know from pharmacoepidemiologic studies is that the Latino community is less interested in medical treatments, and medication in particular, for behavioral and mental health conditions. Therefore, this may pose a different sort of challenge for both primary care providers and specialists who are treating Latino children with ADHD. The influence of race and ethnicity on the treatment plans for children will need to be better understood and considered.
Editor's Note: We would like to hear from you. Is this NSCH report consistent with your own clinical experience? How has the changing epidemiology of ADHD affected your practice? Please join the discussion.
Wednesday, January 19, 2011
Eating Disorders in Pediatric Primary Care
From Medscape Pediatrics
An Expert Interview With David S. Rosen, MD, MPH
Laurie Scudder, DNP, NP
Editor's Note: The American Academy of Pediatrics released a new Clinical Report - Identification and Management of Eating Disorders in Children and Adolescents in December 2010. The report documents an increasing incidence of eating disorders in boys, who now represent up to 10% of all cases, and younger children.
The document emphasizes the importance of early detection and proper evaluation of children suspected of a disorder.
Medical complications of eating disorders can affect any organ system and necessitate a range of management strategies including medical care, mental health treatment, and nutritional intervention.
Medscape talked with the report's lead author, David S. Rosen, MD, MPH, Clinical Professor of Pediatrics, Internal Medicine, and Psychiatry at the University Michigan Medical School, Ann Arbor, about the implications of this information for primary care.
Medscape: Dr. Rosen, the report clearly notes the changing epidemiology of eating disorders, including an increased incidence in boys, younger children, and minority children. Are you able to speculate on some of the reasons for these changes?
Dr. Rosen: Some of it is better case finding. In the past we weren't looking for or recognizing eating disorders in populations where we weren't expecting to see them. Some of it is simply recognizing eating disorders that have probably always been there, but there are probably also changes going on in who develops eating disorders in the first place. As the media change, as our eating habits change, as our nutrition practices change, as our concerns about obesity have become very acute, a lot of kids are thinking about nutrition in ways that they haven't been asked to before. In a certain vulnerable population, that message sometimes gets misdirected. There are unintended consequences, which can result in eating disorders.
Medscape: The report describes the increasing incidence in younger children. The committee looked at genetic and environmental variables as they affect this disorder and examined the role of puberty in activating a potential genetic predisposition to the traits that often accompany eating disorders such as perfectionism and behavior rigidity. Yet, there is a rising incidence in prepubertal children. Can you discuss some of the reasons for this rising incidence?
Dr. Rosen: Again, I think that some of the increase has to do with better case finding, but the impact of that is probably quite small. We really are, in fact, seeing many more younger children with eating disorders than we ever have before. Let's just be clear that we don't have a certain explanation for why that has occurred. However, many of us are concerned that, as we have rushed to address the concerns related to obesity in the United States, we have hurried out interventions to try to encourage healthy eating that have, in some vulnerable populations, had unintended consequences.
If you are taught in school that fat is bad and you happen to be a 9-year-old without the cognitive ability to understand the nuances of that information, you are unable to recognize that that's not really a black and white statement. You decide that fat is bad, and you look at every label and, if that food has fat in it, you don't eat it. If you are even more inclined by virtue of an anxiety issue or obsessive compulsive traits to really dig in and grab hold of that way of eating, it doesn't take very long before you get into trouble.
Medscape: The report also noted a wide variance in estimates of prevalence. For example, the report provided estimates of bulimia nervosa ranging from 0.8% to 14%. Can you offer some insight into the reasons behind this variance, and is it related to differences in applying DSM-IV criteria?
Dr. Rosen: The prevalence of anorexia nervosa is fairly well-understood to be about 0.5%. The prevalence of bulimia nervosa is understood to be somewhere in the neighborhood of 2%-4%. Yes, there are some reports that will cite numbers that are quite different from that, but often those reports have very different ways of looking at populations. Sometimes they're looking at particularly vulnerable populations. Sometimes the definitions they are using are a little bit different, and we probably should acknowledge that the DSM-IV criteria are recognized by many as being something less than perfect in capturing the group of kids that do, in fact, have these disorders.
The biggest concern, of course, is the category of "eating disorder not otherwise specified." That has been sort of a "waste basket" for kids who clearly have disordered eating and certainly have all of the associated psychological and medical risks that go along with that, but they don't meet the strict criteria required to be diagnosed with anorexia or bulimia. They get left out of the statistics for anorexia and bulimia, which artifactually reduces the number of kids who are, in fact, affected by eating disorders. The result is that this other category of "not otherwise specified" eating disorders becomes quite large, very heterogeneous, and hard to get your hands around.
It is hoped that the DSM-V criteria, which are going to come out in the next couple of years, are going to help to better classify patients with eating disorders so that we can be more specific about their treatment and reduce the number that have to fall into that unhelpful "not otherwise specified" category.
Screening and Early Recognition in Primary Care
Medscape: The report provided some important guidance on screening and early recognition of disordered eating in children. What are some best practices for incorporating those screening strategies into the primary care environment?
Dr. Rosen: The first thing, and pediatric primary care providers do this already, is to always look at growth parameters. A child who is not following his or her established growth parameters should raise a red flag and prompt further evaluation. A fall in the height curve, a fall in the weight curve, a body mass index curve that is dropping -- those are all situations in which, at least, some further questions should be asked about what's going on.
In talking with kids about their nutrition and eating habits, something we should all be doing now, we should take note when children talk about dieting and express concerns about their weight. Those children require some further screening and evaluation to see whether these dieting behaviors are, in fact, healthy behaviors or potentially unhealthy behaviors. The same is true for physical activity. Kids who are very compulsive about their physical activity need to be queried further to determine what's driving that activity level.
One of the things that we have recognized is that some children are more vulnerable than others. In the young age group, children with pre-existing anxiety symptoms are more likely, in my experience, to go on to develop eating issues as their anxiety gets juxtaposed with their eating behavior. That's a group that requires further assessment.
We also know that some activities pose higher risk. Dancers, skaters, models, and wrestlers seem to be at increased risk and probably warrant additional attention to their nutrition and eating and activity habits.
Medscape: The report encouraged pediatric providers to seriously consider the possibility of an eating disorder if the child's family member or a friend or a teacher voices some concern.
Dr. Rosen: Correct. We are now out of the realm of preventive care. We are now discussing a child who is brought in because there is concern about a problem. It is absolutely true that, if a child is brought to a pediatric provider's office because somebody has expressed some concern -- whether that's a parent, a brother or sister, a friend, a teacher, or somebody at school -- a careful evaluation must be done despite the protestations of that child or teen. There is a relatively high likelihood that, in fact, something is going on.
Medscape: The report provided a comprehensive overview of the evaluation of children, and the message was that assessment needed to begin in the primary care office. Are there red flags that should alert a primary care provider that a child should instead be immediately referred to a mental health professional?
Dr. Rosen: Absolutely. Pediatric primary care providers should be able to begin the process of evaluating, and I'll use the word managing rather than treating, a patient who has a suspected eating disorder, whatever that eating disorder is. The evaluation includes asking the right questions to decide whether there really is a problem as well as getting a sense of the growth parameters and the direction of the weight trajectory. Look carefully for any signs of medical instability or consequences from the eating issue. Do a first-pass mental health assessment to make sure that child is not acutely suicidal and is safe being at home.
Make sure he or she is, in fact, eating and able to limit vomiting, if that is a problem. All of those are appropriate roles for a pediatric primary care provider at that first visit, whether that visit occurred because the family was concerned or because a problem was identified during a visit that was intended for another reason.
The next step is determined by the experience and comfort of the pediatric provider. There will be many pediatric providers who, once they have made the diagnosis of an eating disorder, will refer that patient to somebody with more expertise and experience in managing children with eating disorders or with the resources, such as dietitians and mental health providers, to provide a more comprehensive plan of care.
However, there are many primary pediatric providers who are comfortable in coordinating care and providing the medical supervision and will simply need to bring in a mental health provider and/or a dietitian to help with care. Let's acknowledge, however, that in some places, ready referral options are not available to the primary provider. Care is going to have to continue in that primary pediatric office because there are no easily accessible alternatives.
Nothing about this care is out of the realm of what a primary pediatric provider can choose to do if they are comfortable doing so. There is no imperative that patients be referred elsewhere. On the other hand, nobody should be forced into an uncomfortable situation of managing a patient who they feel unprepared to manage. Pediatric providers who really feel that this is not their area of expertise should, after that initial evaluation, feel justified in referring that family to someone who is more experienced. Even in that situation, I would contend that the role of the primary pediatric provider is still an important one. You have to make sure your patient gets to that referral and continues to be seen. Families and siblings in situations like this require a lot of support. That is a very important role for primary pediatric providers even in the setting of referral.
Comorbidities of Eating Disorders
Medscape: The report reassured primary care providers that many of the daunting number of medical comorbidities that may accompany eating disorders resolve with refeeding and resolution of purging. One of the exceptions, however, was brain changes. Could you comment on this?
Dr. Rosen: There are actually 3 areas where we have concerns that there may not be complete resolution of symptoms. The first has to do with growth. In very young patients who are still growing when they present with eating disorders, there are at least some data, although not particularly robust, to suggest that there can be permanent limitation of growth as a result of an eating disorder during critical phases of growth.
The second issue has to do with bone health. We know that the period of adolescence is a time when people lay down most of their bone mineral, and an eating disorder that extends throughout much of that period of time can result in lasting, irreversible, unrecoverable limitations in bone mineralization. That, of course, results in problems with bone health and increased potential for fractures not only during adolescence but throughout the rest of life.
The third area, which is the fascinating one, has to do with the brain. We have learned over the last decade and a half that there is loss of brain tissue and increase in cerebrospinal fluid that occurs particularly in anorexia nervosa. That is not surprising because we see lots of changes that seem to reflect changes in the brain, including changes in mood and cognitive ability. Much of the change in brain mass recovers with weight restoration as well, but there do seem to be some lasting deficits that extend even past the point of weight recovery. The implications of that are unknown. What is reassuring is that the associated changes in both mood and cognition do, in fact, resolve with weight restoration.
Medscape: The need for early identification and treatment is underscored by recognition of those changes that may not resolve. Is there a message in that for primary care providers?
Dr. Rosen: I am sad to have to say that I see a lot of patients with very advanced eating disorders who unsuccessfully sought care from other providers prior to coming to see me. Many were told to "just wait and see what happens." "Wait and see" approaches do not make sense when dealing with a condition that has this much potential morbidity, can progress very quickly, and in which treatment is challenging and becomes more so as the child becomes more ill.
The message that I have for providers is: Faced with somebody with an eating disorder, or even the suspicion of an eating disorder, you really need to move very aggressively towards intervention. That intervention may be an evaluation or may, in fact, be actual treatment. "Wait and see" approaches are not usually appropriate in these conditions. The group of kids who are most vulnerable and, by extension, most responsive to early intervention is the younger group. When we see the 10- to12-year-olds with eating disorders who might not meet the criteria for anorexia or bulimia, we are nevertheless very aggressive about treating them because our experience has been that they turn around really quickly if they get appropriate treatment. If you wait 6 or 9 months, these kids become entrenched in their disorders and can be just as difficult to treat as the patients who have had eating disorders for years.
When making the diagnosis of an eating disorder, the first place providers are likely to encounter resistance is with the child. They often deny that they have a problem, that it is as big of a problem as we say it is, or that it is the cause of the consequences that people are recognizing. You have to deal with that resistance. You cannot allow yourself to be steamrolled by it.
The second place where you may meet resistance is from parents who may minimize the problem, not recognize the problem, or who do not have the resources to be able to appropriately address it. To be fair, eating disorders are very costly in terms of time, energy, and money. That resistance needs to be met.
Bottom line: The more quickly we can move kids and families to definitive treatment once a diagnosis has been made, the better the outcome is likely to be.
Conclusion
Medscape: Dr. Rosen, do you have any additional thoughts about the role of the primary care provider in ensuring ongoing care for a disorder that may require years of intervention?
Dr. Rosen: Patients with eating disorders have lots of other health issues too. The primary care pediatric provider is going to be involved in all of those other issues -- immunizations, sports physicals, sore throats, broken arms, and all of the other things that require a pediatric provider. If you know your patient has a chronic illness -- it doesn't matter what the chronic illness is -- and you are seeing that child for their back-to-school physical, you need to make sure that they are also doing well with respect to their chronic illness. That includes ensuring that they are seeing the people they need to see and making sure that the issues related to their chronic illness are not creating additional challenges. An eating disorder is a chronic illness, and primary providers, even if they are not involved in the ongoing management of the eating disorder, certainly need to inquire and follow up, assess, and support the patient and their family. They must also be mindful of the possibility that the same problem could occur in a sibling because these are genetic disorders and they run in families.
Medscape: Do you have any final insights?
Dr. Rosen: If parents or pediatric providers are considering the diagnosis of an eating disorder only when the child shows up with 20 pounds of weight loss and amenorrhea and growth failure, then the diagnosis is too late. We need to be much more attentive to this possibility earlier on. We need to be responding when the kids are beginning to express weight concerns, when they are beginning to talk about dieting or becoming more compulsively overactive. We cannot wait for the point when a child has lost a lot of weight or a young girl has lost her period and is already in medical trouble. That is a message not just for primary care pediatric folks but also for families. Particularly in vulnerable populations, it is a message that pediatric providers must make sure that families are hearing in an anticipatory way. If you are the mom of a ballet dancer, if you are the dad of a wrestler, if you are the parent of a child who has a long history of anxiety issues -- those are folks who need to get a heads up about the things to look for early in the process of a developing eating disorder rather than at those end stages.
A second point that I do not think we've talked about at all but that I think is extraordinarily important is the conventional wisdom that eating disorders never get better: If you have it, you have it for life. You learn to control it. Be prepared to deal with it until you die. That is just incorrect. Eating disorders do get better. Most patients recover fully, which means that they are not only medically healthy but no longer have those dysfunctional thoughts and attitudes about eating and weight and shape and body image.
An even larger majority recover fully from a medical perspective, although they might have some persistently dysfunctional thoughts about weight and body image. It is really important to correct misunderstandings that once you have an eating disorder you have it for life. You do not. The expectation for nearly all children and most adolescents with eating disorders is that they will recover fully. Now it might take a long time. It will be a lot of hard work. It will be frustrating. There is no guarantee. However, our expectation when we meet people with an eating disorder for the first time and are describing what this is going to be like is to emphasize that our finish line is complete cure. We are not being "pie in the sky" when we say that. That really is what we expect is going to happen. It might take a long time, but that truly is our goal, and we achieve it most of the time.
Medscape: That is a very positive message for our conclusion. Thank you very much, Dr. Rosen.
An Expert Interview With David S. Rosen, MD, MPH
Laurie Scudder, DNP, NP
Editor's Note: The American Academy of Pediatrics released a new Clinical Report - Identification and Management of Eating Disorders in Children and Adolescents in December 2010. The report documents an increasing incidence of eating disorders in boys, who now represent up to 10% of all cases, and younger children.
The document emphasizes the importance of early detection and proper evaluation of children suspected of a disorder.
Medical complications of eating disorders can affect any organ system and necessitate a range of management strategies including medical care, mental health treatment, and nutritional intervention.
Medscape talked with the report's lead author, David S. Rosen, MD, MPH, Clinical Professor of Pediatrics, Internal Medicine, and Psychiatry at the University Michigan Medical School, Ann Arbor, about the implications of this information for primary care.
