From Heartwire
Michael O'Riordan
February 3, 2010 (Atlanta, Georgia) — New data from the Centers for Disease Control and Prevention (CDC) shows that one in five youths aged 12 to 19 years has abnormal lipid levels [1]. Also, nearly one-third of these youths are obese or overweight and based on their body-mass index (BMI) are candidates for lipid screening, according to investigators.
In an editorial accompanying the new report [2], the CDC urges clinicians to be aware of the lipid screening guidelines so that interventions for overweight or obese children and youths can be recommended. "Healthcare providers can refer eligible youths to nutritional counseling, community fitness programs, and school-based lifestyle programs," writes the CDC.
The new report, from a combined sample of four National Health and Nutrition Examination Survey (NHANES) surveys taken from 1999 to 2006, includes data on 9187 youths, of which 3733 provided fasting blood samples for lipid testing.
Among the sample, 20% had at least one abnormal lipid measurement, such as elevated LDL cholesterol (>130 mg/dL), reduced HDL cholesterol (<35 mg/dL), or elevated triglyceride levels (>150 mg/dL). Researchers also showed that compared with normal-weight youths, those who were overweight or obese were significantly more likely to have at least one abnormal lipid measurement.
In addition to these findings, the CDC report also showed that boys were more likely than girls to have low HDL cholesterol, while older youths, those aged 18 to 19 years, were more likely to have low HDL and elevated triglyceride levels than kids aged 12 or 13 years.
The researchers point out that, based on the American Academy of Pediatrics (AAP) screening recommendations, 32% of youths would be eligible for lipid screening based solely on their BMI. The AAP recommends screening based on family history of high cholesterol or premature cardiovascular disease or an unknown family history of high cholesterol or premature disease, as well as the presence of at least one major cardiovascular disease risk factor, including overweight/obesity.
Friday, February 12, 2010
Flares in Childhood Eczema
From Skin Therapy Letter
S. M. Langan, MRCP, MSc, PhD
Abstract
Eczema is a major public health problem affecting children worldwide. Few studies have directly assessed triggers for disease flares. This paper presents evidence from a published systematic review and a prospective cohort study looking at flare factors in eczema.
This systematic review suggested that foodstuffs in selected groups, dust exposure, unfamiliar pets, seasonal variation, stress, and irritants may be important in eczema flares.
We performed a prospective cohort study that focused on environmental factors and identified associations between exposure to nylon clothing, dust, unfamiliar pets, sweating, shampoo, and eczema flares.
Results from this study also demonstrated some new key findings. First, the effect of shampoo was found to increase in cold weather, and second, combinations of environmental factors were associated with disease exacerbation, supporting a multiple component disease model.
This information is likely to be useful to families and may lead to the ability to reduce disease flares in the future.
Introduction
Eczema is an important condition that affects 2%-20% of children worldwide, and is associated with significant morbidity for children and their families.[1]
Although some progress has been made in understanding factors that are related to the occurrence of eczema, very little is known about factors associated with disease exacerbation. Most textbooks and review articles quote long lists of exacerbating factors, but we have found very little scientific data to support them.
Defining Flares of Eczema
In order to address the causes of flares, it is first important to define what is meant by an eczema flare. Langan et al. carried out a systematic review that assessed definitions of flare in the literature and sought parallels with definitions used in other relapsing and remitting diseases.[2]
The authors proposed that a flare could be defined as an episode requiring escalation of treatment or additional medical advice. This should be pre-defined by investigators at the onset of a study. For example, in studies of moderate or severe eczema, escalation to the use of topical corticosteroids might constitute a "flare". The need to use potent or super-potent topical corticosteroids, or to attend a primary care physician or dermatologist for disease exacerbation might be more appropriate. It is not possible to develop an entirely standardized definition for "flare", as the true meaning is related to the individual patient and his or her perception of disease worsening above baseline.
A Review of Evidence for Causes of Flares in Eczema
A systematic review was also carried out to assess the evidence for causes of eczema flares. This review highlighted the limited evidence for flare factors, but suggested that there may be a role for foodstuffs in selected groups, dust exposure, unfamiliar pets, seasonal variation, stress, and irritants in eczema flares.[3] However, scientific investigation was required to elucidate the relative impact of these factors in studies of longitudinal design over longer study periods. Another aspect requiring study was whether combinations of factors are more important than single factors, suggesting a complex disease model.
A Study of Environmental Factors
Langan et al. addressed these issues in a prospective cohort study.[4] The objectives were to assess the role of various environmental factors on eczema severity in a cohort of eczematous children with the following identified hypotheses:
Hypothesis 1: In hot weather, the combination of heat, sweating, and grass pollen precipitates increased severity in children with eczema in the UK.
Hypothesis 2: The combination of cold weather, indoor aeroallergen exposure, and reduced relative humidity from central heating led to increased severity in children with eczema in the UK. These first 2 hypotheses were informed by previous research, which proposed "summer" and "winter" types of eczema.[5]
Hypothesis 3: Detergents (i.e., soap or shampoo) increase the propensity to disease flares triggered by other factors at all temperatures, but more so in cold weather due to impaired skin barrier function.
Hypothesis 4: Any combination of greater than or equal to 3 exposures at any time is associated with worsening of eczema. The exposures assessed included dust, pets, shampoo, sweating, swimming, nylon clothing next to the skin, and a change in mean temperature of more than 3°C from the previous weekly average.
Study Methods
A prospective cohort study (n=60) of children with moderate-to-severe eczema between 6 and 9 months of age and up to 15 years were enrolled with overlapping start dates to allow for the study of seasonal factors. The exposures studied included temperature, relative humidity, sun exposure, sweating, clothing, cleansing products/washing, outdoor pollen level, the extent and nature of exposure to household pets, dusty environments, and swimming. On a daily basis, children or their parents completed novel electronic diaries programmed for this study recording eczema severity and exposures. Portable dataloggers were used to record temperature and relative humidity. External meteorological data was obtained from a local monitoring center.
The primary outcome was measured as a daily "bother" score; the secondary outcomes were daily "scratch" scores and flares of eczema outcome measures. The daily bother score was determined in response to the question, "How much bother did your (your child's) eczema cause today?"
Global scores by the patients and their parents were rated on a scale from 0 to 10 (where 0=no bother at all and 10=the most bother you can imagine).
Binary outcomes were recorded with respect to the question, "Have you had to step up your treatment today because your (your child's) eczema was worse?" Stepping up treatment was defined at the outset and patient-specific for each child.
Statistical Methods
A time series method, autoregressive moving average models (ARMA), was used to model the impact of each exposure on eczema severity for each individual. This method was required to deal with the autocorrelation in the data, i.e., the severity of eczema on 1 day has a relationship with the severity of eczema on the next day and the day before. Standard random effects from meta-analysis techniques were used to pool estimated coefficients across participants. Heterogeneity of responses, as detected using Chi-squared tests, represented inter-individual variation. The body site specificity of reactions was also examined.
