Multiple Courses of Antenatal Steroids Not Recommended for Preterm Birth
Laurie Barclay, MD
From Medscape Medical News
December 22, 2008 — Multiple courses of antenatal steroids every 14 days do not improve preterm birth outcomes, are linked to decreased size at birth, and are therefore not recommended, according to the results of a study reported in the December 20/27 issue of The Lancet.
"One course of antenatal corticosteroids reduces the risk of respiratory distress syndrome and neonatal death," write Kellie E. Murphy, from Mount Sinai Hospital, University of Toronto in Toronto, Ontario, Canada, and colleagues from the MACS Collaborative Group.
The study sample consisted of 1,858 women at 25 to 32 weeks of gestation who were at high risk for preterm birth, who were still undelivered 14 to 21 days after an initial course of antenatal corticosteroids, and who continued to be at high risk. Participants were randomly assigned to receive multiple courses of antenatal corticosteroids (n = 937) or placebo (n = 921), every 14 days until week 33 or delivery, whichever came first.
Compared with infants exposed to placebo, those exposed to multiple courses of antenatal corticosteroids had similar morbidity and mortality rates, with the main study endpoint occurring in 150 (12.9%) vs 143 (12.5%). Compared with infants in the placebo group, those in the multiple-dose corticosteroid group had lower birth weight (2,216 vs 2,330 g; P = .0026), shorter length (44.5 vs 45.4 cm; P < .001), and smaller head circumference (31.1 vs 31.7 cm; P < .001).
"Multiple courses of antenatal corticosteroids, every 14 days, do not improve preterm-birth outcomes, and are associated with a decreased weight, length, and head circumference at birth," the study authors write. "Therefore, this treatment schedule is not recommended."
In an accompanying comment, John P. Newnham, from the School of Women's and Infants' Health, University of Western Australia in Perth, and Karen Simmer, from King Edward and Princess Margaret Hospitals in Perth, note that follow-up of the children in this study will help shed light on any long-term effects of multiple doses of antenatal corticosteroids.
"Particular attention should be paid to those areas in which other studies have suggested problems, including behaviour, growth, glucose tolerance, and blood pressure," Drs. Newnham and Simmer write. "In the meantime, the evidence suggests it is prudent for obstetricians not to prescribe repeat injections of antenatal corticosteroids. Single-course therapy is of considerable benefit, but we should be aware of the potential dangers of giving too much of a good thing."
Lancet. 2008;372:2094-2095, 2143-2151.
Thursday, June 18, 2009
Tuesday, June 16, 2009
Long-Term Steroid Asthma Therapy Increases Fracture Risk in Children, Teens
Laurie Barclay & Désirée Lie
MEDSCAPE NEWS
July 7, 2008 — Long-term use of corticosteroids for asthma treatment may increase fracture risk in male children and teens, according to the results of a cohort follow-up study reported in the July issue of Pediatrics.
"Systemic corticosteroids are known to induce osteoporosis and increase the risk for fractures in adults and children," write H. William Kelly, PharmD, from the University of New Mexico Health Sciences Center in Albuquerque, and colleagues from the Childhood Asthma Management Program (CAMP) Research Group.
"Inhaled corticosteroids have been shown to increase the risk for osteoporosis and fractures in adults at risk; however, long-term prospective studies of children to assess risks of multiple short courses of oral corticosteroids and chronic inhaled corticosteroids have not been performed. Thus, we assessed the effects of multiple short courses of oral corticosteroids and long-term inhaled corticosteroids on bone mineral accretion over a period of years."
This study was a follow-up of children with mild to moderate asthma who were initially randomized in the CAMP trial. All patients had serial dual-energy radiographic absorptiometry scans of the lumbar spine for bone mineral density. Median duration of follow-up was 7 years. Of the initial cohort, 84% of those with asthma who were aged 5 to 12 years at baseline (531 boys and 346 girls) underwent calculation of annual bone mineral accretion.