Medscape: Dr. Rosen, the report clearly notes the changing epidemiology of eating disorders, including an increased incidence in boys, younger children, and minority children. Are you able to speculate on some of the reasons for these changes?
Dr. Rosen: Some of it is better case finding. In the past we weren't looking for or recognizing eating disorders in populations where we weren't expecting to see them. Some of it is simply recognizing eating disorders that have probably always been there, but there are probably also changes going on in who develops eating disorders in the first place. As the media change, as our eating habits change, as our nutrition practices change, as our concerns about obesity have become very acute, a lot of kids are thinking about nutrition in ways that they haven't been asked to before. In a certain vulnerable population, that message sometimes gets misdirected. There are unintended consequences, which can result in eating disorders.
Medscape: The report describes the increasing incidence in younger children. The committee looked at genetic and environmental variables as they affect this disorder and examined the role of puberty in activating a potential genetic predisposition to the traits that often accompany eating disorders such as perfectionism and behavior rigidity. Yet, there is a rising incidence in prepubertal children. Can you discuss some of the reasons for this rising incidence?
Dr. Rosen: Again, I think that some of the increase has to do with better case finding, but the impact of that is probably quite small. We really are, in fact, seeing many more younger children with eating disorders than we ever have before. Let's just be clear that we don't have a certain explanation for why that has occurred. However, many of us are concerned that, as we have rushed to address the concerns related to obesity in the United States, we have hurried out interventions to try to encourage healthy eating that have, in some vulnerable populations, had unintended consequences.
If you are taught in school that fat is bad and you happen to be a 9-year-old without the cognitive ability to understand the nuances of that information, you are unable to recognize that that's not really a black and white statement. You decide that fat is bad, and you look at every label and, if that food has fat in it, you don't eat it. If you are even more inclined by virtue of an anxiety issue or obsessive compulsive traits to really dig in and grab hold of that way of eating, it doesn't take very long before you get into trouble.
Medscape: The report also noted a wide variance in estimates of prevalence. For example, the report provided estimates of bulimia nervosa ranging from 0.8% to 14%. Can you offer some insight into the reasons behind this variance, and is it related to differences in applying DSM-IV criteria?
Dr. Rosen: The prevalence of anorexia nervosa is fairly well-understood to be about 0.5%. The prevalence of bulimia nervosa is understood to be somewhere in the neighborhood of 2%-4%. Yes, there are some reports that will cite numbers that are quite different from that, but often those reports have very different ways of looking at populations. Sometimes they're looking at particularly vulnerable populations. Sometimes the definitions they are using are a little bit different, and we probably should acknowledge that the DSM-IV criteria are recognized by many as being something less than perfect in capturing the group of kids that do, in fact, have these disorders.
The biggest concern, of course, is the category of "eating disorder not otherwise specified." That has been sort of a "waste basket" for kids who clearly have disordered eating and certainly have all of the associated psychological and medical risks that go along with that, but they don't meet the strict criteria required to be diagnosed with anorexia or bulimia. They get left out of the statistics for anorexia and bulimia, which artifactually reduces the number of kids who are, in fact, affected by eating disorders. The result is that this other category of "not otherwise specified" eating disorders becomes quite large, very heterogeneous, and hard to get your hands around.
It is hoped that the DSM-V criteria, which are going to come out in the next couple of years, are going to help to better classify patients with eating disorders so that we can be more specific about their treatment and reduce the number that have to fall into that unhelpful "not otherwise specified" category.
Screening and Early Recognition in Primary Care
Medscape: The report provided some important guidance on screening and early recognition of disordered eating in children. What are some best practices for incorporating those screening strategies into the primary care environment?
Dr. Rosen: The first thing, and pediatric primary care providers do this already, is to always look at growth parameters. A child who is not following his or her established growth parameters should raise a red flag and prompt further evaluation. A fall in the height curve, a fall in the weight curve, a body mass index curve that is dropping -- those are all situations in which, at least, some further questions should be asked about what's going on.
In talking with kids about their nutrition and eating habits, something we should all be doing now, we should take note when children talk about dieting and express concerns about their weight. Those children require some further screening and evaluation to see whether these dieting behaviors are, in fact, healthy behaviors or potentially unhealthy behaviors. The same is true for physical activity. Kids who are very compulsive about their physical activity need to be queried further to determine what's driving that activity level.
One of the things that we have recognized is that some children are more vulnerable than others. In the young age group, children with pre-existing anxiety symptoms are more likely, in my experience, to go on to develop eating issues as their anxiety gets juxtaposed with their eating behavior. That's a group that requires further assessment.
We also know that some activities pose higher risk. Dancers, skaters, models, and wrestlers seem to be at increased risk and probably warrant additional attention to their nutrition and eating and activity habits.
Medscape: The report encouraged pediatric providers to seriously consider the possibility of an eating disorder if the child's family member or a friend or a teacher voices some concern.
Dr. Rosen: Correct. We are now out of the realm of preventive care. We are now discussing a child who is brought in because there is concern about a problem. It is absolutely true that, if a child is brought to a pediatric provider's office because somebody has expressed some concern -- whether that's a parent, a brother or sister, a friend, a teacher, or somebody at school -- a careful evaluation must be done despite the protestations of that child or teen. There is a relatively high likelihood that, in fact, something is going on.
Medscape: The report provided a comprehensive overview of the evaluation of children, and the message was that assessment needed to begin in the primary care office. Are there red flags that should alert a primary care provider that a child should instead be immediately referred to a mental health professional?
Dr. Rosen: Absolutely. Pediatric primary care providers should be able to begin the process of evaluating, and I'll use the word managing rather than treating, a patient who has a suspected eating disorder, whatever that eating disorder is. The evaluation includes asking the right questions to decide whether there really is a problem as well as getting a sense of the growth parameters and the direction of the weight trajectory. Look carefully for any signs of medical instability or consequences from the eating issue. Do a first-pass mental health assessment to make sure that child is not acutely suicidal and is safe being at home.
Make sure he or she is, in fact, eating and able to limit vomiting, if that is a problem. All of those are appropriate roles for a pediatric primary care provider at that first visit, whether that visit occurred because the family was concerned or because a problem was identified during a visit that was intended for another reason.
The next step is determined by the experience and comfort of the pediatric provider. There will be many pediatric providers who, once they have made the diagnosis of an eating disorder, will refer that patient to somebody with more expertise and experience in managing children with eating disorders or with the resources, such as dietitians and mental health providers, to provide a more comprehensive plan of care.
However, there are many primary pediatric providers who are comfortable in coordinating care and providing the medical supervision and will simply need to bring in a mental health provider and/or a dietitian to help with care. Let's acknowledge, however, that in some places, ready referral options are not available to the primary provider. Care is going to have to continue in that primary pediatric office because there are no easily accessible alternatives.
Nothing about this care is out of the realm of what a primary pediatric provider can choose to do if they are comfortable doing so. There is no imperative that patients be referred elsewhere. On the other hand, nobody should be forced into an uncomfortable situation of managing a patient who they feel unprepared to manage. Pediatric providers who really feel that this is not their area of expertise should, after that initial evaluation, feel justified in referring that family to someone who is more experienced. Even in that situation, I would contend that the role of the primary pediatric provider is still an important one. You have to make sure your patient gets to that referral and continues to be seen. Families and siblings in situations like this require a lot of support. That is a very important role for primary pediatric providers even in the setting of referral.
Comorbidities of Eating Disorders
Medscape: The report reassured primary care providers that many of the daunting number of medical comorbidities that may accompany eating disorders resolve with refeeding and resolution of purging. One of the exceptions, however, was brain changes. Could you comment on this?
Dr. Rosen: There are actually 3 areas where we have concerns that there may not be complete resolution of symptoms. The first has to do with growth. In very young patients who are still growing when they present with eating disorders, there are at least some data, although not particularly robust, to suggest that there can be permanent limitation of growth as a result of an eating disorder during critical phases of growth.
The second issue has to do with bone health. We know that the period of adolescence is a time when people lay down most of their bone mineral, and an eating disorder that extends throughout much of that period of time can result in lasting, irreversible, unrecoverable limitations in bone mineralization. That, of course, results in problems with bone health and increased potential for fractures not only during adolescence but throughout the rest of life.
The third area, which is the fascinating one, has to do with the brain. We have learned over the last decade and a half that there is loss of brain tissue and increase in cerebrospinal fluid that occurs particularly in anorexia nervosa. That is not surprising because we see lots of changes that seem to reflect changes in the brain, including changes in mood and cognitive ability. Much of the change in brain mass recovers with weight restoration as well, but there do seem to be some lasting deficits that extend even past the point of weight recovery. The implications of that are unknown. What is reassuring is that the associated changes in both mood and cognition do, in fact, resolve with weight restoration.
Medscape: The need for early identification and treatment is underscored by recognition of those changes that may not resolve. Is there a message in that for primary care providers?
Dr. Rosen: I am sad to have to say that I see a lot of patients with very advanced eating disorders who unsuccessfully sought care from other providers prior to coming to see me. Many were told to "just wait and see what happens." "Wait and see" approaches do not make sense when dealing with a condition that has this much potential morbidity, can progress very quickly, and in which treatment is challenging and becomes more so as the child becomes more ill.
The message that I have for providers is: Faced with somebody with an eating disorder, or even the suspicion of an eating disorder, you really need to move very aggressively towards intervention. That intervention may be an evaluation or may, in fact, be actual treatment. "Wait and see" approaches are not usually appropriate in these conditions. The group of kids who are most vulnerable and, by extension, most responsive to early intervention is the younger group. When we see the 10- to12-year-olds with eating disorders who might not meet the criteria for anorexia or bulimia, we are nevertheless very aggressive about treating them because our experience has been that they turn around really quickly if they get appropriate treatment. If you wait 6 or 9 months, these kids become entrenched in their disorders and can be just as difficult to treat as the patients who have had eating disorders for years.
When making the diagnosis of an eating disorder, the first place providers are likely to encounter resistance is with the child. They often deny that they have a problem, that it is as big of a problem as we say it is, or that it is the cause of the consequences that people are recognizing. You have to deal with that resistance. You cannot allow yourself to be steamrolled by it.
The second place where you may meet resistance is from parents who may minimize the problem, not recognize the problem, or who do not have the resources to be able to appropriately address it. To be fair, eating disorders are very costly in terms of time, energy, and money. That resistance needs to be met.
Bottom line: The more quickly we can move kids and families to definitive treatment once a diagnosis has been made, the better the outcome is likely to be.
Conclusion
Medscape: Dr. Rosen, do you have any additional thoughts about the role of the primary care provider in ensuring ongoing care for a disorder that may require years of intervention?
Dr. Rosen: Patients with eating disorders have lots of other health issues too. The primary care pediatric provider is going to be involved in all of those other issues -- immunizations, sports physicals, sore throats, broken arms, and all of the other things that require a pediatric provider. If you know your patient has a chronic illness -- it doesn't matter what the chronic illness is -- and you are seeing that child for their back-to-school physical, you need to make sure that they are also doing well with respect to their chronic illness. That includes ensuring that they are seeing the people they need to see and making sure that the issues related to their chronic illness are not creating additional challenges. An eating disorder is a chronic illness, and primary providers, even if they are not involved in the ongoing management of the eating disorder, certainly need to inquire and follow up, assess, and support the patient and their family. They must also be mindful of the possibility that the same problem could occur in a sibling because these are genetic disorders and they run in families.
Medscape: Do you have any final insights?
Dr. Rosen: If parents or pediatric providers are considering the diagnosis of an eating disorder only when the child shows up with 20 pounds of weight loss and amenorrhea and growth failure, then the diagnosis is too late. We need to be much more attentive to this possibility earlier on. We need to be responding when the kids are beginning to express weight concerns, when they are beginning to talk about dieting or becoming more compulsively overactive. We cannot wait for the point when a child has lost a lot of weight or a young girl has lost her period and is already in medical trouble. That is a message not just for primary care pediatric folks but also for families. Particularly in vulnerable populations, it is a message that pediatric providers must make sure that families are hearing in an anticipatory way. If you are the mom of a ballet dancer, if you are the dad of a wrestler, if you are the parent of a child who has a long history of anxiety issues -- those are folks who need to get a heads up about the things to look for early in the process of a developing eating disorder rather than at those end stages.
A second point that I do not think we've talked about at all but that I think is extraordinarily important is the conventional wisdom that eating disorders never get better: If you have it, you have it for life. You learn to control it. Be prepared to deal with it until you die. That is just incorrect. Eating disorders do get better. Most patients recover fully, which means that they are not only medically healthy but no longer have those dysfunctional thoughts and attitudes about eating and weight and shape and body image.
An even larger majority recover fully from a medical perspective, although they might have some persistently dysfunctional thoughts about weight and body image. It is really important to correct misunderstandings that once you have an eating disorder you have it for life. You do not. The expectation for nearly all children and most adolescents with eating disorders is that they will recover fully. Now it might take a long time. It will be a lot of hard work. It will be frustrating. There is no guarantee. However, our expectation when we meet people with an eating disorder for the first time and are describing what this is going to be like is to emphasize that our finish line is complete cure. We are not being "pie in the sky" when we say that. That really is what we expect is going to happen. It might take a long time, but that truly is our goal, and we achieve it most of the time.
Medscape: That is a very positive message for our conclusion. Thank you very much, Dr. Rosen.
Autism and the MMR Vaccine, Revisited
From Medscape Infectious Diseases
Paul A. Offit, MD
Hi. My name is Paul Offit. I'm talking to you today from the Division of Infectious Diseases and the Vaccine Education Center at Children's Hospital, Philadelphia. I'm sure many of you know that an editorial was published in the British Medical Journal [1,2] on January 5, 2011, looking at the issue of Andrew Wakefield and his 1998 Lancet publication claiming that the combination measles, mumps, and rubella (MMR) vaccine caused autism. The purpose of the editorial was to make the further point that this was indeed an elaborate fraud. It wasn't just that he was wrong -- it was that it was fraudulent and wrong.
I'm sure many of you know that what Dr. Wakefield claimed was that because the MMR vaccine was given as a combination vaccine, it overwhelmed the immune system, allowing the measles component of that vaccine to enter the intestines and cause intestinal damage, which allowed for the ingress of encephalopathic proteins. Not a single aspect of that hypothesis was correct, and more importantly, nothing was studied, because Dr. Wakefield's initial publication was merely a case series. The studies were to come later, and there were 14 of them that looked at hundreds of thousands of children who either did or didn't receive the MMR vaccine. These studies found that the incidence of autism, not surprisingly, was the same in the vaccinated group as it was in the unvaccinated group.
So what did we learn from this? What disappoints me about the British Medical Journal editorial was that the focus was on fraud -- that essentially this man should not be believed because he was fraudulent. But to me it doesn't matter whether you're fraudulent and wrong. In this case, the only thing that matters was that he was wrong and that his paper certainly did a lot of damage. Thousands of parents in England chose to not vaccinate their children. Hundreds were hospitalized and 4 were killed. Three in Ireland and 1 in London died because their parents feared the MMR vaccine more than they feared the measles. You could argue that the Wakefield paper killed 4 children.
I'd like to think that in the future we'd be more circumspect. When an article that could have a tremendous negative impact on the public's health is submitted for publication, both journal reviewers as well as the media should be far more circumspect. Thanks for your attention
Paul A. Offit, MD
Hi. My name is Paul Offit. I'm talking to you today from the Division of Infectious Diseases and the Vaccine Education Center at Children's Hospital, Philadelphia. I'm sure many of you know that an editorial was published in the British Medical Journal [1,2] on January 5, 2011, looking at the issue of Andrew Wakefield and his 1998 Lancet publication claiming that the combination measles, mumps, and rubella (MMR) vaccine caused autism. The purpose of the editorial was to make the further point that this was indeed an elaborate fraud. It wasn't just that he was wrong -- it was that it was fraudulent and wrong.