Findings
Primary Outcome: "Bother" Scores
Increased disease severity was associated with direct contact with nylon clothing (pooled regression coefficient 0.23, 95% confidence interval [CI] 0.03-0.43), increasing exposure to dust (pooled regression coefficient 0.53, 0.23-0.83), exposure to unfamiliar pets (pooled regression coefficient 0.22, 0.10-0.34), sweating (pooled regression coefficient 0.24, 0.09-0.39) and shampoo exposure (pooled regression coefficient 0.07, 0.01-0.13). The association between shampoo use and eczema exacerbation was enhanced in cold weather (pooled regression coefficient 0.30, 0.04-0.57). Body site specificity was observed for the reactions to nylon clothing, which was greater on covered sites [trunk (p=0.02), limbs (p=0.03)], and reactions to wool clothing on truncal covered sites (p=0.03), but not limbs (p=0.62), while exacerbation of hand eczema was associated with exposure to pets (p‹0.001). Significant heterogeneity of responses between individuals was observed for exposure to grass pollen and outdoor temperature. With regard to the final hypothesis, a combination of any 3 of 7 likely variables was associated with exacerbation of eczema (pooled regression coefficient 0.41, 0.20-0.63).
Secondary Outcome: "Scratch" Scores
Increased disease severity was seen associated with swimming (pooled regression coefficient 0.14, 95% CI 0.00-0.28), exposure to wool clothing (pooled regression coefficient 0.28, 0.11-0.45), sweating (pooled regression coefficient 0.15, 0.04-0.26), and shampoo (pooled regression coefficient 0.07, 0.01-0.13).
Secondary Outcome: Eczema Flares
Only swimming was clearly associated with eczema exacerbation using this outcome measure (pooled regression coefficient 0.42, 0.05-0.80).
A summary of exposure factors associated with exacerbation of eczema includes:
Dust
Nylon
Shampoo
Shampoo + cold weather
Sweating
Swimming
Unfamiliar pets
Wool
Relative to the study hypotheses, the association between shampoo exposure and eczema exacerbation was shown to be increased in cold weather. There was also evidence showing an association between various combinations of exposures and disease worsening. There was insufficient evidence to support the other hypotheses tested in this study, but this may be explained by a low prevalence of these combinations of exposures. The implications of these study findings for clinical practice are that for the first time, it has been shown that shampoo exposure may be associated with eczema exacerbation and this effect is more pronounced in cold weather. This study also strengthens the systematic review findings that support disease worsening with dust, pet, and irritant exposure. Furthermore, this investigation suggests that eczema exacerbation may be more complicated in that multiple exposures acting in concert may be associated with worsening of the disease. The impact of food and stress were not examined in this prospective study.
Conclusion
Future research is required to specifically explore possible gene-environmental interactions with filaggrin mutations and their relevance in relation to disease flares, and to look at shampoo formulations in relation to eczema exacerbation.
S. M. Langan, MRCP, MSc, PhD
Abstract
Eczema is a major public health problem affecting children worldwide. Few studies have directly assessed triggers for disease flares. This paper presents evidence from a published systematic review and a prospective cohort study looking at flare factors in eczema.
This systematic review suggested that foodstuffs in selected groups, dust exposure, unfamiliar pets, seasonal variation, stress, and irritants may be important in eczema flares.
We performed a prospective cohort study that focused on environmental factors and identified associations between exposure to nylon clothing, dust, unfamiliar pets, sweating, shampoo, and eczema flares.
Results from this study also demonstrated some new key findings. First, the effect of shampoo was found to increase in cold weather, and second, combinations of environmental factors were associated with disease exacerbation, supporting a multiple component disease model.
This information is likely to be useful to families and may lead to the ability to reduce disease flares in the future.
Introduction
Eczema is an important condition that affects 2%-20% of children worldwide, and is associated with significant morbidity for children and their families.[1]
Although some progress has been made in understanding factors that are related to the occurrence of eczema, very little is known about factors associated with disease exacerbation. Most textbooks and review articles quote long lists of exacerbating factors, but we have found very little scientific data to support them.
Defining Flares of Eczema
In order to address the causes of flares, it is first important to define what is meant by an eczema flare. Langan et al. carried out a systematic review that assessed definitions of flare in the literature and sought parallels with definitions used in other relapsing and remitting diseases.[2]
The authors proposed that a flare could be defined as an episode requiring escalation of treatment or additional medical advice. This should be pre-defined by investigators at the onset of a study. For example, in studies of moderate or severe eczema, escalation to the use of topical corticosteroids might constitute a "flare". The need to use potent or super-potent topical corticosteroids, or to attend a primary care physician or dermatologist for disease exacerbation might be more appropriate. It is not possible to develop an entirely standardized definition for "flare", as the true meaning is related to the individual patient and his or her perception of disease worsening above baseline.
A Review of Evidence for Causes of Flares in Eczema
A systematic review was also carried out to assess the evidence for causes of eczema flares. This review highlighted the limited evidence for flare factors, but suggested that there may be a role for foodstuffs in selected groups, dust exposure, unfamiliar pets, seasonal variation, stress, and irritants in eczema flares.[3] However, scientific investigation was required to elucidate the relative impact of these factors in studies of longitudinal design over longer study periods. Another aspect requiring study was whether combinations of factors are more important than single factors, suggesting a complex disease model.
A Study of Environmental Factors
Langan et al. addressed these issues in a prospective cohort study.[4] The objectives were to assess the role of various environmental factors on eczema severity in a cohort of eczematous children with the following identified hypotheses:
Hypothesis 1: In hot weather, the combination of heat, sweating, and grass pollen precipitates increased severity in children with eczema in the UK.
Hypothesis 2: The combination of cold weather, indoor aeroallergen exposure, and reduced relative humidity from central heating led to increased severity in children with eczema in the UK. These first 2 hypotheses were informed by previous research, which proposed "summer" and "winter" types of eczema.[5]
Hypothesis 3: Detergents (i.e., soap or shampoo) increase the propensity to disease flares triggered by other factors at all temperatures, but more so in cold weather due to impaired skin barrier function.
Hypothesis 4: Any combination of greater than or equal to 3 exposures at any time is associated with worsening of eczema. The exposures assessed included dust, pets, shampoo, sweating, swimming, nylon clothing next to the skin, and a change in mean temperature of more than 3°C from the previous weekly average.
Study Methods
A prospective cohort study (n=60) of children with moderate-to-severe eczema between 6 and 9 months of age and up to 15 years were enrolled with overlapping start dates to allow for the study of seasonal factors. The exposures studied included temperature, relative humidity, sun exposure, sweating, clothing, cleansing products/washing, outdoor pollen level, the extent and nature of exposure to household pets, dusty environments, and swimming. On a daily basis, children or their parents completed novel electronic diaries programmed for this study recording eczema severity and exposures. Portable dataloggers were used to record temperature and relative humidity. External meteorological data was obtained from a local monitoring center.
The primary outcome was measured as a daily "bother" score; the secondary outcomes were daily "scratch" scores and flares of eczema outcome measures. The daily bother score was determined in response to the question, "How much bother did your (your child's) eczema cause today?"
Global scores by the patients and their parents were rated on a scale from 0 to 10 (where 0=no bother at all and 10=the most bother you can imagine).
Binary outcomes were recorded with respect to the question, "Have you had to step up your treatment today because your (your child's) eczema was worse?" Stepping up treatment was defined at the outset and patient-specific for each child.
Statistical Methods
A time series method, autoregressive moving average models (ARMA), was used to model the impact of each exposure on eczema severity for each individual. This method was required to deal with the autocorrelation in the data, i.e., the severity of eczema on 1 day has a relationship with the severity of eczema on the next day and the day before. Standard random effects from meta-analysis techniques were used to pool estimated coefficients across participants. Heterogeneity of responses, as detected using Chi-squared tests, represented inter-individual variation. The body site specificity of reactions was also examined.
Findings
Primary Outcome: "Bother" Scores
Increased disease severity was associated with direct contact with nylon clothing (pooled regression coefficient 0.23, 95% confidence interval [CI] 0.03-0.43), increasing exposure to dust (pooled regression coefficient 0.53, 0.23-0.83), exposure to unfamiliar pets (pooled regression coefficient 0.22, 0.10-0.34), sweating (pooled regression coefficient 0.24, 0.09-0.39) and shampoo exposure (pooled regression coefficient 0.07, 0.01-0.13). The association between shampoo use and eczema exacerbation was enhanced in cold weather (pooled regression coefficient 0.30, 0.04-0.57). Body site specificity was observed for the reactions to nylon clothing, which was greater on covered sites [trunk (p=0.02), limbs (p=0.03)], and reactions to wool clothing on truncal covered sites (p=0.03), but not limbs (p=0.62), while exacerbation of hand eczema was associated with exposure to pets (p‹0.001). Significant heterogeneity of responses between individuals was observed for exposure to grass pollen and outdoor temperature. With regard to the final hypothesis, a combination of any 3 of 7 likely variables was associated with exacerbation of eczema (pooled regression coefficient 0.41, 0.20-0.63).
Secondary Outcome: "Scratch" Scores
Increased disease severity was seen associated with swimming (pooled regression coefficient 0.14, 95% CI 0.00-0.28), exposure to wool clothing (pooled regression coefficient 0.28, 0.11-0.45), sweating (pooled regression coefficient 0.15, 0.04-0.26), and shampoo (pooled regression coefficient 0.07, 0.01-0.13).
Secondary Outcome: Eczema Flares
Only swimming was clearly associated with eczema exacerbation using this outcome measure (pooled regression coefficient 0.42, 0.05-0.80).
A summary of exposure factors associated with exacerbation of eczema includes:
Dust
Nylon
Shampoo
Shampoo + cold weather
Sweating
Swimming
Unfamiliar pets
Wool
Relative to the study hypotheses, the association between shampoo exposure and eczema exacerbation was shown to be increased in cold weather. There was also evidence showing an association between various combinations of exposures and disease worsening. There was insufficient evidence to support the other hypotheses tested in this study, but this may be explained by a low prevalence of these combinations of exposures. The implications of these study findings for clinical practice are that for the first time, it has been shown that shampoo exposure may be associated with eczema exacerbation and this effect is more pronounced in cold weather. This study also strengthens the systematic review findings that support disease worsening with dust, pet, and irritant exposure. Furthermore, this investigation suggests that eczema exacerbation may be more complicated in that multiple exposures acting in concert may be associated with worsening of the disease. The impact of food and stress were not examined in this prospective study.
Conclusion
Future research is required to specifically explore possible gene-environmental interactions with filaggrin mutations and their relevance in relation to disease flares, and to look at shampoo formulations in relation to eczema exacerbation.
Influenza Virus Infection in Infants Less than Three Months of Age
From The Pediatric Infectious Disease Journal®
Bender, Jeffrey M. MD; Ampofo, Krow MD; Gesteland, Per MD, MSc; Sheng, Xiaoming PhD; Korgenski, Kent MS; Raines, Bill; Daly, Judy A. PhD; Valentine, Karen MS; Srivastava, Rajendu MD, FRCP(C), MPH; Pavia, Andrew T. MD; Byington, Carrie L. MD
Abstract
Objective: We evaluated the presentation, outcomes, and the risk of serious bacterial infection (SBI) in infants < 3 months old with influenza virus infection.
Patients and Methods: We identified demographic, hospitalization, and microbiologic data from computerized medical records for all infants and children < 24 months of age, with laboratory confirmed influenza infection cared for at a tertiary care children's hospital during 4 winter seasons (2004–2008). We compared those < 3 months of age with older groups.
Results: We identified 833 children < 24 months of age with laboratory-confirmed influenza. Of those, 218 were < 3 months old. Influenza accounted for 3.6% of all evaluations of febrile infants and 12% of febrile infant encounters during winter. Infants < 3 months of age were less likely to have a high risk chronic medical condition, but were more likely to be hospitalized than children 3 to < 24 months old (P < 0.005). Infants < 3 months with influenza had fewer prolonged hospital stays than those 3 to < 6 months old [P = 0.056; OR: 0.5 (0.24–1.0)] and 6 to < 12 months old [P = 0.011; OR: 0.43 (0.24–0.83)]. Five (2.3%) infants < 3 months old had SBI.
Conclusions: Infants < 3 months of age with influenza virus infection often present with fever alone. Although they are more likely to be hospitalized than those 3 to < 24 months old, hospital stays are short and outcomes generally good. Infants with influenza virus infection have a low risk of concomitant SBI.
Introduction
Febrile infants younger than 3 months are often evaluated for serious bacterial infection (SBI). Approximately 8.5% to 9.5% of these infants have a SBI, with the remaining fevers presumably caused by viral illness.[1,2] Many studies have demonstrated that febrile infants with the clinical diagnosis of a specific viral illness such as bronchiolitis or a laboratory confirmed diagnosis of enterovirus or respiratory syncytial virus (RSV), are at lower risk for SBI than those with otherwise undifferentiated fever.[2–11] There are few data on the risk of SBI and outcomes of young infants with laboratory-confirmed influenza.
Influenza is a common viral cause of fever in young children during the winter.[12,13] Unlike other respiratory viruses, influenza frequently presents with high fever[14] that can be difficult to differentiate from SBI. In infants younger than 3 months, this often results in an evaluation for SBI and hospitalization.
Influenza vaccination is recommended for infants and children 6 months and older. Recent studies have demonstrated significant morbidity and mortality associated with influenza infection in infants younger than 6 months who are too young to be immunized.[15–17] Likewise, influenza infection in infants 6 months and younger may lead to high hospitalization rates and associated hospital costs.[17–19]
The objective of this study was to describe the outcomes, including rates of concomitant SBI, of a large cohort of infants younger than 3 months of age with laboratory confirmed influenza. We compare the outcomes of this group of infants with the outcomes among infants and children 3 to < 24 months old.
http://www.medscape.com/viewarticle/714806?src=mp&spon=9&uac=71630FV
Bender, Jeffrey M. MD; Ampofo, Krow MD; Gesteland, Per MD, MSc; Sheng, Xiaoming PhD; Korgenski, Kent MS; Raines, Bill; Daly, Judy A. PhD; Valentine, Karen MS; Srivastava, Rajendu MD, FRCP(C), MPH; Pavia, Andrew T. MD; Byington, Carrie L. MD
Abstract
Objective: We evaluated the presentation, outcomes, and the risk of serious bacterial infection (SBI) in infants < 3 months old with influenza virus infection.
Patients and Methods: We identified demographic, hospitalization, and microbiologic data from computerized medical records for all infants and children < 24 months of age, with laboratory confirmed influenza infection cared for at a tertiary care children's hospital during 4 winter seasons (2004–2008). We compared those < 3 months of age with older groups.