I'm sure many of you know that what Dr. Wakefield claimed was that because the MMR vaccine was given as a combination vaccine, it overwhelmed the immune system, allowing the measles component of that vaccine to enter the intestines and cause intestinal damage, which allowed for the ingress of encephalopathic proteins. Not a single aspect of that hypothesis was correct, and more importantly, nothing was studied, because Dr. Wakefield's initial publication was merely a case series. The studies were to come later, and there were 14 of them that looked at hundreds of thousands of children who either did or didn't receive the MMR vaccine. These studies found that the incidence of autism, not surprisingly, was the same in the vaccinated group as it was in the unvaccinated group.
So what did we learn from this? What disappoints me about the British Medical Journal editorial was that the focus was on fraud -- that essentially this man should not be believed because he was fraudulent. But to me it doesn't matter whether you're fraudulent and wrong. In this case, the only thing that matters was that he was wrong and that his paper certainly did a lot of damage. Thousands of parents in England chose to not vaccinate their children. Hundreds were hospitalized and 4 were killed. Three in Ireland and 1 in London died because their parents feared the MMR vaccine more than they feared the measles. You could argue that the Wakefield paper killed 4 children.
I'd like to think that in the future we'd be more circumspect. When an article that could have a tremendous negative impact on the public's health is submitted for publication, both journal reviewers as well as the media should be far more circumspect. Thanks for your attention
Monday, January 17, 2011
FDA Limits Acetaminophen in Prescription Analgesics
From Medscape Medical News > Alerts,
Robert Lowes
January 13, 2011 — The US Food and Drug Administration (FDA) today announced that it is asking drug makers to limit the amount of acetaminophen in prescription combination pain relievers to no more than 325 mg per tablet or capsule to reduce overdoses and the severe liver injury that can follow.
The decision, to be phased in over 3 years, affects dozens of prescription analgesics that contain both acetaminophen and another ingredient, typically opioids such as codeine, oxycodone, and hydrocodone. Some of these combination products now have as much as 750 mg of acetaminophen per dose.
The new dose restriction does not apply to numerous over-the-counter (OTC) pain relievers and cold, sinus, and cough medicines that contain acetaminophen. Normally, the maximum level allowed for these products is 500 mg, although a few extended-action pain relievers that are taken less frequently can go up to 650 mg.
The FDA also is requiring manufacturers to update the labels of all prescription products containing acetaminophen with a boxed warning on the risk of severe liver injury if too much of the ingredient is taken or consumed with alcohol.
Agency officials stress that patients prescribed analgesics with acetaminophen at doses above 325 mg can safely continue to take them under a physician’s supervision.
The key to safety, they say, is not exceeding the maximum daily dose of 4000 mg, whether it comes in the form of prescription medications, OTC medications, or both.
"When taken as directed, acetaminophen is a very safe product, and our goal is to make it safer," said Sandra Kweder, MD, deputy director of the Office of New Drugs in the FDA’s Center for Drug Evaluation and Research, at a press conference today.
Accidental overdoses are all too common because patients may be taking a cough medicine containing the ingredient, for example, as well as a prescription analgesic for back pain without knowing the latter also includes acetaminophen. That mistake can easily happen, said Dr. Kweder, because labels for prescription analgesics do not make it crystal clear that acetaminophen is an ingredient. They often use an abbreviation for the medication — APAP — that consumers may not understand.
Overdoses from prescription combination analgesics account for nearly half of all cases of acetaminophen-related liver failure, which often leads to liver transplantation or death, according to the FDA.
More information about today’s announcement is available on the FDA Web site.
To report adverse events related to products containing acetaminophen, contact MedWatch, the FDA's safety information and adverse event reporting program, by telephone at 1-800-FDA-1088, by fax at 1-800-FDA-0178, online at http://www.fda.gov/medwatch, or by mail to MedWatch, FDA, 5600 Fishers Lane, Rockville, Maryland 20852-9787.
Robert Lowes
January 13, 2011 — The US Food and Drug Administration (FDA) today announced that it is asking drug makers to limit the amount of acetaminophen in prescription combination pain relievers to no more than 325 mg per tablet or capsule to reduce overdoses and the severe liver injury that can follow.
The decision, to be phased in over 3 years, affects dozens of prescription analgesics that contain both acetaminophen and another ingredient, typically opioids such as codeine, oxycodone, and hydrocodone. Some of these combination products now have as much as 750 mg of acetaminophen per dose.
The new dose restriction does not apply to numerous over-the-counter (OTC) pain relievers and cold, sinus, and cough medicines that contain acetaminophen. Normally, the maximum level allowed for these products is 500 mg, although a few extended-action pain relievers that are taken less frequently can go up to 650 mg.
The FDA also is requiring manufacturers to update the labels of all prescription products containing acetaminophen with a boxed warning on the risk of severe liver injury if too much of the ingredient is taken or consumed with alcohol.
Agency officials stress that patients prescribed analgesics with acetaminophen at doses above 325 mg can safely continue to take them under a physician’s supervision.
The key to safety, they say, is not exceeding the maximum daily dose of 4000 mg, whether it comes in the form of prescription medications, OTC medications, or both.
"When taken as directed, acetaminophen is a very safe product, and our goal is to make it safer," said Sandra Kweder, MD, deputy director of the Office of New Drugs in the FDA’s Center for Drug Evaluation and Research, at a press conference today.
Accidental overdoses are all too common because patients may be taking a cough medicine containing the ingredient, for example, as well as a prescription analgesic for back pain without knowing the latter also includes acetaminophen. That mistake can easily happen, said Dr. Kweder, because labels for prescription analgesics do not make it crystal clear that acetaminophen is an ingredient. They often use an abbreviation for the medication — APAP — that consumers may not understand.
Overdoses from prescription combination analgesics account for nearly half of all cases of acetaminophen-related liver failure, which often leads to liver transplantation or death, according to the FDA.
More information about today’s announcement is available on the FDA Web site.
To report adverse events related to products containing acetaminophen, contact MedWatch, the FDA's safety information and adverse event reporting program, by telephone at 1-800-FDA-1088, by fax at 1-800-FDA-0178, online at http://www.fda.gov/medwatch, or by mail to MedWatch, FDA, 5600 Fishers Lane, Rockville, Maryland 20852-9787.
Friday, January 14, 2011
DHHS Updates Treatment Guidelines for HIV-Infected Adults, Teens
From Medscape Medical News
Laurie Barclay, MD
January 13, 2011 — The Department of Health and Human Services (DHHS) Panel on Antiretroviral Guidelines for Adults and Adolescents has updated guidelines for the use of antiretroviral (ARV) agents for HIV-1-infection in this population. The guidelines were posted online January 10.
The DHHS panel, a working group of the Office of AIDS Research Advisory Council, aimed to provide recommendations for clinicians based on current evidence regarding ARV drugs used to treat adults and adolescents with HIV infection in the United States. The new guidelines, which update those issued December 1, 2009, highlight baseline evaluation; treatment goals; indications to begin ARV therapy (ART); choice of initial therapy in ART-naive patients; drugs or combinations that should be avoided; management of adverse effects, drug interactions, and treatment failure; and specific ART-related considerations applicable to various patient subgroups.
"...ART for the treatment of ...HIV infection has improved steadily since the advent of potent combination therapy in 1996," write panel co-chairs John G. Bartlett, MD, from Johns Hopkins University in Baltimore, Maryland, and H. Clifford Lane, MD, from National Institutes of Health in Bethesda, Maryland, and colleagues. "New drugs have been approved that offer new mechanisms of action, improvements in potency and activity even against multidrug-resistant viruses, dosing convenience, and tolerability."
Specific Updated Changes
Specific changes in these updated guidelines from the December 1, 2009, version of the guidelines include the following:
* The DHHS panel highlighted the importance of clinical research to answer remaining questions concerning the optimal safety and efficacy of ART, and it therefore encourages both protocol development and patient enrollment in well-designed, Institutional Review Board–approved clinical trials.
* For a patient receiving a suppressive ART regimen with a CD4 T-cell count well above the threshold for risk for opportunistic infection, clinicians seldom use changes in CD4 T-cell count to make decisions regarding ART changes. Therefore, the panel now recommends that the CD4 T-cell count may be monitored less often in such patients, such as every 6 to 12 months vs every 3 to 6 months, provided there are no clinical status changes, including the patient having new HIV-associated clinical symptoms or beginning treatment with interferon, corticosteroids, or antineoplastic agents.
* For some viral load assays, low-level positive viral load results (usually < 200 copies/mL) have been commonly reported. To eliminate most cases of viremia caused by isolated blips or test variability, the panel now defines virologic failure as a confirmed viral load of more than 200 copies/mL for the purpose of patient monitoring.
Recommendations on Drug-Resistance Testing
New recommendations regarding drug-resistance testing include the following:
* More specific recommendations are given regarding when to use genotypic testing to identify resistance to integrase strand transfer inhibitors (INSTIs).
* If transmitted INSTI resistance is suspected, it may be helpful to include genotypic testing for INSTI resistance because standard genotypic drug-resistance testing involves testing only for mutations in the reverse transcriptase and protease genes.
* For patients in whom an INSTI-based regimen fails, genotypic testing for INSTI resistance should be considered to help decide whether a drug from this class should be included in subsequent regimens.
Combination Regimens
Changes to the "What to Start" recommendations regarding initial combination regimens for the ARV-naive patient include the following:
* Maraviroc plus zidovudine/lamivudine is now considered to be an "Acceptable Regimen" after US Food and Drug Adminstration approval of maraviroc for use in ART-naive patients, based on findings from a randomized controlled trial using maraviroc plus zidovudine/lamivudine.
* Maraviroc plus tenofovir/emtricitabine and maraviroc plus abacavir/lamivudine are now considered to be regimens that may be acceptable, although additional definitive data are needed.
* Ritonavir-boosted saquinavir–based regimens are now designated as "Regimens that are Acceptable but Should be Used with Caution" vs "Alternative PI[Protease Inhibitor]-based Regimens." This change reflects a recent change in the Invirase (Roche Laboratories) product label because significant PR and QT interval prolongations were found in a healthy volunteer study.
Coinfection With Hepatitis B Virus
More specific recommendations are offered for treatment of patients with HIV coinfected with hepatitis B virus, including recommendations for patients with lamivudine/emtricitabine–resistant hepatitis B virus infection and for those unable to tolerate tenofovir-based regimens.
Coinfection With Tuberculosis
Updates to management of Mycobacterium tuberculosis/HIV coinfection reflect survival and clinical benefits of starting ART earlier in treatment-naive patients with active tuberculosis (TB) disease, based on findings from recent randomized controlled trials. The following recommendations address initiating ART in patients being treated for active TB but not yet on ART:
* ART should be given to all HIV-infected patients with diagnosed active TB.
* Patients with a CD4 T-cell count of less than 200 cells/mm3 should start ART within 2 to 4 weeks of starting TB treatment.
* Patients with a CD4 T-cell count of 200 to 500 cells/mm3 should start ART within 2 to 4 weeks, or at least by 8 weeks after starting TB treatment.
* Most panel members also recommend that patients with a CD4 T-cell count of more than 500 cells/mm3 start ART within 8 weeks of TB therapy.
New Table Formats
The most common and/or severe known ARV-associated adverse events, listed by ARV drug class, are displayed in a new table format.
Several sections and pertinent tables have also been updated, including those on coreceptor tropism assays, treatment goals, starting ART in treatment-naive patients, what drugs and regimens not to use, virologic and immunologic failure, regimen simplification, exposure-response relationship and therapeutic drug monitoring for ARV agents, acute HIV infection, HIV and illicit drug users, HIV-2 infection, drug interactions, and drug characteristics.
"The provider can make recommendations most likely to lead to positive outcomes only if the patient's own point of view and social context are well known," the panel concludes. "...The Panel anticipates continued progress in the simplicity of regimens, improved potency and barrier to resistance, and reduced toxicity. The Panel hopes the guidelines are useful and is committed to their continued adjustment and improvement."
Financial disclosures for members of the DHHS Panel on Antiretroviral Guidelines for Adults and Adolescents are available on the DHHS' AIDS Info site.
Panel on Antiretroviral Guidelines for Adults and Adolescents. Guidelines for the use of antiretroviral agents in HIV-1-infected adults and adolescents. Department of Health and Human Services. January 10, 2011.
Laurie Barclay, MD
January 13, 2011 — The Department of Health and Human Services (DHHS) Panel on Antiretroviral Guidelines for Adults and Adolescents has updated guidelines for the use of antiretroviral (ARV) agents for HIV-1-infection in this population. The guidelines were posted online January 10.
The DHHS panel, a working group of the Office of AIDS Research Advisory Council, aimed to provide recommendations for clinicians based on current evidence regarding ARV drugs used to treat adults and adolescents with HIV infection in the United States. The new guidelines, which update those issued December 1, 2009, highlight baseline evaluation; treatment goals; indications to begin ARV therapy (ART); choice of initial therapy in ART-naive patients; drugs or combinations that should be avoided; management of adverse effects, drug interactions, and treatment failure; and specific ART-related considerations applicable to various patient subgroups.
"...ART for the treatment of ...HIV infection has improved steadily since the advent of potent combination therapy in 1996," write panel co-chairs John G. Bartlett, MD, from Johns Hopkins University in Baltimore, Maryland, and H. Clifford Lane, MD, from National Institutes of Health in Bethesda, Maryland, and colleagues. "New drugs have been approved that offer new mechanisms of action, improvements in potency and activity even against multidrug-resistant viruses, dosing convenience, and tolerability."
Specific Updated Changes
Specific changes in these updated guidelines from the December 1, 2009, version of the guidelines include the following:
* The DHHS panel highlighted the importance of clinical research to answer remaining questions concerning the optimal safety and efficacy of ART, and it therefore encourages both protocol development and patient enrollment in well-designed, Institutional Review Board–approved clinical trials.
* For a patient receiving a suppressive ART regimen with a CD4 T-cell count well above the threshold for risk for opportunistic infection, clinicians seldom use changes in CD4 T-cell count to make decisions regarding ART changes. Therefore, the panel now recommends that the CD4 T-cell count may be monitored less often in such patients, such as every 6 to 12 months vs every 3 to 6 months, provided there are no clinical status changes, including the patient having new HIV-associated clinical symptoms or beginning treatment with interferon, corticosteroids, or antineoplastic agents.
* For some viral load assays, low-level positive viral load results (usually < 200 copies/mL) have been commonly reported. To eliminate most cases of viremia caused by isolated blips or test variability, the panel now defines virologic failure as a confirmed viral load of more than 200 copies/mL for the purpose of patient monitoring.
Recommendations on Drug-Resistance Testing
New recommendations regarding drug-resistance testing include the following:
* More specific recommendations are given regarding when to use genotypic testing to identify resistance to integrase strand transfer inhibitors (INSTIs).
* If transmitted INSTI resistance is suspected, it may be helpful to include genotypic testing for INSTI resistance because standard genotypic drug-resistance testing involves testing only for mutations in the reverse transcriptase and protease genes.
* For patients in whom an INSTI-based regimen fails, genotypic testing for INSTI resistance should be considered to help decide whether a drug from this class should be included in subsequent regimens.