Results: We identified 833 children < 24 months of age with laboratory-confirmed influenza. Of those, 218 were < 3 months old. Influenza accounted for 3.6% of all evaluations of febrile infants and 12% of febrile infant encounters during winter. Infants < 3 months of age were less likely to have a high risk chronic medical condition, but were more likely to be hospitalized than children 3 to < 24 months old (P < 0.005). Infants < 3 months with influenza had fewer prolonged hospital stays than those 3 to < 6 months old [P = 0.056; OR: 0.5 (0.24–1.0)] and 6 to < 12 months old [P = 0.011; OR: 0.43 (0.24–0.83)]. Five (2.3%) infants < 3 months old had SBI.
Conclusions: Infants < 3 months of age with influenza virus infection often present with fever alone. Although they are more likely to be hospitalized than those 3 to < 24 months old, hospital stays are short and outcomes generally good. Infants with influenza virus infection have a low risk of concomitant SBI.
Introduction
Febrile infants younger than 3 months are often evaluated for serious bacterial infection (SBI). Approximately 8.5% to 9.5% of these infants have a SBI, with the remaining fevers presumably caused by viral illness.[1,2] Many studies have demonstrated that febrile infants with the clinical diagnosis of a specific viral illness such as bronchiolitis or a laboratory confirmed diagnosis of enterovirus or respiratory syncytial virus (RSV), are at lower risk for SBI than those with otherwise undifferentiated fever.[2–11] There are few data on the risk of SBI and outcomes of young infants with laboratory-confirmed influenza.
Influenza is a common viral cause of fever in young children during the winter.[12,13] Unlike other respiratory viruses, influenza frequently presents with high fever[14] that can be difficult to differentiate from SBI. In infants younger than 3 months, this often results in an evaluation for SBI and hospitalization.
Influenza vaccination is recommended for infants and children 6 months and older. Recent studies have demonstrated significant morbidity and mortality associated with influenza infection in infants younger than 6 months who are too young to be immunized.[15–17] Likewise, influenza infection in infants 6 months and younger may lead to high hospitalization rates and associated hospital costs.[17–19]
The objective of this study was to describe the outcomes, including rates of concomitant SBI, of a large cohort of infants younger than 3 months of age with laboratory confirmed influenza. We compare the outcomes of this group of infants with the outcomes among infants and children 3 to < 24 months old.
http://www.medscape.com/viewarticle/714806?src=mp&spon=9&uac=71630FV
The Effect of Backpacks on the Lumbar Spine in Children: A Standing Magnetic Resonance Imaging Study
From Spine
Timothy B. Neuschwander, MD; John Cutrone, MD; Brandon R. Macias, BA; Samantha Cutrone; Gita Murthy, PhD; Henry Chambers, MD; Alan R. Hargens, MD
Abstract
Study Design: This study is a repeated measures design to measure the lumbar spine response to typical school backpack loads in healthy children. The lumbar spine in this setting was measured for the first time by an upright magnetic resonance imaging (MRI) scanner.
Objective: The purpose of this study is to measure the lumbar spine response to typical school backpack loads in healthy children. We hypothesize that backpack loads significantly increase disc compression and lumbar curvature.
Summary of Background Data: Children commonly carry school backpacks of 10% to 22% bodyweight. Despite growing concern among parents about safety, there are no imaging studies which describe the effect of backpack loads on the spine in children.
Methods: Three boys and 5 girls, age 11 ± 2 years (mean ± SD) underwent T2 weighted sagittal and coronal MRI scans of the lumbar spine while standing. Scans were repeated with 4, 8, and 12 kg backpack loads, which represented approximately 10%, 20%, and 30% body weight for our sample. Main outcome measures were disc compression, defined as post- minus preloading disc height, and lumbar asymmetry, defined as the coronal Cobb angle between the superior endplates of S1 and L1.
Results:
Increasing backpack loads significantly compressed lumbar disc heights measured in the midline sagittal plane (P < 0.05, repeated-measures analysis of variance [ANOVA]). Lumbar asymmetry was: 2.23° ± 1.07° standing, 5.46° ± 2.50° with 4 kg, 9.18° ± 2.25° with 8 kg, and 5.68° ± 1.76° with 12 kg (mean ± SE).
Backpack loads significantly increased lumbar asymmetry (P < 0.03, one-way ANOVA). Four of the 8 subjects had Cobb angles greater than 10° during 8-kg backpack loads. Using a visual-analogue scale to rate their pain (0-no pain, 10-worst pain imaginable), subjects reported significant increases in back pain associated with backpack loads of 4, 8, and 12 kg (P < 0.001, 1-way ANOVA).
Conclusion: Backpack loads are responsible for a significant amount of back pain in children, which in part, may be due to changes in lumbar disc height or curvature. This is the first upright MRI study to document reduced disc height and greater lumbar asymmetry for common backpack loads in children.
Timothy B. Neuschwander, MD; John Cutrone, MD; Brandon R. Macias, BA; Samantha Cutrone; Gita Murthy, PhD; Henry Chambers, MD; Alan R. Hargens, MD
Abstract
Study Design: This study is a repeated measures design to measure the lumbar spine response to typical school backpack loads in healthy children. The lumbar spine in this setting was measured for the first time by an upright magnetic resonance imaging (MRI) scanner.
Objective: The purpose of this study is to measure the lumbar spine response to typical school backpack loads in healthy children. We hypothesize that backpack loads significantly increase disc compression and lumbar curvature.
Summary of Background Data: Children commonly carry school backpacks of 10% to 22% bodyweight. Despite growing concern among parents about safety, there are no imaging studies which describe the effect of backpack loads on the spine in children.
Methods: Three boys and 5 girls, age 11 ± 2 years (mean ± SD) underwent T2 weighted sagittal and coronal MRI scans of the lumbar spine while standing. Scans were repeated with 4, 8, and 12 kg backpack loads, which represented approximately 10%, 20%, and 30% body weight for our sample. Main outcome measures were disc compression, defined as post- minus preloading disc height, and lumbar asymmetry, defined as the coronal Cobb angle between the superior endplates of S1 and L1.
Results:
Increasing backpack loads significantly compressed lumbar disc heights measured in the midline sagittal plane (P < 0.05, repeated-measures analysis of variance [ANOVA]). Lumbar asymmetry was: 2.23° ± 1.07° standing, 5.46° ± 2.50° with 4 kg, 9.18° ± 2.25° with 8 kg, and 5.68° ± 1.76° with 12 kg (mean ± SE).
Backpack loads significantly increased lumbar asymmetry (P < 0.03, one-way ANOVA). Four of the 8 subjects had Cobb angles greater than 10° during 8-kg backpack loads. Using a visual-analogue scale to rate their pain (0-no pain, 10-worst pain imaginable), subjects reported significant increases in back pain associated with backpack loads of 4, 8, and 12 kg (P < 0.001, 1-way ANOVA).
Conclusion: Backpack loads are responsible for a significant amount of back pain in children, which in part, may be due to changes in lumbar disc height or curvature. This is the first upright MRI study to document reduced disc height and greater lumbar asymmetry for common backpack loads in children.
Friday, February 5, 2010
Tylenol, Motrin, Benadryl, St. Joseph Aspirin, Rolaids Recall
From WebMD Health News > Alerts, Approvals and Safety Changes > Alerts
Daniel J. DeNoon
January 15, 2010 — Because of a sickening smell in some containers, 54 million packages of 27 different over-the-counter remedies now are being recalled.
Products include various types of child and/or adult Tylenol, Motrin, Benadryl, St. Joseph Aspirin, Rolaids, and Simply Sleep. This adds to the 6 million packages of Tylenol recalled late last year, bringing the total number of recalled products to 60 million.
A musty, moldy odor coming from the products has sickened at least 70 people with nausea, stomach pain, vomiting, and diarrhea. The symptoms go away by themselves and no one has been seriously injured.
The FDA says Johnson & Johnson's McNeil Consumer Health Care knew of the problem for more than a year. When the company did act in November and December 2008, it did too little too late, said Deborah M. Autor, director of the FDA's Office of Compliance.
"When something smells bad, literally or figuratively, companies must aggressively investigate and take all actions necessary to solve the problem," Autor said at a news conference. "McNeil should have acted faster."
The odor comes from a chemical, 2,4,6-tribromoanisole or TBA. TBA is produced when fungi break down a commonly used fungicide called 2,4,6-tribromophenol. The full health effects of TBA are not known.
Before being filled with product, product containers were stored on wooden pallets apparently treated with the fungicide. TBA seems to have infiltrated the product containers before they were filled.
The FDA inspected McNeil's main plant at Las Piedras, Puerto Rico, and was not happy with what it found. The FDA says McNeil began receiving complaints in May 2008, but failed to investigate fully or to warn consumers in a timely manner.
The FDA has given McNeil 15 days to respond to its seven-point warning letter. In addition to the contamination issue, the FDA says there are product-quality issues with some Motrin products.
Specific products included in the recall include:
Children's Motrin
Children's Tylenol
Extra Strength Tylenol
Regular Strength Tylenol
Tylenol 8 Hour
Tylenol Arthritis
Tylenol PM
Benadryl
Motrin IB
Rolaids
Simply Sleep
St. Joseph Aspirin
A complete list of the recalled products, including package sizes, product types, lot numbers, and UPC codes, can be seen at www.mcneilproductrecall.com. Consumers with question can call McNeil at 888-222-6036.
Consumers who think they may have suffered ill effects from the products should contact the FDA at www.FDA.gov/medwatch.
SOURCES:
Daniel J. DeNoon
January 15, 2010 — Because of a sickening smell in some containers, 54 million packages of 27 different over-the-counter remedies now are being recalled.
Products include various types of child and/or adult Tylenol, Motrin, Benadryl, St. Joseph Aspirin, Rolaids, and Simply Sleep. This adds to the 6 million packages of Tylenol recalled late last year, bringing the total number of recalled products to 60 million.
A musty, moldy odor coming from the products has sickened at least 70 people with nausea, stomach pain, vomiting, and diarrhea. The symptoms go away by themselves and no one has been seriously injured.
The FDA says Johnson & Johnson's McNeil Consumer Health Care knew of the problem for more than a year. When the company did act in November and December 2008, it did too little too late, said Deborah M. Autor, director of the FDA's Office of Compliance.
"When something smells bad, literally or figuratively, companies must aggressively investigate and take all actions necessary to solve the problem," Autor said at a news conference. "McNeil should have acted faster."
The odor comes from a chemical, 2,4,6-tribromoanisole or TBA. TBA is produced when fungi break down a commonly used fungicide called 2,4,6-tribromophenol. The full health effects of TBA are not known.
Before being filled with product, product containers were stored on wooden pallets apparently treated with the fungicide. TBA seems to have infiltrated the product containers before they were filled.
The FDA inspected McNeil's main plant at Las Piedras, Puerto Rico, and was not happy with what it found. The FDA says McNeil began receiving complaints in May 2008, but failed to investigate fully or to warn consumers in a timely manner.
The FDA has given McNeil 15 days to respond to its seven-point warning letter. In addition to the contamination issue, the FDA says there are product-quality issues with some Motrin products.
Specific products included in the recall include:
Children's Motrin
Children's Tylenol
Extra Strength Tylenol
Regular Strength Tylenol
Tylenol 8 Hour
Tylenol Arthritis
Tylenol PM
Benadryl
Motrin IB
Rolaids
Simply Sleep
St. Joseph Aspirin
A complete list of the recalled products, including package sizes, product types, lot numbers, and UPC codes, can be seen at www.mcneilproductrecall.com. Consumers with question can call McNeil at 888-222-6036.
Consumers who think they may have suffered ill effects from the products should contact the FDA at www.FDA.gov/medwatch.
SOURCES:
Cell Phones May Be Linked to Increase in Tumors, But Evidence Still Inconclusive
From Medscape Medical News
Roxanne Nelson
February 5, 2010 — Cell phones have become an integral part of everyday life, but concerns about their safety persist. A meta-analysis, published in the November 20 issue of the Journal of Clinical Oncology, which found evidence linking cell phone use to an increased risk for tumors has since attracted criticism.
The meta-analysis found that, overall, the use of cell phones was not significantly associated with the risk for tumors in a random-effects model meta-analysis. Compared with people who never or rarely used a cell phone, the odds ratio (OR) for the overall use of cell phones was 0.98 for malignant and benign tumors (95% confidence interval [CI], 0.89 - 1.07).
However, it also found that cell-phone use of 10 years or longer was associated with a risk for tumors in 13 studies that reported this association (OR, 1.18; 95% CI, 1.04 - 1.34).
The authors, led by Seung-Kwon Myung, MD, MS, from the National Cancer Center in Goyang, South Korea, write that the results of the studies included in their analysis varied widely, and appeared to depend on who conducted and funded the research and the controls used for bias and errors.
"We found a large discrepancy in the association between [cell] phone use and tumor risk by research group, which is confounded with the methodologic quality of the research," they noted.
However, in subsequent letters to the editor, published online January 25 in the journal, the meta-analysis was criticized for having methodologic flaws and issues and a number of limitations.
No Conclusive Evidence
A number of epidemiologic studies have reported associations between the use of cell phones and malignant or benign tumors of the brain and of the head and neck, non-Hodgkin's lymphoma, and testicular cancer. Results have been inconclusive or even contradictory. But as previously reported by Medscape Oncology, a report released in August 2009 by the International Electromagnetic Field Collaborative suggested that the regular use of cell phones can result in a "significant" risk for brain tumors.
Soon after the release of that report, a US Senate hearing on the health effects of cell-phone use was held; it concluded that more and better research is needed to determine if there is a risk to human health. Several nations have decided not to wait for additional data, have issued warnings about the use of cell phones, and advise taking precautionary measures. In the United States, the state of Maine is considering legislation that would require placing warnings on all cell phones.
Long-Term Use Associated With Benign Tumors
The meta-analysis was conducted to investigate the association between cell-phone use and the risk for malignant and benign conditions. It included 23 case–control studies, and involved 37,916 participants (12,344 patient cases and 25,572 control subjects).
They observed that the studies included in their meta-analysis varied in quality, and some that suggested there was little to no risk did not correct for bias. In 8 high-quality studies that used blinding, a significant positive association (harmful effect) was observed; in a fixed-effects analysis of 15 studies that did not use blinding, a significant negative association (protective effect) was observed.