Combination Regimens
Changes to the "What to Start" recommendations regarding initial combination regimens for the ARV-naive patient include the following:
* Maraviroc plus zidovudine/lamivudine is now considered to be an "Acceptable Regimen" after US Food and Drug Adminstration approval of maraviroc for use in ART-naive patients, based on findings from a randomized controlled trial using maraviroc plus zidovudine/lamivudine.
* Maraviroc plus tenofovir/emtricitabine and maraviroc plus abacavir/lamivudine are now considered to be regimens that may be acceptable, although additional definitive data are needed.
* Ritonavir-boosted saquinavir–based regimens are now designated as "Regimens that are Acceptable but Should be Used with Caution" vs "Alternative PI[Protease Inhibitor]-based Regimens." This change reflects a recent change in the Invirase (Roche Laboratories) product label because significant PR and QT interval prolongations were found in a healthy volunteer study.
Coinfection With Hepatitis B Virus
More specific recommendations are offered for treatment of patients with HIV coinfected with hepatitis B virus, including recommendations for patients with lamivudine/emtricitabine–resistant hepatitis B virus infection and for those unable to tolerate tenofovir-based regimens.
Coinfection With Tuberculosis
Updates to management of Mycobacterium tuberculosis/HIV coinfection reflect survival and clinical benefits of starting ART earlier in treatment-naive patients with active tuberculosis (TB) disease, based on findings from recent randomized controlled trials. The following recommendations address initiating ART in patients being treated for active TB but not yet on ART:
* ART should be given to all HIV-infected patients with diagnosed active TB.
* Patients with a CD4 T-cell count of less than 200 cells/mm3 should start ART within 2 to 4 weeks of starting TB treatment.
* Patients with a CD4 T-cell count of 200 to 500 cells/mm3 should start ART within 2 to 4 weeks, or at least by 8 weeks after starting TB treatment.
* Most panel members also recommend that patients with a CD4 T-cell count of more than 500 cells/mm3 start ART within 8 weeks of TB therapy.
New Table Formats
The most common and/or severe known ARV-associated adverse events, listed by ARV drug class, are displayed in a new table format.
Several sections and pertinent tables have also been updated, including those on coreceptor tropism assays, treatment goals, starting ART in treatment-naive patients, what drugs and regimens not to use, virologic and immunologic failure, regimen simplification, exposure-response relationship and therapeutic drug monitoring for ARV agents, acute HIV infection, HIV and illicit drug users, HIV-2 infection, drug interactions, and drug characteristics.
"The provider can make recommendations most likely to lead to positive outcomes only if the patient's own point of view and social context are well known," the panel concludes. "...The Panel anticipates continued progress in the simplicity of regimens, improved potency and barrier to resistance, and reduced toxicity. The Panel hopes the guidelines are useful and is committed to their continued adjustment and improvement."
Financial disclosures for members of the DHHS Panel on Antiretroviral Guidelines for Adults and Adolescents are available on the DHHS' AIDS Info site.
Panel on Antiretroviral Guidelines for Adults and Adolescents. Guidelines for the use of antiretroviral agents in HIV-1-infected adults and adolescents. Department of Health and Human Services. January 10, 2011.
ACIP Updates Guidelines for Use of Tdap Vaccine
From Medscape Medical News
Laurie Barclay, MD
January 14, 2011 — Vaccination with tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis (Tdap) vaccine is the best way for adolescents and adults to protect themselves and others against pertussis, according to updated recommendations for use of Tdap from the Advisory Committee on Immunization Practices (ACIP), published in the January 14 issue of Morbidity and Mortality Weekly Report.
Tdap vaccine for adults and DTaP vaccine for infants
A 1-time dose of Tdap vaccine is recommended for all adolescents and adults to boost their immunity to pertussis. In 2009, there were 16,858 pertussis cases and 12 infant deaths reported to the US Centers for Disease Control and Prevention. The report of the updated guidelines also summarizes safety and efficacy data reviewed by the ACIP and offers guidance for implementing the recommendations.
"Despite sustained high coverage for childhood pertussis vaccination, pertussis remains poorly controlled in the United States," the guidelines authors write. "Although 2005 recommendations by the ...ACIP called for vaccination with ...Tdap for adolescents and adults to improve immunity against pertussis, Tdap coverage is 56% among adolescents and <6% among adults. In October 2010, ACIP recommended expanded use of Tdap."
In the United States, 2 Tdap vaccines are available: Boostrix (GlaxoSmithKline Biologicals, Rixensart, Belgium) licensed for use in persons aged 10 through 64 years old, and Adacel (Sanofi Pasteur, Toronto, Canada) licensed for use in persons aged 11 through 64 years.
Specific recommendations in the updated guidelines include the following:
* A single dose of Tdap should be given routinely to adults aged 19 through 64 years and also to adolescents aged 11 through 18 years who completed the recommended childhood diphtheria and tetanus toxoids and pertussis/diphtheria and tetanus toxoids and acellular pertussis (DTP/DTaP) vaccination series.
* Tdap should preferably be given to adolescents at their 11- to 12-year-old preventive healthcare visit.
* Tdap can be given regardless of the time elapsed since the last vaccine containing tetanus toxoid or diphtheria toxoid.
* Tdap should be given to adults 65 years or older who are or who anticipate being in close contact with an infant younger than 12 months. A single dose of Tdap may also be given to other adults 65 years or older.
* A single dose of Tdap should be given to children aged 7 through 10 years who are not fully vaccinated against pertussis (5 doses of DTaP or 4 doses of DTaP if the fourth dose was given on or after the fourth birthday), provided they have no contraindication to pertussis vaccine.
* Children aged 7 through 10 years who were never vaccinated against tetanus, diphtheria, or pertussis, or who have unknown vaccination status, should receive a series of 3 vaccinations containing tetanus and diphtheria toxoids, with Tdap as the first of these 3 doses.
"ACIP recommends that pertussis vaccination, when indicated, should not be delayed and that Tdap should be administered regardless of interval since the last tetanus or diphtheria toxoid-containing vaccine," the report authors write.
"ACIP concluded that while longer intervals between Td and Tdap vaccination could decrease the occurrence of local reactions, the benefits of protection against pertussis outweigh the potential risk for adverse events."
MMWR Morb Mortal Wkly Rep. 2011;60:13-15. Abstract
Laurie Barclay, MD
January 14, 2011 — Vaccination with tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis (Tdap) vaccine is the best way for adolescents and adults to protect themselves and others against pertussis, according to updated recommendations for use of Tdap from the Advisory Committee on Immunization Practices (ACIP), published in the January 14 issue of Morbidity and Mortality Weekly Report.
Tdap vaccine for adults and DTaP vaccine for infants
A 1-time dose of Tdap vaccine is recommended for all adolescents and adults to boost their immunity to pertussis. In 2009, there were 16,858 pertussis cases and 12 infant deaths reported to the US Centers for Disease Control and Prevention. The report of the updated guidelines also summarizes safety and efficacy data reviewed by the ACIP and offers guidance for implementing the recommendations.
"Despite sustained high coverage for childhood pertussis vaccination, pertussis remains poorly controlled in the United States," the guidelines authors write. "Although 2005 recommendations by the ...ACIP called for vaccination with ...Tdap for adolescents and adults to improve immunity against pertussis, Tdap coverage is 56% among adolescents and <6% among adults. In October 2010, ACIP recommended expanded use of Tdap."
In the United States, 2 Tdap vaccines are available: Boostrix (GlaxoSmithKline Biologicals, Rixensart, Belgium) licensed for use in persons aged 10 through 64 years old, and Adacel (Sanofi Pasteur, Toronto, Canada) licensed for use in persons aged 11 through 64 years.
Specific recommendations in the updated guidelines include the following:
* A single dose of Tdap should be given routinely to adults aged 19 through 64 years and also to adolescents aged 11 through 18 years who completed the recommended childhood diphtheria and tetanus toxoids and pertussis/diphtheria and tetanus toxoids and acellular pertussis (DTP/DTaP) vaccination series.
* Tdap should preferably be given to adolescents at their 11- to 12-year-old preventive healthcare visit.
* Tdap can be given regardless of the time elapsed since the last vaccine containing tetanus toxoid or diphtheria toxoid.
* Tdap should be given to adults 65 years or older who are or who anticipate being in close contact with an infant younger than 12 months. A single dose of Tdap may also be given to other adults 65 years or older.
* A single dose of Tdap should be given to children aged 7 through 10 years who are not fully vaccinated against pertussis (5 doses of DTaP or 4 doses of DTaP if the fourth dose was given on or after the fourth birthday), provided they have no contraindication to pertussis vaccine.
* Children aged 7 through 10 years who were never vaccinated against tetanus, diphtheria, or pertussis, or who have unknown vaccination status, should receive a series of 3 vaccinations containing tetanus and diphtheria toxoids, with Tdap as the first of these 3 doses.
"ACIP recommends that pertussis vaccination, when indicated, should not be delayed and that Tdap should be administered regardless of interval since the last tetanus or diphtheria toxoid-containing vaccine," the report authors write.
"ACIP concluded that while longer intervals between Td and Tdap vaccination could decrease the occurrence of local reactions, the benefits of protection against pertussis outweigh the potential risk for adverse events."
MMWR Morb Mortal Wkly Rep. 2011;60:13-15. Abstract
Parental Smoking Ups BP of Kids Aged Four and Five
From Heartwire
Lisa Nainggolan
January 14, 2011 (Heidelberg, Germany) — The preschool children of smokers have a 20% increased risk of having blood pressure in the highest normal value even after other risk factors are adjusted for, new research from Germany shows [1]. This is the first study to show that breathing tobacco smoke increases the BP of children as young as four or five, say Dr Giacomo D Simonetti (University of Berne, Switzerland) and colleagues in their paper published online January 10, 2011 in Circulation.
Simonetti, who conducted the research while working at the University of Heidelberg in Germany, told heartwire : "Parental smoking is not only negative for children's lung function, it poses a risk to their future cardiovascular health.
We know childhood BP tracks to adult BP, so the most important conclusion here is that if you avoid risk factors--such as secondhand smoke--as a child, you will have lower BP and probably lower BP values as an adult."
The findings "complete the picture of tobacco exposure interfering with cardiovascular maturation and health from gestation to adulthood," say Simonetti and colleagues.
He adds that parents should be counseled to stop smoking, as the benefits would likely extend even to the youngest family members.
And at the very least, a strictly smoke-free environment should be implemented in the home.
Maternal Smoking Had More Impact Than Paternal Smoking
In an extension of a standard school health exam, Simonetti and colleagues measured the BP of 4236 kindergarten boys and girls (average age 5.7). Parents had to say whether they smoked or not: in 28.5% of the families the father smoked; in 20.7% it was the mother; and in 11.9% of cases, both parents were smokers. The mean number of cigarettes smoked per day was 11.6 for mothers and 13.9 for fathers.
Children with a smoking parent were 21% more likely to have systolic blood pressure in the highest normal value (ie, above the 85th percentile). Although this is a small BP-raising effect, it was consistent and remained significant event even after adjustment for all known risk factors that could influence BP--including body-mass index and height of the children and whether the mother suffered from pregnancy-related hypertension, for example.
Simonetti said they did not try to differentiate between people who did not smoke in the home and those who did, because this would have been too difficult to determine. Of interest, smoking by mothers had a larger impact than smoking by fathers, probably because more of their smoking was done in the home, while fathers smoked more at their workplaces, he suggests.
"Smoking adds to other risk factors," says Simonetti. "Passive smoking increased the risk of having blood pressure at the upper end of normal, and some of these children already had high blood pressure."
"The findings of this study add an important pediatric perspective to the issue of prevention and containment of active and passive smoking," he and his colleagues conclude.
Lisa Nainggolan
January 14, 2011 (Heidelberg, Germany) — The preschool children of smokers have a 20% increased risk of having blood pressure in the highest normal value even after other risk factors are adjusted for, new research from Germany shows [1]. This is the first study to show that breathing tobacco smoke increases the BP of children as young as four or five, say Dr Giacomo D Simonetti (University of Berne, Switzerland) and colleagues in their paper published online January 10, 2011 in Circulation.
Simonetti, who conducted the research while working at the University of Heidelberg in Germany, told heartwire : "Parental smoking is not only negative for children's lung function, it poses a risk to their future cardiovascular health.
We know childhood BP tracks to adult BP, so the most important conclusion here is that if you avoid risk factors--such as secondhand smoke--as a child, you will have lower BP and probably lower BP values as an adult."
The findings "complete the picture of tobacco exposure interfering with cardiovascular maturation and health from gestation to adulthood," say Simonetti and colleagues.
He adds that parents should be counseled to stop smoking, as the benefits would likely extend even to the youngest family members.
And at the very least, a strictly smoke-free environment should be implemented in the home.
Maternal Smoking Had More Impact Than Paternal Smoking
In an extension of a standard school health exam, Simonetti and colleagues measured the BP of 4236 kindergarten boys and girls (average age 5.7). Parents had to say whether they smoked or not: in 28.5% of the families the father smoked; in 20.7% it was the mother; and in 11.9% of cases, both parents were smokers. The mean number of cigarettes smoked per day was 11.6 for mothers and 13.9 for fathers.
Children with a smoking parent were 21% more likely to have systolic blood pressure in the highest normal value (ie, above the 85th percentile). Although this is a small BP-raising effect, it was consistent and remained significant event even after adjustment for all known risk factors that could influence BP--including body-mass index and height of the children and whether the mother suffered from pregnancy-related hypertension, for example.
Simonetti said they did not try to differentiate between people who did not smoke in the home and those who did, because this would have been too difficult to determine. Of interest, smoking by mothers had a larger impact than smoking by fathers, probably because more of their smoking was done in the home, while fathers smoked more at their workplaces, he suggests.
"Smoking adds to other risk factors," says Simonetti. "Passive smoking increased the risk of having blood pressure at the upper end of normal, and some of these children already had high blood pressure."
"The findings of this study add an important pediatric perspective to the issue of prevention and containment of active and passive smoking," he and his colleagues conclude.
Monday, January 10, 2011
HHS Recommends Lower Fluoride Levels in Drinking Water
From Medscape Medical News
Robert Lowes
January 10, 2011 — Two federal agencies have announced that they are taking new measures to reduce levels of fluoride in drinking water because Americans increasingly encounter the mineral from other sources, such as fluoridated toothpaste.
The overriding goal of the US Department of Health and Human Services (HHS) and the Environmental Protection Agency (EPA) is to reverse a slow rise in fluorosis, which leads to cracks in the enamel and discoloration of the teeth. In extreme cases, it also may adversely affect bone, increasing fracture risk.
At the same time, federal health officials affirmed the value and safety of adding fluoride to drinking water to prevent tooth decay.
"The Centers for Disease Control and Prevention...has named community water fluoridation as 1 of the 10 top public health achievements of the 20th century," said Howard Koh, MD, MPH, assistant secretary for health at HHS in a press conference January 7.
"It still remains a cost-effective method of delivering fluoride to all members of a community to prevent and control tooth decay and improve oral health."
This stance immediately drew fire from fluoridation opponents, who claim the mineral is a public health threat.
HHS proposes to lower its recommended optimal level for community water fluoridation from a range of 0.7 to 1.2 mg/L to the single figure at the lower end — 0.7 mg/L. Local municipalities that opt to fluoridate their water supplies stay within this range, with the average concentration being 0.8 mg/L, Cynthia Dougherty, director of the Office of Ground water and Drinking Water at the EPA, said at the news conference.