A subgroup meta-analysis by methodologic quality showed a significant positive association in the high-quality studies (OR, 1.09; 95% CI, 1.01 - 1.18), whereas a negative association was observed in the low-quality studies. In that subgroup meta-analysis, cell-phone use of 10 years or longer was significantly positively associated with the risk for benign tumors but not for malignant tumors.
"Distinct Pattern" Seen
Another factor affecting the validity of the meta-analysis is the funding sources of each research group, "because it is possible that these may have influenced the respective study designs and results," the authors write. In subgroup meta-analyses by research group/funding source, they observed a "distinct pattern" in their findings. A positive association was seen in 7 studies, conducted by Swedish oncologist Lennart Hardell, MD, and colleagues, that were independent of industry funding. Conversely, a negative association was seen in the industry-funded INTERPHONE studies. No association was seen in studies conducted by other groups.
In an analysis of 15 studies involving brain tumors, a significant association was not observed. A preventive effect was observed for meningiomas, and the authors note that this effect was largely the result of a decreased OR in the INTERPHONE studies. A significant negative association was found when studies involving benign brain tumors were analyzed and, again, this was largely the result of a decreased OR in the INTERPHONE studies, report the authors.
They note that all of the studies conducted by Hardell et al used blinding to the status of patient cases or control subjects and were categorized as having a high methodologic quality, whereas most of the INTERPHONE studies and studies by other groups did not use blinding and were "thus categorized as having low methodologic quality."
The authors conclude that they "found a large discrepancy in the association between [cell] phone use and tumor risk by research group, which is confounded with the methodologic quality of the research," and that "our findings should be confirmed in prospective cohort studies to provide a higher level of evidence."
Critique and Response
In a letter to the editor, Andreas Stang, MD, Andrea Schmidt-Pokrzywniak, PhD, and Oliver Kuss, PhD, all from the Martin-Luther-Universität Halle-Wittenberg, Halle (Saale), Germany, expressed their concerns about some of the methodology in the meta-analysis. In particular, they point out that the study authors used the Newcastle-Ottawa Scale (NOS) to assess the quality of published case–control studies, but that "the validity of this checklist approach is at best unknown or doubtful."
Dr. Myung and colleagues, in their published response, "acknowledge that several methodologic issues raised by Stang et al are important for our main conclusions," and agree that the NOS is not an ideal quality-assessment tool for case–control studies because it has not yet been fully validated. However, they note that other checklists used to assess the quality of observational studies in systematic reviews have not been fully validated either. Of these tools, they considered the NOS to be comprehensive for case–control studies, and selected it for their quality assessment.
A second letter from Jack T. Rowley, PhD, from GSM Association in London, United Kingdom, and Michael J. Milligan, secretary general of Mobile Manufacturers Forum in Brussels, Belgium, rejected the "suggestion that there was any influence by our organizations on the scientific conduct of the INTERPHONE studies." They acknowledge that, in some cases, partial funding was provided by the GSM Association and Mobile Manufacturers Forum, but explain that funding was also received from noncommercial sources.
They also point out that a higher quality score was given to the Hardell group of studies, even though other analyses have raised methodologic questions about them.
Funding sources can influence research in subtle ways.
In response, the meta-analysis authors write that although they would prefer to believe that the design and conduct of the INTERPHONE studies were not influenced by the cell-phone industry, "nonetheless, we recommend that research on the topic of [cell]-phone use and health should not be funded by the industry because funding sources can influence research in subtle ways, and to preserve the credibility of the research it is important to avoid even the appearance of a conflict of interest."
However, they agree that the Hardell studies might have some methodologic limitations and acknowledge that they did not consider information and recall bias or validation of the self-reported indices of cell-phone use because the NOS does not include these items.
In a third letter, Florence Samkange-Zeeb, MPH, from the Universitätsmedizin der Johannes Gutenberg-Universität Mainz in Germany, and colleagues note that the authors "give no rationale" for pooling studies that cover a broad spectrum of heterogeneous and biologically diverse cancer sites, for which the localized exposure from the use of cell phones is completely different.
They also did not "understand why blinding is used as the major quality criteria," and found it surprising that there was no mention of the concerns that have been raised about the Hardell studies. As an example, they write, there have been questions about selection of the target population and the way the response rates were defined.
"In our opinion, this meta-analysis is an example of what happens when authors may have the technical skills [to perform] a meta-analysis, but are unfamiliar with the topic," they write.
The study authors responded by noting that there is "substantial precedent for pooling studies to examine the association of a potential risk factor with tumor risk in biologically diverse sites." They point out that researchers have pooled study results that reported the association between smoking and various heterogeneous diseases, including diabetes, cardiovascular disease, and cancers, to determine morbidity.
They reiterate the importance of blinding in this analysis, because "blinding and comparable response rates among case and control groups constituted the most important items in quality assessment using the NOS." These 2 items differentiated the 2 largest groups of studies in the meta-analysis, which were the Hardell and INTERPHONE studies.
"One of the problems in case–control studies is bias due to measurement error caused by the retrospective approach to measuring the predictor variable, and a recommended strategy for avoiding measurement error is blinding," they add.
Regarding the Hardell series, they agree with the critics that the differences in the methodologies, analyses, and presentation between the Hardell and other studies should have been explored. These issues and other potential confounding factors in the Hardell studies need to be explored in further studies, they write, and this issue was already discussed in their paper.
"We had no vested interest in the outcome of our meta-analysis" they point out.
The study was supported in part by the Centers for Disease Control and Prevention. The authors have disclosed no relevant financial relationships.
J Clin Oncol. 2009; 27:5565-5572. Abstract
J Clin Oncol. Published online January 25, 2010. Abstract, Abstract, Abstract, Abstract
.
Roxanne Nelson
February 5, 2010 — Cell phones have become an integral part of everyday life, but concerns about their safety persist. A meta-analysis, published in the November 20 issue of the Journal of Clinical Oncology, which found evidence linking cell phone use to an increased risk for tumors has since attracted criticism.
The meta-analysis found that, overall, the use of cell phones was not significantly associated with the risk for tumors in a random-effects model meta-analysis. Compared with people who never or rarely used a cell phone, the odds ratio (OR) for the overall use of cell phones was 0.98 for malignant and benign tumors (95% confidence interval [CI], 0.89 - 1.07).
However, it also found that cell-phone use of 10 years or longer was associated with a risk for tumors in 13 studies that reported this association (OR, 1.18; 95% CI, 1.04 - 1.34).
The authors, led by Seung-Kwon Myung, MD, MS, from the National Cancer Center in Goyang, South Korea, write that the results of the studies included in their analysis varied widely, and appeared to depend on who conducted and funded the research and the controls used for bias and errors.
"We found a large discrepancy in the association between [cell] phone use and tumor risk by research group, which is confounded with the methodologic quality of the research," they noted.
However, in subsequent letters to the editor, published online January 25 in the journal, the meta-analysis was criticized for having methodologic flaws and issues and a number of limitations.
No Conclusive Evidence
A number of epidemiologic studies have reported associations between the use of cell phones and malignant or benign tumors of the brain and of the head and neck, non-Hodgkin's lymphoma, and testicular cancer. Results have been inconclusive or even contradictory. But as previously reported by Medscape Oncology, a report released in August 2009 by the International Electromagnetic Field Collaborative suggested that the regular use of cell phones can result in a "significant" risk for brain tumors.
Soon after the release of that report, a US Senate hearing on the health effects of cell-phone use was held; it concluded that more and better research is needed to determine if there is a risk to human health. Several nations have decided not to wait for additional data, have issued warnings about the use of cell phones, and advise taking precautionary measures. In the United States, the state of Maine is considering legislation that would require placing warnings on all cell phones.
Long-Term Use Associated With Benign Tumors
The meta-analysis was conducted to investigate the association between cell-phone use and the risk for malignant and benign conditions. It included 23 case–control studies, and involved 37,916 participants (12,344 patient cases and 25,572 control subjects).
They observed that the studies included in their meta-analysis varied in quality, and some that suggested there was little to no risk did not correct for bias. In 8 high-quality studies that used blinding, a significant positive association (harmful effect) was observed; in a fixed-effects analysis of 15 studies that did not use blinding, a significant negative association (protective effect) was observed.
A subgroup meta-analysis by methodologic quality showed a significant positive association in the high-quality studies (OR, 1.09; 95% CI, 1.01 - 1.18), whereas a negative association was observed in the low-quality studies. In that subgroup meta-analysis, cell-phone use of 10 years or longer was significantly positively associated with the risk for benign tumors but not for malignant tumors.
"Distinct Pattern" Seen
Another factor affecting the validity of the meta-analysis is the funding sources of each research group, "because it is possible that these may have influenced the respective study designs and results," the authors write. In subgroup meta-analyses by research group/funding source, they observed a "distinct pattern" in their findings. A positive association was seen in 7 studies, conducted by Swedish oncologist Lennart Hardell, MD, and colleagues, that were independent of industry funding. Conversely, a negative association was seen in the industry-funded INTERPHONE studies. No association was seen in studies conducted by other groups.
In an analysis of 15 studies involving brain tumors, a significant association was not observed. A preventive effect was observed for meningiomas, and the authors note that this effect was largely the result of a decreased OR in the INTERPHONE studies. A significant negative association was found when studies involving benign brain tumors were analyzed and, again, this was largely the result of a decreased OR in the INTERPHONE studies, report the authors.
They note that all of the studies conducted by Hardell et al used blinding to the status of patient cases or control subjects and were categorized as having a high methodologic quality, whereas most of the INTERPHONE studies and studies by other groups did not use blinding and were "thus categorized as having low methodologic quality."
The authors conclude that they "found a large discrepancy in the association between [cell] phone use and tumor risk by research group, which is confounded with the methodologic quality of the research," and that "our findings should be confirmed in prospective cohort studies to provide a higher level of evidence."
Critique and Response
In a letter to the editor, Andreas Stang, MD, Andrea Schmidt-Pokrzywniak, PhD, and Oliver Kuss, PhD, all from the Martin-Luther-Universität Halle-Wittenberg, Halle (Saale), Germany, expressed their concerns about some of the methodology in the meta-analysis. In particular, they point out that the study authors used the Newcastle-Ottawa Scale (NOS) to assess the quality of published case–control studies, but that "the validity of this checklist approach is at best unknown or doubtful."
Dr. Myung and colleagues, in their published response, "acknowledge that several methodologic issues raised by Stang et al are important for our main conclusions," and agree that the NOS is not an ideal quality-assessment tool for case–control studies because it has not yet been fully validated. However, they note that other checklists used to assess the quality of observational studies in systematic reviews have not been fully validated either. Of these tools, they considered the NOS to be comprehensive for case–control studies, and selected it for their quality assessment.
A second letter from Jack T. Rowley, PhD, from GSM Association in London, United Kingdom, and Michael J. Milligan, secretary general of Mobile Manufacturers Forum in Brussels, Belgium, rejected the "suggestion that there was any influence by our organizations on the scientific conduct of the INTERPHONE studies." They acknowledge that, in some cases, partial funding was provided by the GSM Association and Mobile Manufacturers Forum, but explain that funding was also received from noncommercial sources.
They also point out that a higher quality score was given to the Hardell group of studies, even though other analyses have raised methodologic questions about them.
Funding sources can influence research in subtle ways.
In response, the meta-analysis authors write that although they would prefer to believe that the design and conduct of the INTERPHONE studies were not influenced by the cell-phone industry, "nonetheless, we recommend that research on the topic of [cell]-phone use and health should not be funded by the industry because funding sources can influence research in subtle ways, and to preserve the credibility of the research it is important to avoid even the appearance of a conflict of interest."
However, they agree that the Hardell studies might have some methodologic limitations and acknowledge that they did not consider information and recall bias or validation of the self-reported indices of cell-phone use because the NOS does not include these items.
In a third letter, Florence Samkange-Zeeb, MPH, from the Universitätsmedizin der Johannes Gutenberg-Universität Mainz in Germany, and colleagues note that the authors "give no rationale" for pooling studies that cover a broad spectrum of heterogeneous and biologically diverse cancer sites, for which the localized exposure from the use of cell phones is completely different.
They also did not "understand why blinding is used as the major quality criteria," and found it surprising that there was no mention of the concerns that have been raised about the Hardell studies. As an example, they write, there have been questions about selection of the target population and the way the response rates were defined.
"In our opinion, this meta-analysis is an example of what happens when authors may have the technical skills [to perform] a meta-analysis, but are unfamiliar with the topic," they write.
The study authors responded by noting that there is "substantial precedent for pooling studies to examine the association of a potential risk factor with tumor risk in biologically diverse sites." They point out that researchers have pooled study results that reported the association between smoking and various heterogeneous diseases, including diabetes, cardiovascular disease, and cancers, to determine morbidity.
They reiterate the importance of blinding in this analysis, because "blinding and comparable response rates among case and control groups constituted the most important items in quality assessment using the NOS." These 2 items differentiated the 2 largest groups of studies in the meta-analysis, which were the Hardell and INTERPHONE studies.
"One of the problems in case–control studies is bias due to measurement error caused by the retrospective approach to measuring the predictor variable, and a recommended strategy for avoiding measurement error is blinding," they add.
Regarding the Hardell series, they agree with the critics that the differences in the methodologies, analyses, and presentation between the Hardell and other studies should have been explored. These issues and other potential confounding factors in the Hardell studies need to be explored in further studies, they write, and this issue was already discussed in their paper.
"We had no vested interest in the outcome of our meta-analysis" they point out.
The study was supported in part by the Centers for Disease Control and Prevention. The authors have disclosed no relevant financial relationships.
J Clin Oncol. 2009; 27:5565-5572. Abstract
J Clin Oncol. Published online January 25, 2010. Abstract, Abstract, Abstract, Abstract
.
Tuesday, February 2, 2010
Study Linking Vaccine to Autism Broke Research Rules, U.K. Regulators Say
From WebMD Health News
Nicky Broyd
February 2, 2010 — The British doctor who led a study suggesting a link between the measles/ mumps/rubella (MMR) vaccine and autism acted "dishonestly and irresponsibly," a U.K. regulatory panel has ruled.