Meanwhile, the EPA will consider whether it should lower its current maximum allowable level of fluoride, now set at 4 mg/L. The agency is following the recommendation of the National Academies of Science, which in 2006 called for an updated assessment of the mineral's effect on teeth and bone that accounts for all sources of exposure.
Too Much Fluoride Can Damage Bones
The HHS and EPA fluoride levels serve 2 different purposes. The recommended HHS concentration refers to a fluoride level high enough to effectively reduce the incidence of tooth decay, while minimizing the rate of fluorosis. The EPA standard of 4 mg/L, which is the law, as opposed to a recommendation, is the maximum concentration of fluoride that is considered safe.
State regulations on fluoride levels must be as strict as the EPA's, although states are free to set the bar lower, and some have done so, said Jim Taft, executive director of a group called the Association of State Drinking Water Administrators, in an interview with Medscape Medical News.
HHS and EPA are revisiting the subject of fluoride concentration levels in water because sources of fluoride exposure have become more plentiful. For starters, almost all water contains naturally occurring fluoride, but US communities also began adding the mineral to their water supplies more than 60 years ago to prevent tooth decay. As a result, Americans took in fluoride not only from drinking water but also from foods and beverages prepared with fluoridated water. Since the early 1960s, fluoride also has found its way into consumer dental products such as toothpaste and mouthwash, as well as professionally applied dental varnishes and gels.
More fluoride exposure has been accompanied by higher rates of dental fluorosis. In about 92% of cases, the condition is mild, appearing as white spots on the teeth, according to HHS.
In severe but rare cases, fluorosis can leave the teeth pitted. Children aged 8 years and younger are at greatest risk for fluorosis and possible pitting because fluoride adversely affects their teeth while they are still forming.
In addition, excessive fluoride consumption during a lifetime may lead to skeletal fluorosis, which may increase the likelihood of bone pain, tenderness, and fracture, as well as disrupt endocrine and neurological processes.
By lowering the recommended optimal level of fluoride in drinking water to 0.7 mg/L, HHS hopes to compensate for increased fluoride exposure elsewhere. In addition, studies show that although tooth decay gradually declines as fluoride concentrations approach 0.7 mg/L, there is little change in tooth decay between that level and 1.2 mg/L.
The proposed recommendation will soon be published in the Federal Register. HHS will accept comments from the public for 30 days. It expects to issue a final recommendation for community water fluoridation by this spring.
Fluoridation Opponents Not Impressed
The move by HSS to lower fluoride levels in drinking water met with kudos from the American Dental Association.
"This is a superb example of a government agency fulfilling its mission to protect and enhance the health of the American people," said American Dental Association President Raymond Gist, DDS. "The recommended levels for optimal fluoridation may be reduced, but the health benefits of fluoridation remain."
Opponents of fluoridated water, in contrast, were not impressed.
"[The federal government is] trying to keep the issue focused on teeth, when the science is becoming clearer and clearer that fluoride damages other tissues," said Paul Connett, PhD, executive director of the Fluoride Action Network based in Canton, New York. His group asserts that health risks associated with low to moderate doses of fluoride include joint pain, skin rash, reduced thyroid activity, bone cancer, and even IQ deficits. A recent study published in a peer-reviewed journal of the federal National Institute of Environmental Health Sciences suggests such a link between fluoride and intelligence.
Dr. Connett, a professor emeritus of environmental chemistry at St. Lawrence University in Canton, told Medscape Medical News that the United States should stop fluoridating water and instead address the root causes of tooth decay — poverty and poor diet.
"There is no difference in dental caries between fluoridated and nonfluoridated countries, fluoridated and nonfluoridated states, and fluoridated and nonfluoridated cities," added Dr. Connett.
Robert Lowes
January 10, 2011 — Two federal agencies have announced that they are taking new measures to reduce levels of fluoride in drinking water because Americans increasingly encounter the mineral from other sources, such as fluoridated toothpaste.
The overriding goal of the US Department of Health and Human Services (HHS) and the Environmental Protection Agency (EPA) is to reverse a slow rise in fluorosis, which leads to cracks in the enamel and discoloration of the teeth. In extreme cases, it also may adversely affect bone, increasing fracture risk.
At the same time, federal health officials affirmed the value and safety of adding fluoride to drinking water to prevent tooth decay.
"The Centers for Disease Control and Prevention...has named community water fluoridation as 1 of the 10 top public health achievements of the 20th century," said Howard Koh, MD, MPH, assistant secretary for health at HHS in a press conference January 7.
"It still remains a cost-effective method of delivering fluoride to all members of a community to prevent and control tooth decay and improve oral health."
This stance immediately drew fire from fluoridation opponents, who claim the mineral is a public health threat.
HHS proposes to lower its recommended optimal level for community water fluoridation from a range of 0.7 to 1.2 mg/L to the single figure at the lower end — 0.7 mg/L. Local municipalities that opt to fluoridate their water supplies stay within this range, with the average concentration being 0.8 mg/L, Cynthia Dougherty, director of the Office of Ground water and Drinking Water at the EPA, said at the news conference.
Meanwhile, the EPA will consider whether it should lower its current maximum allowable level of fluoride, now set at 4 mg/L. The agency is following the recommendation of the National Academies of Science, which in 2006 called for an updated assessment of the mineral's effect on teeth and bone that accounts for all sources of exposure.
Too Much Fluoride Can Damage Bones
The HHS and EPA fluoride levels serve 2 different purposes. The recommended HHS concentration refers to a fluoride level high enough to effectively reduce the incidence of tooth decay, while minimizing the rate of fluorosis. The EPA standard of 4 mg/L, which is the law, as opposed to a recommendation, is the maximum concentration of fluoride that is considered safe.
State regulations on fluoride levels must be as strict as the EPA's, although states are free to set the bar lower, and some have done so, said Jim Taft, executive director of a group called the Association of State Drinking Water Administrators, in an interview with Medscape Medical News.
HHS and EPA are revisiting the subject of fluoride concentration levels in water because sources of fluoride exposure have become more plentiful. For starters, almost all water contains naturally occurring fluoride, but US communities also began adding the mineral to their water supplies more than 60 years ago to prevent tooth decay. As a result, Americans took in fluoride not only from drinking water but also from foods and beverages prepared with fluoridated water. Since the early 1960s, fluoride also has found its way into consumer dental products such as toothpaste and mouthwash, as well as professionally applied dental varnishes and gels.
More fluoride exposure has been accompanied by higher rates of dental fluorosis. In about 92% of cases, the condition is mild, appearing as white spots on the teeth, according to HHS.
In severe but rare cases, fluorosis can leave the teeth pitted. Children aged 8 years and younger are at greatest risk for fluorosis and possible pitting because fluoride adversely affects their teeth while they are still forming.
In addition, excessive fluoride consumption during a lifetime may lead to skeletal fluorosis, which may increase the likelihood of bone pain, tenderness, and fracture, as well as disrupt endocrine and neurological processes.
By lowering the recommended optimal level of fluoride in drinking water to 0.7 mg/L, HHS hopes to compensate for increased fluoride exposure elsewhere. In addition, studies show that although tooth decay gradually declines as fluoride concentrations approach 0.7 mg/L, there is little change in tooth decay between that level and 1.2 mg/L.
The proposed recommendation will soon be published in the Federal Register. HHS will accept comments from the public for 30 days. It expects to issue a final recommendation for community water fluoridation by this spring.
Fluoridation Opponents Not Impressed
The move by HSS to lower fluoride levels in drinking water met with kudos from the American Dental Association.
"This is a superb example of a government agency fulfilling its mission to protect and enhance the health of the American people," said American Dental Association President Raymond Gist, DDS. "The recommended levels for optimal fluoridation may be reduced, but the health benefits of fluoridation remain."
Opponents of fluoridated water, in contrast, were not impressed.
"[The federal government is] trying to keep the issue focused on teeth, when the science is becoming clearer and clearer that fluoride damages other tissues," said Paul Connett, PhD, executive director of the Fluoride Action Network based in Canton, New York. His group asserts that health risks associated with low to moderate doses of fluoride include joint pain, skin rash, reduced thyroid activity, bone cancer, and even IQ deficits. A recent study published in a peer-reviewed journal of the federal National Institute of Environmental Health Sciences suggests such a link between fluoride and intelligence.
Dr. Connett, a professor emeritus of environmental chemistry at St. Lawrence University in Canton, told Medscape Medical News that the United States should stop fluoridating water and instead address the root causes of tooth decay — poverty and poor diet.
"There is no difference in dental caries between fluoridated and nonfluoridated countries, fluoridated and nonfluoridated states, and fluoridated and nonfluoridated cities," added Dr. Connett.
Thursday, January 6, 2011
Autism and MMR Vaccine Study an 'Elaborate Fraud,' Charges BMJ
From Medscape Medical News > Psychiatry
Deborah Brauser
January 6, 2011 — BMJ is publishing a series of 3 articles and editorials charging that the study published in The Lancet in 1998 by Andrew Wakefield and colleagues linking the childhood measles-mumps-rubella (MMR) vaccine to a "new syndrome" of regressive autism and bowel disease was not just bad science but "an elaborate fraud."
According to the first article published in BMJ today by London-based investigative reporter Brian Deer, the study's investigators altered and falsified medical records and facts, misrepresented information to families, and treated the 12 children involved unethically.
In addition, Mr. Wakefield accepted consultancy fees from lawyers who were building a lawsuit against vaccine manufacturers, and many of the study participants were referred by an antivaccine organization.
In an accompanying editorial, BMJ Editor-in-Chief Fiona Godlee, MD, Deputy BMJ Editor Jane Smith, and Associate BMJ Editor Harvey Marcovitch write that there is no doubt that Mr. Wakefield perpetrated fraud.
A great deal of thought and effort must have gone into drafting the paper to achieve the results he wanted: the discrepancies all led in 1 direction; misreporting was gross.
Although The Lancet published a retraction of the study last year right after the UK General Medical Council (GMC) announced that the investigators acted "dishonestly" and irresponsibly," the BMJ editors note that the journal did not go far enough.
"The Lancet retraction was prompted by the results from the [General Medical Council] hearing and was very much based on the concerns about the ethics of the study," Dr. Godlee told Medscape Medical News.
"What we found was that it was definite fraud and that is a very important thing for the world to know. This article shows that the science was falsified and should be discounted," continued Dr. Godlee.
This evidence "should now close the door on this damaging vaccine scare," the editorial authors add.
Damage to Public Health
Although it included only 12 patients, faced almost immediate criticism, and never had its findings replicated, the study received wide media coverage and set off a panic among parents, with the result that MMR vaccinations decreased dramatically.
The 2003 to 2004 vaccination rate of 80% has now recovered slightly in the United Kingdom, but it is still well below the recommended 95% level recommended to ensure "herd immunity." A measles epidemic was also declared in England and Wales in 2008.
"Perhaps as important as the scare's effect on infectious disease is the energy, emotion, and money that have been diverted away from efforts to understand the real cause of autism and how to help children and families who live with it," the editorialists write.
Mr. Deer did his first investigative stories on the Wakefield paper in 2004 for the Sunday Times in London and a UK television network. On the basis of his findings, the GMC's Fitness to Practice panel convened in 2007 and heard from 36 witnesses during a period of 2 and a half years.
At the end of January last year, as reported by Medscape Medical News , the panel used strong language in condemning the study's methods and noted that Mr. Wakefield and 2 other colleagues had broken guidelines.
The Lancet issued its retraction 5 days later, citing the panel's findings that the participants were not consecutive patients seeking treatment and that the study had falsely reported being approved by an ethics committee.
Although the GMC later found that Mr. Wakefield and coauthor John Walker-Smith committed serious misconduct and struck them off the medical register, Mr. Wakefield has repeatedly denied doing anything wrong. In addition, he was not among the 10 of 13 coauthors who disavowed the study's findings in 2004.
"Instead, although now disgraced and stripped of his clinical and academic credentials, he continues to push his views. Meanwhile, the damage to public health continues," the editorialists write.
Multiple Discrepancies Found
Last spring, the BMJ went to Mr. Deer to ask if there was more to this story. In this newest article, he reports that "multiple discrepancies" were found, including the following:
* Only one of the studied 9 children actually had clear regressive autism and 3 did not have a diagnosis of any autism type;
* Five had preexisting development concerns — although all 12 were classified in the study as "previously normal"; and
* The exclusion of important allegations helped create "the appearance of a 14-day temporal link."
In addition, none of the 12 patients were "free of misreporting or alteration," he writes.
It cost a tremendous amount of time and money to penetrate the veil of confidentiality that surrounded just these 12 children. So how on earth would anybody penetrate the veil over other larger medical research? When Wakefield did what he did, it was on the assumption that no one would ever be able to find out the truth.
"My number 1 takeaway is that it cost a tremendous amount of time and money to penetrate the veil of confidentiality that surrounded just these 12 children. So how on earth would anybody penetrate the veil over other larger medical research? When Wakefield did what he did, it was on the assumption that no one would ever be able to find out the truth," Mr. Deer told Medscape Medical News.
BMJ fact-checked Mr. Deer's article against the 6 million–word transcript of the GMC panel's hearing. Dr. Godlee said she is now calling for reexamination of all of Wakefield's past studies to determine whether others should be retracted. "Past experience tells us that research misconduct is rarely isolated behavior," she writes.
But how did a small case-control study like this set off such a panic in the first place? "I think a lot of people would like to know the answer to that," said Dr. Godlee.
"I think Andrew Wakefield is a terrifically good publicist. He managed to convince his institution to run a press conference for this very small piece of research. The media attention for this grew, and concerns were raised with his subsequent publications."
In addition, she said that many parents have questions about why their children have developed autism and are looking for reasons to explain the onset of its behavioral symptoms. "MMR is a very common intervention, it seemed to fit the picture, and it's very hard to prove that something is safe despite overwhelming evidence that there is no link.
"If you're looking for an explanation, this may seem plausible, although the science is nonsense. Overall, I think it's a combination of very desperate parents looking for answers and a very clever man who was willing to lie and cheat, who was willing to try to advance his own career and financial benefits," noted Dr. Godlee.
Editor's Dread
With questions raised almost from the start, how culpable is The Lancet? And how can other journals protect themselves from publishing falsified studies?
"That is the dread of any editor," said Dr. Godlee. "I think editors' main responsibility is to make sure that what is published is valid in terms of being good research. And I think The Lancet's decision to publish this is the first place was a very questionable decision, especially as it dealt with such a serious issue.
"Why publish research that is not going to advance science and is going to create a vaccine scare? I think there is culpability there. But as for fraud, that is very tricky because science is based on trust," she added.
"None of us go back and ask for the case records of patients involved. But we need to become aware that any article that comes in could be fraudulent. And we have to be absolutely vigilant and investigate properly when concerns are raised. It's a constant cycle of oversight that needs to be done."
Medscape Medical News contacted The Lancet for its reaction to the BMJ series of articles, but officials there had "no comment on this."
Dr. Godlee said that she would also hope that coauthors would serve as backup for honesty in reporting and that all of this study's investigators "failed in their duties as authors" — especially since there were only 12 patients involved.
Adding a name to a paper carries a responsibility to ensure that no fraud has been committed. This should serve as a wake-up call for other researchers in the future. It's their reputation that can be damaged if they are found to be associated with someone else's failures of integrity.
"Adding a name to a paper carries a responsibility to ensure that no fraud has been committed. This should serve as a wake-up call for other researchers in the future. It's their reputation that can be damaged if they are found to be associated with someone else's failures of integrity."
Diversion of Research Funds
The editors write that although a breach of trust this large is "almost certainly rare," it raises questions about what could have been done earlier, what further inquiry is needed, and what can be done to keep it from happening again.
Future BMJ articles in the series, to be published during the next 2 weeks, will deal with these questions and about The Lancet's actions from study publication through retraction.
"We wanted to also look at what motivated Andrew Wakefield, looking at the commercial schemes he established to exploit the MMR scare, and then we examine what happened when the issues of concern were first raised back in 2004 and why it was not taken more seriously at that time," explained Dr. Godlee.
"To people who might ask why we're interested in all of this now, the answer is that what Brian Deer has unearthed is much more substantial than what most of us knew or what came out in the GMC hearing. This study was not only bad research but fraudulent as well. And it's taken an enormous amount of time and effort and money away from legitimate lines of inquiry," she concluded.
Mr. Deer's original investigation was funded by the Sunday Times of London and the Channel 4 television network. The current articles were funded by the BMJ. He reported receiving no other funding except for legal costs from the Medical Protection Society on behalf of Mr. Wakefield. The editorial authors have disclosed no relevant financial relationships.
BMJ. Published online January 6, 2011.
Deborah Brauser
January 6, 2011 — BMJ is publishing a series of 3 articles and editorials charging that the study published in The Lancet in 1998 by Andrew Wakefield and colleagues linking the childhood measles-mumps-rubella (MMR) vaccine to a "new syndrome" of regressive autism and bowel disease was not just bad science but "an elaborate fraud."
According to the first article published in BMJ today by London-based investigative reporter Brian Deer, the study's investigators altered and falsified medical records and facts, misrepresented information to families, and treated the 12 children involved unethically.
In addition, Mr. Wakefield accepted consultancy fees from lawyers who were building a lawsuit against vaccine manufacturers, and many of the study participants were referred by an antivaccine organization.
In an accompanying editorial, BMJ Editor-in-Chief Fiona Godlee, MD, Deputy BMJ Editor Jane Smith, and Associate BMJ Editor Harvey Marcovitch write that there is no doubt that Mr. Wakefield perpetrated fraud.
A great deal of thought and effort must have gone into drafting the paper to achieve the results he wanted: the discrepancies all led in 1 direction; misreporting was gross.
Although The Lancet published a retraction of the study last year right after the UK General Medical Council (GMC) announced that the investigators acted "dishonestly" and irresponsibly," the BMJ editors note that the journal did not go far enough.
"The Lancet retraction was prompted by the results from the [General Medical Council] hearing and was very much based on the concerns about the ethics of the study," Dr. Godlee told Medscape Medical News.
"What we found was that it was definite fraud and that is a very important thing for the world to know. This article shows that the science was falsified and should be discounted," continued Dr. Godlee.
This evidence "should now close the door on this damaging vaccine scare," the editorial authors add.
Damage to Public Health
Although it included only 12 patients, faced almost immediate criticism, and never had its findings replicated, the study received wide media coverage and set off a panic among parents, with the result that MMR vaccinations decreased dramatically.
The 2003 to 2004 vaccination rate of 80% has now recovered slightly in the United Kingdom, but it is still well below the recommended 95% level recommended to ensure "herd immunity." A measles epidemic was also declared in England and Wales in 2008.
"Perhaps as important as the scare's effect on infectious disease is the energy, emotion, and money that have been diverted away from efforts to understand the real cause of autism and how to help children and families who live with it," the editorialists write.
Mr. Deer did his first investigative stories on the Wakefield paper in 2004 for the Sunday Times in London and a UK television network. On the basis of his findings, the GMC's Fitness to Practice panel convened in 2007 and heard from 36 witnesses during a period of 2 and a half years.
At the end of January last year, as reported by Medscape Medical News , the panel used strong language in condemning the study's methods and noted that Mr. Wakefield and 2 other colleagues had broken guidelines.
The Lancet issued its retraction 5 days later, citing the panel's findings that the participants were not consecutive patients seeking treatment and that the study had falsely reported being approved by an ethics committee.
Although the GMC later found that Mr. Wakefield and coauthor John Walker-Smith committed serious misconduct and struck them off the medical register, Mr. Wakefield has repeatedly denied doing anything wrong. In addition, he was not among the 10 of 13 coauthors who disavowed the study's findings in 2004.
"Instead, although now disgraced and stripped of his clinical and academic credentials, he continues to push his views. Meanwhile, the damage to public health continues," the editorialists write.
Multiple Discrepancies Found
Last spring, the BMJ went to Mr. Deer to ask if there was more to this story. In this newest article, he reports that "multiple discrepancies" were found, including the following:
* Only one of the studied 9 children actually had clear regressive autism and 3 did not have a diagnosis of any autism type;
* Five had preexisting development concerns — although all 12 were classified in the study as "previously normal"; and
* The exclusion of important allegations helped create "the appearance of a 14-day temporal link."
In addition, none of the 12 patients were "free of misreporting or alteration," he writes.
It cost a tremendous amount of time and money to penetrate the veil of confidentiality that surrounded just these 12 children. So how on earth would anybody penetrate the veil over other larger medical research? When Wakefield did what he did, it was on the assumption that no one would ever be able to find out the truth.
"My number 1 takeaway is that it cost a tremendous amount of time and money to penetrate the veil of confidentiality that surrounded just these 12 children. So how on earth would anybody penetrate the veil over other larger medical research? When Wakefield did what he did, it was on the assumption that no one would ever be able to find out the truth," Mr. Deer told Medscape Medical News.
BMJ fact-checked Mr. Deer's article against the 6 million–word transcript of the GMC panel's hearing. Dr. Godlee said she is now calling for reexamination of all of Wakefield's past studies to determine whether others should be retracted. "Past experience tells us that research misconduct is rarely isolated behavior," she writes.
But how did a small case-control study like this set off such a panic in the first place? "I think a lot of people would like to know the answer to that," said Dr. Godlee.
"I think Andrew Wakefield is a terrifically good publicist. He managed to convince his institution to run a press conference for this very small piece of research. The media attention for this grew, and concerns were raised with his subsequent publications."
In addition, she said that many parents have questions about why their children have developed autism and are looking for reasons to explain the onset of its behavioral symptoms. "MMR is a very common intervention, it seemed to fit the picture, and it's very hard to prove that something is safe despite overwhelming evidence that there is no link.
"If you're looking for an explanation, this may seem plausible, although the science is nonsense. Overall, I think it's a combination of very desperate parents looking for answers and a very clever man who was willing to lie and cheat, who was willing to try to advance his own career and financial benefits," noted Dr. Godlee.
Editor's Dread
With questions raised almost from the start, how culpable is The Lancet? And how can other journals protect themselves from publishing falsified studies?
"That is the dread of any editor," said Dr. Godlee. "I think editors' main responsibility is to make sure that what is published is valid in terms of being good research. And I think The Lancet's decision to publish this is the first place was a very questionable decision, especially as it dealt with such a serious issue.
"Why publish research that is not going to advance science and is going to create a vaccine scare? I think there is culpability there. But as for fraud, that is very tricky because science is based on trust," she added.
"None of us go back and ask for the case records of patients involved. But we need to become aware that any article that comes in could be fraudulent. And we have to be absolutely vigilant and investigate properly when concerns are raised. It's a constant cycle of oversight that needs to be done."
Medscape Medical News contacted The Lancet for its reaction to the BMJ series of articles, but officials there had "no comment on this."
Dr. Godlee said that she would also hope that coauthors would serve as backup for honesty in reporting and that all of this study's investigators "failed in their duties as authors" — especially since there were only 12 patients involved.
Adding a name to a paper carries a responsibility to ensure that no fraud has been committed. This should serve as a wake-up call for other researchers in the future. It's their reputation that can be damaged if they are found to be associated with someone else's failures of integrity.
"Adding a name to a paper carries a responsibility to ensure that no fraud has been committed. This should serve as a wake-up call for other researchers in the future. It's their reputation that can be damaged if they are found to be associated with someone else's failures of integrity."
Diversion of Research Funds
The editors write that although a breach of trust this large is "almost certainly rare," it raises questions about what could have been done earlier, what further inquiry is needed, and what can be done to keep it from happening again.
Future BMJ articles in the series, to be published during the next 2 weeks, will deal with these questions and about The Lancet's actions from study publication through retraction.
"We wanted to also look at what motivated Andrew Wakefield, looking at the commercial schemes he established to exploit the MMR scare, and then we examine what happened when the issues of concern were first raised back in 2004 and why it was not taken more seriously at that time," explained Dr. Godlee.
"To people who might ask why we're interested in all of this now, the answer is that what Brian Deer has unearthed is much more substantial than what most of us knew or what came out in the GMC hearing. This study was not only bad research but fraudulent as well. And it's taken an enormous amount of time and effort and money away from legitimate lines of inquiry," she concluded.
Mr. Deer's original investigation was funded by the Sunday Times of London and the Channel 4 television network. The current articles were funded by the BMJ. He reported receiving no other funding except for legal costs from the Medical Protection Society on behalf of Mr. Wakefield. The editorial authors have disclosed no relevant financial relationships.
BMJ. Published online January 6, 2011.
Wednesday, January 5, 2011
AAP Issues New Guidelines for Management of Iron Deficiency
Medscape Medical News from the American Academy of Pediatrics (AAP) 2010 National Conference and Exhibition
Jim Kling
October 14, 2010 — Correction: The original text of this article described the daily iron dose for infants 6 to 12 months as 11 mg/kg. This is incorrect. The dose should be 11 mg/day.
October 5, 2010 (San Francisco, California) — Iron deficiency is one of the most common, yet undetected, problems among children. Here at the American Academy of Pediatrics (AAP) 2010 National Conference and Exhibition, the American Association of Pediatrics released a clinical report, with guidelines for iron intake in infants and children and to improve screening methods.
The clinical report, entitled Diagnosis and Prevention of Iron Deficiency and Iron Deficiency Anemia in Infants and Young Children (0–3 Years of Age), was published online October 5 in Pediatrics. It is a revision of a 1999 policy statement.
Iron deficiency can have long-term irreversible effects on a child's cognitive and behavioral development. By the time a child develops iron-deficiency anemia, it might be too late to prevent future problems. "The body has a preferential tracking of iron. Red blood cells take precedence over the iron requirements of the brain. By the time you get iron-deficiency anemia, you've been iron-deficient for a long time," said Frank Greer, MD, professor of pediatrics at the University of Wisconsin School of Medicine and Public Health in Madison, and a coauthor of the report.
The 1999 guidelines call for children to have their hemoglobin checked sometime between 9 and 12 months of age, and again between 15 and 18 months of age. However, the existing test misses many children with iron deficiency and iron-deficiency anemia. Even those found to be iron deficient frequently receive no follow-up testing or treatment, according to Dr. Greer.
Although supplementing all children with iron would reduce iron deficiency, such a program does not have widespread support in the medical community at this point. That's partly because toddlers, who are the most widely affected group, have a wide range of diets and it is unclear what foods to fortify.
Liquid iron supplements or vitamins could be used, but there is a risk for iron overload in some populations, according to Michael K. Georgieff, MD, professor of pediatrics and child psychology and director of the Center for Neurobehavioral Development at the University of Minnesota in Minneapolis. Dr. Georgieff was on the AAP's committee on nutrition from 1993 to 1999 and played a key role in the 1999 guidelines.
"Iron supplementation and awareness of iron nutrition has probably been one of the most successful public health programs in the United States. In the 1960s, iron deficiency was probably 30% to 40%. Today, it may be under 10%. But in trying to eliminate that last 10%, you have to consider it in terms of exposing kids to [too much] iron," said Dr. Georgieff.
No single screening test is available that will accurately characterize the iron status of a child, he noted. In the report, the AAP recommends 4 protocols for screening for iron deficiency and iron-deficiency anemia, including combinations of several tests and follow-up protocols. "It's burdensome," Dr. Greer admitted.
"Since we're not going to do universal supplementation, we need to identify kids who are at risk for iron deficiency and start targeting them," said Dr. Georgieff, who studies the neurodevelopmental effects of iron deficiency in children.
The AAP report identified several factors associated with iron deficiency and iron-deficiency anemia, including prematurity or low birth-weight, lead exposure, exclusive breastfeeding past 4 months of age without iron supplements, and weaning to foods that don't include iron-fortified cereals or iron-rich foods. Infants with special healthcare needs might also be at risk. Children of low economic status, particularly those of Mexican American descent, are also of concern, according to the report, which recommends selective screening for these individuals.
The guidelines also address means to prevent iron deficiency through a diet of foods naturally rich in iron, such as meat, shellfish, legumes, iron-rich fruits and vegetables, and iron-fortified cereals. Fruits rich in vitamin C help iron absorption. Some children might require liquid iron supplements or chewable vitamins to get sufficient iron.
The AAP recommends varying amounts of iron based on a child's age:
* Term, healthy infants have sufficient iron for the first 4 months of life. Because human breast milk contains very little iron, breastfed infants should be supplemented with 1 mg/kg per day of oral iron from 4 months of age until iron-rich foods (such as iron-fortified cereals) are introduced.
* Formula-fed infants will receive adequate iron from formula and complementary foods. Whole milk should not be used before 12 months.
* Infants 6 to 12 months of age need 11 mg/day of iron a day. When infants are given complementary foods, red meat and vegetables with high iron content should be introduced early. Liquid iron supplements can be used if iron needs are not met by formula and complementary foods.
* Toddlers 1 to 3 years of age need 7 mg per day of iron. It is best if this comes from foods such as red meats, iron-rich vegetables, and fruits with vitamin C, which enhance iron absorption. Liquid supplements and chewable multivitamins can also be used.
* All preterm infants should have at least 2 mg/kg of iron per day until 12 months of age, which is the amount of iron in iron-fortified formulas. Preterm infants fed human milk should receive an iron supplement of 2 mg/kg per day by 1 month of age; this should be continued until the infant is weaned to iron-fortified formula or begins eating foods that supply the required 2 mg/kg of iron.
Dr. Greer and Dr. Georgieff have disclosed no relevant financial relationships.
American Academy of Pediatrics (AAP) 2010 National Conference and Exhibition.
Jim Kling
October 14, 2010 — Correction: The original text of this article described the daily iron dose for infants 6 to 12 months as 11 mg/kg. This is incorrect. The dose should be 11 mg/day.
October 5, 2010 (San Francisco, California) — Iron deficiency is one of the most common, yet undetected, problems among children. Here at the American Academy of Pediatrics (AAP) 2010 National Conference and Exhibition, the American Association of Pediatrics released a clinical report, with guidelines for iron intake in infants and children and to improve screening methods.
The clinical report, entitled Diagnosis and Prevention of Iron Deficiency and Iron Deficiency Anemia in Infants and Young Children (0–3 Years of Age), was published online October 5 in Pediatrics. It is a revision of a 1999 policy statement.
Iron deficiency can have long-term irreversible effects on a child's cognitive and behavioral development. By the time a child develops iron-deficiency anemia, it might be too late to prevent future problems. "The body has a preferential tracking of iron. Red blood cells take precedence over the iron requirements of the brain. By the time you get iron-deficiency anemia, you've been iron-deficient for a long time," said Frank Greer, MD, professor of pediatrics at the University of Wisconsin School of Medicine and Public Health in Madison, and a coauthor of the report.