The panel represents the U.K. General Medical Council (GMC), which regulates the medical profession. It ruled only on whether Andrew Wakefield, MD, and two colleagues acted properly in carrying out their research, and not on whether MMR vaccine has anything to do with autism.
In the ruling, the GMC used strong language to condemn the methods used by Wakefield in conducting the study.
In the study, published 12 years ago, Wakefield and colleagues suggested there was a link between the MMR vaccine and autism.
Their study included only 12 children, but wide media coverage set off a panic among parents. Vaccinations plummeted; there was a subsequent increase in U.K. measles cases.
In 2004, 10 of the study's 13 authors disavowed the findings. The Lancet, which originally published the paper, retracted it after learning that Wakefield -- prior to designing the study -- had accepted payment from lawyers suing vaccine manufacturers for causing autism.
Fitness to Practice
The GMC's Fitness to Practise panel heard evidence and submissions for 148 days over two and a half years, hearing from 36 witnesses. It then spent 45 days deciding the outcome of the hearing. Besides Wakefield, two former colleagues went before the panel -John Walker-Smith and Simon Murch. They were all found to have broken guidelines.
The disciplinary hearing found Wakefield showed a "callous disregard" for the suffering of children and abused his position of trust. He'd also "failed in his duties as a responsible consultant."
He'd taken blood samples from children attending his son's birthday party in return for money, and was later filmed joking about it at a conference.
He'd also failed to disclose he'd received money for advising lawyers acting for parents who claimed their children had been harmed by the triple vaccine.
Not Over Yet
The GMC will next decide whether Wakefield and his former colleagues committed serious professional misconduct. That could lead to being struck off the medical register. That decision may not be taken for several more months.
Wakefield wasn't in the hearing, but outside the GMC offices he told reporters, "Naturally I am extremely disappointed by the outcome of today's proceedings. The allegations against me and against my colleagues are both unfounded and unjust." He continued, "I invite anyone to examine the contents of these proceedings and come to their own conclusion."
Wakefield was cheered by a group of parents outside the hearing who are still sure he is right, even though his findings have been widely discredited.
"It remains for me to thank the parents whose commitment and loyalty has been extraordinary," he said. "I want to reassure them that science will continue in earnest."
Wakefield now works in the U.S. at an autism center called Thoughtful House, which he helped found. In a statement on its web site the center states that it is "disappointed" by the GMC decision, believing the charges against the three doctors were "unfounded and unfair."
On the web site's "frequently asked questions" the center asks: "Has Dr. Wakefield been accused of any breach of medical ethics while serving as the Executive Director of Thoughtful House?" The answer is "Absolutely not."
Safety of MMR Vaccine
The government and medical experts continue to stress that the MMR vaccine is safe.
The MMR triple vaccine was licensed in the U.S. in 1971 and first used in the U.K. in 1988. Over 100 countries now use it, and it is estimated that more than 500 million doses have been administered.
At the peak of the MMR scare in 2002, there were 1,531 articles about MMR in the U.K. national press; in 1998 there had been just 86.
Between 2001 and 2003, U.K. opinion polls showed that the percent of people believing the MMR vaccine to be safe dropped from over 70% to just over 50%.
U.K. Health Protection Agency figures show measles incidence increased dramatically following the drop in the number of children being vaccinated. The number of confirmed cases between 2007 and 2008 was 2,349, roughly equal to the combined total for the previous eleven years.
SOURCES:
U.K. General Medical Council.
General Medical Counsel, "Fitness to Practise Panel Hearing, 28 January 2010."
Andrew Wakefield, MD.
Nicky Broyd
February 2, 2010 — The British doctor who led a study suggesting a link between the measles/ mumps/rubella (MMR) vaccine and autism acted "dishonestly and irresponsibly," a U.K. regulatory panel has ruled.
The panel represents the U.K. General Medical Council (GMC), which regulates the medical profession. It ruled only on whether Andrew Wakefield, MD, and two colleagues acted properly in carrying out their research, and not on whether MMR vaccine has anything to do with autism.
In the ruling, the GMC used strong language to condemn the methods used by Wakefield in conducting the study.
In the study, published 12 years ago, Wakefield and colleagues suggested there was a link between the MMR vaccine and autism.
Their study included only 12 children, but wide media coverage set off a panic among parents. Vaccinations plummeted; there was a subsequent increase in U.K. measles cases.
In 2004, 10 of the study's 13 authors disavowed the findings. The Lancet, which originally published the paper, retracted it after learning that Wakefield -- prior to designing the study -- had accepted payment from lawyers suing vaccine manufacturers for causing autism.
Fitness to Practice
The GMC's Fitness to Practise panel heard evidence and submissions for 148 days over two and a half years, hearing from 36 witnesses. It then spent 45 days deciding the outcome of the hearing. Besides Wakefield, two former colleagues went before the panel -John Walker-Smith and Simon Murch. They were all found to have broken guidelines.
The disciplinary hearing found Wakefield showed a "callous disregard" for the suffering of children and abused his position of trust. He'd also "failed in his duties as a responsible consultant."
He'd taken blood samples from children attending his son's birthday party in return for money, and was later filmed joking about it at a conference.
He'd also failed to disclose he'd received money for advising lawyers acting for parents who claimed their children had been harmed by the triple vaccine.
Not Over Yet
The GMC will next decide whether Wakefield and his former colleagues committed serious professional misconduct. That could lead to being struck off the medical register. That decision may not be taken for several more months.
Wakefield wasn't in the hearing, but outside the GMC offices he told reporters, "Naturally I am extremely disappointed by the outcome of today's proceedings. The allegations against me and against my colleagues are both unfounded and unjust." He continued, "I invite anyone to examine the contents of these proceedings and come to their own conclusion."
Wakefield was cheered by a group of parents outside the hearing who are still sure he is right, even though his findings have been widely discredited.
"It remains for me to thank the parents whose commitment and loyalty has been extraordinary," he said. "I want to reassure them that science will continue in earnest."
Wakefield now works in the U.S. at an autism center called Thoughtful House, which he helped found. In a statement on its web site the center states that it is "disappointed" by the GMC decision, believing the charges against the three doctors were "unfounded and unfair."
On the web site's "frequently asked questions" the center asks: "Has Dr. Wakefield been accused of any breach of medical ethics while serving as the Executive Director of Thoughtful House?" The answer is "Absolutely not."
Safety of MMR Vaccine
The government and medical experts continue to stress that the MMR vaccine is safe.
The MMR triple vaccine was licensed in the U.S. in 1971 and first used in the U.K. in 1988. Over 100 countries now use it, and it is estimated that more than 500 million doses have been administered.
At the peak of the MMR scare in 2002, there were 1,531 articles about MMR in the U.K. national press; in 1998 there had been just 86.
Between 2001 and 2003, U.K. opinion polls showed that the percent of people believing the MMR vaccine to be safe dropped from over 70% to just over 50%.
U.K. Health Protection Agency figures show measles incidence increased dramatically following the drop in the number of children being vaccinated. The number of confirmed cases between 2007 and 2008 was 2,349, roughly equal to the combined total for the previous eleven years.
SOURCES:
U.K. General Medical Council.
General Medical Counsel, "Fitness to Practise Panel Hearing, 28 January 2010."
Andrew Wakefield, MD.
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