The 1999 guidelines call for children to have their hemoglobin checked sometime between 9 and 12 months of age, and again between 15 and 18 months of age. However, the existing test misses many children with iron deficiency and iron-deficiency anemia. Even those found to be iron deficient frequently receive no follow-up testing or treatment, according to Dr. Greer.
Although supplementing all children with iron would reduce iron deficiency, such a program does not have widespread support in the medical community at this point. That's partly because toddlers, who are the most widely affected group, have a wide range of diets and it is unclear what foods to fortify.
Liquid iron supplements or vitamins could be used, but there is a risk for iron overload in some populations, according to Michael K. Georgieff, MD, professor of pediatrics and child psychology and director of the Center for Neurobehavioral Development at the University of Minnesota in Minneapolis. Dr. Georgieff was on the AAP's committee on nutrition from 1993 to 1999 and played a key role in the 1999 guidelines.
"Iron supplementation and awareness of iron nutrition has probably been one of the most successful public health programs in the United States. In the 1960s, iron deficiency was probably 30% to 40%. Today, it may be under 10%. But in trying to eliminate that last 10%, you have to consider it in terms of exposing kids to [too much] iron," said Dr. Georgieff.
No single screening test is available that will accurately characterize the iron status of a child, he noted. In the report, the AAP recommends 4 protocols for screening for iron deficiency and iron-deficiency anemia, including combinations of several tests and follow-up protocols. "It's burdensome," Dr. Greer admitted.
"Since we're not going to do universal supplementation, we need to identify kids who are at risk for iron deficiency and start targeting them," said Dr. Georgieff, who studies the neurodevelopmental effects of iron deficiency in children.
The AAP report identified several factors associated with iron deficiency and iron-deficiency anemia, including prematurity or low birth-weight, lead exposure, exclusive breastfeeding past 4 months of age without iron supplements, and weaning to foods that don't include iron-fortified cereals or iron-rich foods. Infants with special healthcare needs might also be at risk. Children of low economic status, particularly those of Mexican American descent, are also of concern, according to the report, which recommends selective screening for these individuals.
The guidelines also address means to prevent iron deficiency through a diet of foods naturally rich in iron, such as meat, shellfish, legumes, iron-rich fruits and vegetables, and iron-fortified cereals. Fruits rich in vitamin C help iron absorption. Some children might require liquid iron supplements or chewable vitamins to get sufficient iron.
The AAP recommends varying amounts of iron based on a child's age:
* Term, healthy infants have sufficient iron for the first 4 months of life. Because human breast milk contains very little iron, breastfed infants should be supplemented with 1 mg/kg per day of oral iron from 4 months of age until iron-rich foods (such as iron-fortified cereals) are introduced.
* Formula-fed infants will receive adequate iron from formula and complementary foods. Whole milk should not be used before 12 months.
* Infants 6 to 12 months of age need 11 mg/day of iron a day. When infants are given complementary foods, red meat and vegetables with high iron content should be introduced early. Liquid iron supplements can be used if iron needs are not met by formula and complementary foods.
* Toddlers 1 to 3 years of age need 7 mg per day of iron. It is best if this comes from foods such as red meats, iron-rich vegetables, and fruits with vitamin C, which enhance iron absorption. Liquid supplements and chewable multivitamins can also be used.
* All preterm infants should have at least 2 mg/kg of iron per day until 12 months of age, which is the amount of iron in iron-fortified formulas. Preterm infants fed human milk should receive an iron supplement of 2 mg/kg per day by 1 month of age; this should be continued until the infant is weaned to iron-fortified formula or begins eating foods that supply the required 2 mg/kg of iron.
Dr. Greer and Dr. Georgieff have disclosed no relevant financial relationships.
American Academy of Pediatrics (AAP) 2010 National Conference and Exhibition.
Food Allergy: The Definitive Guide to Clinical Practice
From Medscape Allergy & Clinical Immunology
Laura A. Stokowski, RN, MS
content:
* The Definitive Guide to Clinical Practice in Food Allergy
* A Uniform Definition of Food Allergy
* A Reliable Approach to Diagnosis
* A Consistent Management Plan
* Misconceptions and Misunderstandings About Food Allergy
* Emergency Management of Severe Reactions and Anaphylaxis
* What Do the Guidelines Mean to Practitioners and Patients?
* References
http://www.medscape.com/viewarticle/734431
The Definitive Guide to Clinical Practice in Food Allergy
As many as 90% of self-reported food allergies might not be allergies at all. So -- if they aren't food allergies, what are they, and why does this level of misunderstanding exist?
True food allergies affect only about 5% of children and 4% of adults in the United States.[1] Some experts speculate that the incidence might be increasing, but want of a uniform definition for food allergy has hampered the determination of its actual rates.
That is, until now. The National Institute for Allergy and Infectious Diseases (NIAID) has just released its Guidelines for the Diagnosis and Management of Food Allergy in the United States ,[2] the much-anticipated culmination of a 2-year effort on the part of medical organizations, federal agencies, and patient advocacy groups.[3]
The real value of the guidelines is that they are written not just for allergy specialists, but also for general and specialty practitioners in other fields -- such as primary care, dermatology, gastroenterology or emergency medicine -- who often encounter patients with symptoms or claims of food allergy or food reaction. The guidelines define food allergy and distinguish it from other adverse food reactions, spell out the diagnostic process for potential food allergy (which tests are useful and which are not), and describe the "best practices" for management of food allergy and its symptoms, including anaphylaxis.
"Previous food allergy guidelines were developed by allergists for allergists," explained Matthew Fenton, PhD, Chief of the Asthma, Allergy, and Inflammation Branch of the Division of Allergy, Immunology, and Transplantation, NIAID, and one of the guideline's authors. "This is a major advance, and one that I hope will translate into better patient health and patient care. This effort represents the biggest and broadest attempt to develop evidence-based guidelines -- guidelines that are based on data that has been thoroughly reviewed and graded by experts and that also incorporates expert clinical opinion. Most importantly, this process was conducted by healthcare professionals across a wide range of specialty areas -- everyone who is involved in food allergy, from the advocacy groups to the government public policymakers to the clinical practitioners. It is a departure from previous guidelines. We want the family practice physician in Fargo, North Dakota, to pick up the guidelines and use them as easily as the allergy specialist in Manhattan."
"The guidelines put as much emphasis as possible on evidence-based information, complemented by expert opinions," added American Academy of Allergy and Clinical Immunology President Sami Bahna, MD."They will be very useful to allergists as well as other practitioners because the guidelines incorporate updated literature that has been critically interpreted."
Food allergy doesn't have a cure, or even, in a conventional sense, a treatment. It boils down to proper diagnosis, on the basis of a uniform definition, and management that is consistent and safe for the patient, and most of all, backed up by scientific evidence.
What Do the Guidelines Offer?
The guidelines offer exactly what most practitioners need -- criteria for food allergy that clear up questions such as what is a true food allergy, and what isn't a food allergy at all? They provide reliable diagnostic strategies for patients with reported food allergies -- which tests are useful, which are not -- and when it is best to refer to a specialist. The guidelines outline a consistent approach to management of food allergy, including the appropriate and timely response to severe food allergy symptoms and anaphylaxis. Finally, the guidelines clear up common misconceptions about food allergy, and answer lingering questions such as "is it possible to prevent food allergy"?
A Uniform Definition of Food Allergy
When the scientific literature was examined to identify best practices related to food allergy, many divergent definitions for "food allergy" were found. The first task, therefore, was to define food allergy:
An "adverse health effect arising from a specific immune response that occurs reproducibly on exposure to a given food." [2]
A food is any substance that is intended for human consumption, and may include drinks, chewing gum, food additives, and dietary supplements. A food allergen is the specific component of or ingredient in food (protein or chemical hapten) that is recognized by allergen-specific immune cells and elicits specific immunologic reactions (mediated by immunoglobulin E [IgE] antibodies and/or T cells), resulting in characteristic symptoms.[2]
A food allergy reaction occurs minutes to hours after smelling, touching, or ingesting a specific food -- the trigger -- and results in symptoms of hives, itching, trouble breathing, wheezing, or even anaphylaxis. A food allergy reaction is reproducible; the trigger does not change, and the trigger always sets off the same immune response. Even so, the intensity of a response can vary from event to event.
The guidelines point out that "because individuals can develop immunologic sensitization (as evidenced by the presence of allergen-specific IgE (sIgE) to food allergens) without having clinical symptoms on exposure to those foods, an sIgE-mediated food allergy requires boththe presence of sensitization andthe development of specific signs and symptoms on exposure to that food. Sensitization alone is not sufficient to define food allergy."[2]
Also provided are concise definitions for food allergy syndromes, including food-induced anaphylaxis, gastrointestinal food allergies (immediate gastrointestinal hypersensitivity, eosinophilic esophagitis, eosinophilic gastroenteritis, dietary protein-induced proctitis, food protein-induced enterocolitis syndrome, oral allergy syndrome), cutaneous reactions to food (acute urticaria, angioedema), and respiratory manifestations of food allergy.
Food Allergy vs Food Intolerance
The 50% to 90% of self-reported food allergies that are not really allergies are actually reactions to food that are not mediated by the immune system. This is the critical difference. Non-allergic food reactions, referred to as "food intolerances," typically occur 3-4 hours after ingesting a certain food or similar food and produce symptoms that vary depending on the nature of the intolerance. "With the exception of lactose intolerance, not much is known about other food intolerances," admitted Dr. Fenton. "These people aren't overreacting; it's a real disease. Food intolerances are quite common and can share symptoms with food allergy."
Because they can mimic immune reactions, food intolerances are often confused with food allergies, but the underlying mechanisms differ. Food intolerance can be metabolic, pharmacologic, or toxic in nature, and can involve components of food or additives such as lactose, caffeine, monosodium glutamate, tyramine, artificial colors, or sulfites.
A Reliable Approach to Diagnosis
"With all the attention to food allergy in the press, more people are asking to be tested," observed Dr. Fenton. "It can create stress; people are afraid to eat certain foods."
History and Physical Examination
A detailed medical history and physical examination are the starting points in a patient with possible food allergy, although the findings of neither can be considered diagnostic of food allergy. Parent or patient reportsof self-diagnosed food allergies have low positive predictive value and must be confirmed by other means.[2] A table of systems-specific food allergy symptoms can be found in the guidelines. An individual presenting with any combination of these symptoms shortly after ingesting a food should be evaluated for food allergy, particularly if the symptoms have occurred on more than a single occasion. The guidelines emphasize that diagnosing food allergy on the basis of history or physical examination alone can lead to erroneous diagnosis of food allergy and result in unnecessary dietary restriction that could have adverse nutritional consequences.[2]
Objective Testing
A practical feature of the guidelines that will be invaluable to clinicians is information about which "food allergy tests" have been scientifically validated to make a diagnosis of food allergy and which have not.
"We often hear from practitioners who ask about various products and tests on the market that purport to diagnose food allergies," explains Matthew Fenton. "It is astounding how many products that claim to be diagnostic or therapeutic are not supported by the evidence. So the new guidelines narrow the list to those things any physician would want to use to diagnose and manage food allergy. Practitioners are relieved to hear this, because they are bombarded with these useless products."
Confusion persists about some commonly employed food allergy tests. Dr. Fenton finds that practitioners often obtain total IgE or allergen-specific IgE (sIgE) blood tests without realizing that abnormally high IgE levels or the presence of sIgE are not solely diagnostic of food allergy but mean only that the patient has been sensitized to the allergen -- and they are not necessarily evidence of clinical disease.
Intradermal testing, total serum IgE, or atopy patch tests are not recommended in the diagnosis of food allergy, either alone or in combination.[2] "These tests are easy to do, and might point to a food allergy, but they don't give a definitive diagnosis," explained Dr. Fenton. Some methods, such as skin prick test and sIgE can assist in identifying the causative food in a patient with confirmed food allergy. Food elimination diets or food/symptom diaries, although evidence for usefulness is lacking, may have a role in confirming food allergy when an oral food challenge is not practical.
The Oral Food Challenge
"The gold standard test for diagnosis of food allergy is the oral food challenge," continued Dr. Fenton. "But many primary care providers will be reluctant to do an oral food challenge, if they've never done one before. It has some level of risk and should be performed only by someone with experience, and in the appropriate setting. General practitioners can be trained to do the oral food challenge, but they need to have the right equipment and support -- epinephrine on hand to treat anaphylaxis and easy access to an inpatient facility if a transfer is required."
Oral food challenges are recommended to cut down on misdiagnosis of food allergy. The double-blind, placebo-controlled food challenge (DBPCFC) is the most specific test for diagnosing food allergy, but this test can be expensive and inconvenient to administer outside of research. Therefore, the guidelines state that single-blind and open-food challenges may be used in the clinical setting.[2] A negative oral food challenge rules out food allergy, whereas a positive oral challenge supported by medical history and laboratory tests is diagnostic of food allergy. Patients should be advised not to attempt an oral food challenge on their own -- it must be designed and performed under medical supervision to document the dose that provokes the reaction and to administer symptomatic treatment, which may require management of anaphylaxis. The dose, timing, and escalation must be carefully controlled. Practitioners who aren't comfortable conducting oral food challenges should refer these patients to allergy specialists.
Multiple Allergies
With more than 170 foods capable of causing IgE-mediated reactions, pinpointing a patient's trigger can be onerous. Prior to initiating an oral food challenge, suspected foods are eliminated from the diet for 2 to 8 weeks. When multiple allergies are suspected, all foods in question must be strictly avoided simultaneously.[2] During the oral food challenge, ingestion of each food is separated by a break of about 2 hours.[4] Depending on the number of suspect foods, it might be necessary to conduct the food challenges in multiple sessions.
Laura A. Stokowski, RN, MS
content:
* The Definitive Guide to Clinical Practice in Food Allergy
* A Uniform Definition of Food Allergy
* A Reliable Approach to Diagnosis
* A Consistent Management Plan
* Misconceptions and Misunderstandings About Food Allergy
* Emergency Management of Severe Reactions and Anaphylaxis
* What Do the Guidelines Mean to Practitioners and Patients?
* References
http://www.medscape.com/viewarticle/734431
The Definitive Guide to Clinical Practice in Food Allergy
As many as 90% of self-reported food allergies might not be allergies at all. So -- if they aren't food allergies, what are they, and why does this level of misunderstanding exist?
True food allergies affect only about 5% of children and 4% of adults in the United States.[1] Some experts speculate that the incidence might be increasing, but want of a uniform definition for food allergy has hampered the determination of its actual rates.
That is, until now. The National Institute for Allergy and Infectious Diseases (NIAID) has just released its Guidelines for the Diagnosis and Management of Food Allergy in the United States ,[2] the much-anticipated culmination of a 2-year effort on the part of medical organizations, federal agencies, and patient advocacy groups.[3]
The real value of the guidelines is that they are written not just for allergy specialists, but also for general and specialty practitioners in other fields -- such as primary care, dermatology, gastroenterology or emergency medicine -- who often encounter patients with symptoms or claims of food allergy or food reaction. The guidelines define food allergy and distinguish it from other adverse food reactions, spell out the diagnostic process for potential food allergy (which tests are useful and which are not), and describe the "best practices" for management of food allergy and its symptoms, including anaphylaxis.
"Previous food allergy guidelines were developed by allergists for allergists," explained Matthew Fenton, PhD, Chief of the Asthma, Allergy, and Inflammation Branch of the Division of Allergy, Immunology, and Transplantation, NIAID, and one of the guideline's authors. "This is a major advance, and one that I hope will translate into better patient health and patient care. This effort represents the biggest and broadest attempt to develop evidence-based guidelines -- guidelines that are based on data that has been thoroughly reviewed and graded by experts and that also incorporates expert clinical opinion. Most importantly, this process was conducted by healthcare professionals across a wide range of specialty areas -- everyone who is involved in food allergy, from the advocacy groups to the government public policymakers to the clinical practitioners. It is a departure from previous guidelines. We want the family practice physician in Fargo, North Dakota, to pick up the guidelines and use them as easily as the allergy specialist in Manhattan."
"The guidelines put as much emphasis as possible on evidence-based information, complemented by expert opinions," added American Academy of Allergy and Clinical Immunology President Sami Bahna, MD."They will be very useful to allergists as well as other practitioners because the guidelines incorporate updated literature that has been critically interpreted."
Food allergy doesn't have a cure, or even, in a conventional sense, a treatment. It boils down to proper diagnosis, on the basis of a uniform definition, and management that is consistent and safe for the patient, and most of all, backed up by scientific evidence.
What Do the Guidelines Offer?
The guidelines offer exactly what most practitioners need -- criteria for food allergy that clear up questions such as what is a true food allergy, and what isn't a food allergy at all? They provide reliable diagnostic strategies for patients with reported food allergies -- which tests are useful, which are not -- and when it is best to refer to a specialist. The guidelines outline a consistent approach to management of food allergy, including the appropriate and timely response to severe food allergy symptoms and anaphylaxis. Finally, the guidelines clear up common misconceptions about food allergy, and answer lingering questions such as "is it possible to prevent food allergy"?
A Uniform Definition of Food Allergy
When the scientific literature was examined to identify best practices related to food allergy, many divergent definitions for "food allergy" were found. The first task, therefore, was to define food allergy:
An "adverse health effect arising from a specific immune response that occurs reproducibly on exposure to a given food." [2]
A food is any substance that is intended for human consumption, and may include drinks, chewing gum, food additives, and dietary supplements. A food allergen is the specific component of or ingredient in food (protein or chemical hapten) that is recognized by allergen-specific immune cells and elicits specific immunologic reactions (mediated by immunoglobulin E [IgE] antibodies and/or T cells), resulting in characteristic symptoms.[2]
A food allergy reaction occurs minutes to hours after smelling, touching, or ingesting a specific food -- the trigger -- and results in symptoms of hives, itching, trouble breathing, wheezing, or even anaphylaxis. A food allergy reaction is reproducible; the trigger does not change, and the trigger always sets off the same immune response. Even so, the intensity of a response can vary from event to event.
The guidelines point out that "because individuals can develop immunologic sensitization (as evidenced by the presence of allergen-specific IgE (sIgE) to food allergens) without having clinical symptoms on exposure to those foods, an sIgE-mediated food allergy requires boththe presence of sensitization andthe development of specific signs and symptoms on exposure to that food. Sensitization alone is not sufficient to define food allergy."[2]
Also provided are concise definitions for food allergy syndromes, including food-induced anaphylaxis, gastrointestinal food allergies (immediate gastrointestinal hypersensitivity, eosinophilic esophagitis, eosinophilic gastroenteritis, dietary protein-induced proctitis, food protein-induced enterocolitis syndrome, oral allergy syndrome), cutaneous reactions to food (acute urticaria, angioedema), and respiratory manifestations of food allergy.
Food Allergy vs Food Intolerance
The 50% to 90% of self-reported food allergies that are not really allergies are actually reactions to food that are not mediated by the immune system. This is the critical difference. Non-allergic food reactions, referred to as "food intolerances," typically occur 3-4 hours after ingesting a certain food or similar food and produce symptoms that vary depending on the nature of the intolerance. "With the exception of lactose intolerance, not much is known about other food intolerances," admitted Dr. Fenton. "These people aren't overreacting; it's a real disease. Food intolerances are quite common and can share symptoms with food allergy."
Because they can mimic immune reactions, food intolerances are often confused with food allergies, but the underlying mechanisms differ. Food intolerance can be metabolic, pharmacologic, or toxic in nature, and can involve components of food or additives such as lactose, caffeine, monosodium glutamate, tyramine, artificial colors, or sulfites.
A Reliable Approach to Diagnosis
"With all the attention to food allergy in the press, more people are asking to be tested," observed Dr. Fenton. "It can create stress; people are afraid to eat certain foods."
History and Physical Examination
A detailed medical history and physical examination are the starting points in a patient with possible food allergy, although the findings of neither can be considered diagnostic of food allergy. Parent or patient reportsof self-diagnosed food allergies have low positive predictive value and must be confirmed by other means.[2] A table of systems-specific food allergy symptoms can be found in the guidelines. An individual presenting with any combination of these symptoms shortly after ingesting a food should be evaluated for food allergy, particularly if the symptoms have occurred on more than a single occasion. The guidelines emphasize that diagnosing food allergy on the basis of history or physical examination alone can lead to erroneous diagnosis of food allergy and result in unnecessary dietary restriction that could have adverse nutritional consequences.[2]
Objective Testing
A practical feature of the guidelines that will be invaluable to clinicians is information about which "food allergy tests" have been scientifically validated to make a diagnosis of food allergy and which have not.
"We often hear from practitioners who ask about various products and tests on the market that purport to diagnose food allergies," explains Matthew Fenton. "It is astounding how many products that claim to be diagnostic or therapeutic are not supported by the evidence. So the new guidelines narrow the list to those things any physician would want to use to diagnose and manage food allergy. Practitioners are relieved to hear this, because they are bombarded with these useless products."
Confusion persists about some commonly employed food allergy tests. Dr. Fenton finds that practitioners often obtain total IgE or allergen-specific IgE (sIgE) blood tests without realizing that abnormally high IgE levels or the presence of sIgE are not solely diagnostic of food allergy but mean only that the patient has been sensitized to the allergen -- and they are not necessarily evidence of clinical disease.
Intradermal testing, total serum IgE, or atopy patch tests are not recommended in the diagnosis of food allergy, either alone or in combination.[2] "These tests are easy to do, and might point to a food allergy, but they don't give a definitive diagnosis," explained Dr. Fenton. Some methods, such as skin prick test and sIgE can assist in identifying the causative food in a patient with confirmed food allergy. Food elimination diets or food/symptom diaries, although evidence for usefulness is lacking, may have a role in confirming food allergy when an oral food challenge is not practical.
The Oral Food Challenge
"The gold standard test for diagnosis of food allergy is the oral food challenge," continued Dr. Fenton. "But many primary care providers will be reluctant to do an oral food challenge, if they've never done one before. It has some level of risk and should be performed only by someone with experience, and in the appropriate setting. General practitioners can be trained to do the oral food challenge, but they need to have the right equipment and support -- epinephrine on hand to treat anaphylaxis and easy access to an inpatient facility if a transfer is required."
Oral food challenges are recommended to cut down on misdiagnosis of food allergy. The double-blind, placebo-controlled food challenge (DBPCFC) is the most specific test for diagnosing food allergy, but this test can be expensive and inconvenient to administer outside of research. Therefore, the guidelines state that single-blind and open-food challenges may be used in the clinical setting.[2] A negative oral food challenge rules out food allergy, whereas a positive oral challenge supported by medical history and laboratory tests is diagnostic of food allergy. Patients should be advised not to attempt an oral food challenge on their own -- it must be designed and performed under medical supervision to document the dose that provokes the reaction and to administer symptomatic treatment, which may require management of anaphylaxis. The dose, timing, and escalation must be carefully controlled. Practitioners who aren't comfortable conducting oral food challenges should refer these patients to allergy specialists.
Multiple Allergies
With more than 170 foods capable of causing IgE-mediated reactions, pinpointing a patient's trigger can be onerous. Prior to initiating an oral food challenge, suspected foods are eliminated from the diet for 2 to 8 weeks. When multiple allergies are suspected, all foods in question must be strictly avoided simultaneously.[2] During the oral food challenge, ingestion of each food is separated by a break of about 2 hours.[4] Depending on the number of suspect foods, it might be necessary to conduct the food challenges in multiple sessions.
Tuesday, January 4, 2011
Caffeine Intake May Negatively Affect Children
From Medscape Education Clinical Briefs
Laurie Barclay, MD
Hien T. Nghiem, MD
December 23, 2010 — Caffeine intake is prevalent in children and may have negative effects on sleep duration, according to the results of a study reported online in the December 16 issue of the Journal of Pediatrics.
"Caffeine's diuretic properties have encouraged behavioural health practitioners to eliminate caffeine from the diet of children with enuresis," write William Warzak, MD, from the Munroe-Meyer Institute and the Department of Pediatrics, University of Nebraska Medical Center in Omaha, and colleagues. "The Food and Drug Administration has not developed pediatric guidelines for caffeine consumption, but Canadian guidelines recommend that children aged 4 to 6 years old consume no more than 45 mg/d, approximately equivalent to the amount of caffeine found in a 12-ounce can of cola.... The most recent caffeine consumption data for children living in the United States is almost a decade old, and most of this research has been conducted with older children, adolescents, and adults."
The study goals were to obtain current data for caffeine intake in children, to evaluate the associations between caffeine, enuresis, and sleep, and to assess cross-cultural differences in caffeine consumption by Spanish- and English-speaking children aged 5 to 12 years.
During routine clinical visits at a pediatric clinic in Omaha, parents were surveyed about their child's daily consumption of various types of snacks and beverages. Of 228 young children whose parents were surveyed, about three quarters regularly consumed caffeine. Mean daily caffeine intake was approximately 52 mg in children aged 5 to 7 years and approximately 109 mg in children aged 8 to 12 years. Older children drank more caffeinated beverages than younger children.
"Some children as young as 5 years old were consuming the equivalent of a can of soda a day," Dr. Warzak said in a news release. "Children between the ages of 8 and 12 years consumed an average of 109 mg a day, the equivalent of almost 3 12-ounce cans of soda."
This study authors note that 109 mg caffeine daily is almost twice the amount recommended by Canadian pediatric guidelines and in excess of the amount shown to create physiological effects in adults.
Although caffeine intake was significantly negatively correlated with hours slept, caffeine consumption and enuresis were not significantly correlated. Compared with English-speaking parents, Spanish-speaking parents reported fewer events of enuresis in their children.
"Contrary to popular belief, children were not more likely to wet the bed if they consumed caffeine, despite the fact that caffeine is a diuretic," said coauthor Shelby Evans, PhD, also from the University of Nebraska Medical Center.
Children aged 5 to 7 years slept an average of 9.46 hours per night, which is above the minimum 9 hours recommended by the US Centers for Disease Control and Prevention (CDC), but approximately one quarter of these children slept less than 9 hours per night. Children aged 8 to 12 years old slept an average of 8.47 hours per night, which is below the minimum proposed by the CDC.
Limitations of this study include the inability to determine causal relationships, potential recall and parental bias, and a modest sample size of Spanish-speaking children. In addition, this study did not address the specific physiological and psychological effects of caffeine consumption on young children.
"Parents should be aware of the potentially negative influence of caffeine on a child's sleep quality and daily functioning," Dr. Warzak concluded.
The study authors have disclosed no relevant financial relationships.
J Pediatr. Published online December 16, 2010.
Clinical Context
Because of caffeine's diuretic properties, children with enuresis are encouraged to eliminate caffeine from their diet. At this time, the Food and Drug Administration has no pediatric guidelines for caffeine consumption. Canadian guidelines recommend that children aged 4 to 6 years old consume no more than 45 mg/day, which is approximately equivalent to the amount of caffeine found in a 12-ounce can of cola. For 7- to 9-year-old and 10- to 12-year-old children, the recommendations are no more than 62 mg/day and 85 mg/day, respectively. Caffeine consumption data for children living in the United States are outdated.
The aim of this study was to obtain current caffeine consumption data for children and examine the relationships between caffeine, enuresis, and sleep.
Laurie Barclay, MD
Hien T. Nghiem, MD
December 23, 2010 — Caffeine intake is prevalent in children and may have negative effects on sleep duration, according to the results of a study reported online in the December 16 issue of the Journal of Pediatrics.
"Caffeine's diuretic properties have encouraged behavioural health practitioners to eliminate caffeine from the diet of children with enuresis," write William Warzak, MD, from the Munroe-Meyer Institute and the Department of Pediatrics, University of Nebraska Medical Center in Omaha, and colleagues. "The Food and Drug Administration has not developed pediatric guidelines for caffeine consumption, but Canadian guidelines recommend that children aged 4 to 6 years old consume no more than 45 mg/d, approximately equivalent to the amount of caffeine found in a 12-ounce can of cola.... The most recent caffeine consumption data for children living in the United States is almost a decade old, and most of this research has been conducted with older children, adolescents, and adults."
The study goals were to obtain current data for caffeine intake in children, to evaluate the associations between caffeine, enuresis, and sleep, and to assess cross-cultural differences in caffeine consumption by Spanish- and English-speaking children aged 5 to 12 years.
During routine clinical visits at a pediatric clinic in Omaha, parents were surveyed about their child's daily consumption of various types of snacks and beverages. Of 228 young children whose parents were surveyed, about three quarters regularly consumed caffeine. Mean daily caffeine intake was approximately 52 mg in children aged 5 to 7 years and approximately 109 mg in children aged 8 to 12 years. Older children drank more caffeinated beverages than younger children.
"Some children as young as 5 years old were consuming the equivalent of a can of soda a day," Dr. Warzak said in a news release. "Children between the ages of 8 and 12 years consumed an average of 109 mg a day, the equivalent of almost 3 12-ounce cans of soda."
This study authors note that 109 mg caffeine daily is almost twice the amount recommended by Canadian pediatric guidelines and in excess of the amount shown to create physiological effects in adults.
Although caffeine intake was significantly negatively correlated with hours slept, caffeine consumption and enuresis were not significantly correlated. Compared with English-speaking parents, Spanish-speaking parents reported fewer events of enuresis in their children.
"Contrary to popular belief, children were not more likely to wet the bed if they consumed caffeine, despite the fact that caffeine is a diuretic," said coauthor Shelby Evans, PhD, also from the University of Nebraska Medical Center.
Children aged 5 to 7 years slept an average of 9.46 hours per night, which is above the minimum 9 hours recommended by the US Centers for Disease Control and Prevention (CDC), but approximately one quarter of these children slept less than 9 hours per night. Children aged 8 to 12 years old slept an average of 8.47 hours per night, which is below the minimum proposed by the CDC.
Limitations of this study include the inability to determine causal relationships, potential recall and parental bias, and a modest sample size of Spanish-speaking children. In addition, this study did not address the specific physiological and psychological effects of caffeine consumption on young children.
"Parents should be aware of the potentially negative influence of caffeine on a child's sleep quality and daily functioning," Dr. Warzak concluded.
The study authors have disclosed no relevant financial relationships.
J Pediatr. Published online December 16, 2010.
Clinical Context
Because of caffeine's diuretic properties, children with enuresis are encouraged to eliminate caffeine from their diet. At this time, the Food and Drug Administration has no pediatric guidelines for caffeine consumption. Canadian guidelines recommend that children aged 4 to 6 years old consume no more than 45 mg/day, which is approximately equivalent to the amount of caffeine found in a 12-ounce can of cola. For 7- to 9-year-old and 10- to 12-year-old children, the recommendations are no more than 62 mg/day and 85 mg/day, respectively. Caffeine consumption data for children living in the United States are outdated.
The aim of this study was to obtain current caffeine consumption data for children and examine the relationships between caffeine, enuresis, and sleep.
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