In boys but not girls, therapy with oral corticosteroid bursts was associated with a dosage-dependent decrease in bone mineral accretion (0.052, 0.049, and 0.046 g/cm2 per year) and an increased risk for osteopenia (10%, 14%, and 21%) for 0, 1 to 4, and 5 or more courses, respectively.
Cumulative inhaled corticosteroid use was linked to a small reduction in bone mineral accretion in boys but not in girls, but not to an increased risk for osteopenia in children of either sex.
Limitations of this study include therapy during follow-up controlled by the primary care clinician, failure to control for asthma severity, and lack of accepted normal values for bone mineral density in children to establish z scores to define osteopenia and osteoporosis.
"Multiple oral corticosteroid bursts over a period of years can produce a dosage-dependent reduction in bone mineral accretion and increased risk for osteopenia in children with asthma," the study authors write.
"Inhaled corticosteroid use has the potential for reducing bone mineral accretion in male children progressing through puberty, but this risk is likely to be outweighed by the ability to reduce the amount of oral corticosteroids used in these children."
Pediatrics. 2008;122:e53-e61.
MEDSCAPE NEWS
July 7, 2008 — Long-term use of corticosteroids for asthma treatment may increase fracture risk in male children and teens, according to the results of a cohort follow-up study reported in the July issue of Pediatrics.
"Systemic corticosteroids are known to induce osteoporosis and increase the risk for fractures in adults and children," write H. William Kelly, PharmD, from the University of New Mexico Health Sciences Center in Albuquerque, and colleagues from the Childhood Asthma Management Program (CAMP) Research Group.
"Inhaled corticosteroids have been shown to increase the risk for osteoporosis and fractures in adults at risk; however, long-term prospective studies of children to assess risks of multiple short courses of oral corticosteroids and chronic inhaled corticosteroids have not been performed. Thus, we assessed the effects of multiple short courses of oral corticosteroids and long-term inhaled corticosteroids on bone mineral accretion over a period of years."
This study was a follow-up of children with mild to moderate asthma who were initially randomized in the CAMP trial. All patients had serial dual-energy radiographic absorptiometry scans of the lumbar spine for bone mineral density. Median duration of follow-up was 7 years. Of the initial cohort, 84% of those with asthma who were aged 5 to 12 years at baseline (531 boys and 346 girls) underwent calculation of annual bone mineral accretion.
In boys but not girls, therapy with oral corticosteroid bursts was associated with a dosage-dependent decrease in bone mineral accretion (0.052, 0.049, and 0.046 g/cm2 per year) and an increased risk for osteopenia (10%, 14%, and 21%) for 0, 1 to 4, and 5 or more courses, respectively.
Cumulative inhaled corticosteroid use was linked to a small reduction in bone mineral accretion in boys but not in girls, but not to an increased risk for osteopenia in children of either sex.
Limitations of this study include therapy during follow-up controlled by the primary care clinician, failure to control for asthma severity, and lack of accepted normal values for bone mineral density in children to establish z scores to define osteopenia and osteoporosis.
"Multiple oral corticosteroid bursts over a period of years can produce a dosage-dependent reduction in bone mineral accretion and increased risk for osteopenia in children with asthma," the study authors write.
"Inhaled corticosteroid use has the potential for reducing bone mineral accretion in male children progressing through puberty, but this risk is likely to be outweighed by the ability to reduce the amount of oral corticosteroids used in these children."
Pediatrics. 2008;122:e53-e61.
Rapid Weight Gain in First Three Months of Life -not good
Rapid Growth in Infancy Linked to Cardiovascular and Metabolic Risk Factors Later in Life
by Michael O’Riordan & Penny Murata
Medscape News
June 12, 2009 — Important determinants of cardiovascular disease and type 2 diabetes mellitus in adulthood are increased in infants who gain weight rapidly early in life, a new study has shown. Increased weight gain relative to height in early infancy is associated with reduced insulin sensitivity and serum high-density lipoprotein (HDL)-cholesterol levels, as well as increased waist circumference and serum triglyceride levels, report investigators.
"Rapid weight gain in the first three months of life," write Dr Ralph Leunissen (Erasmus Medical Center, Rotterdam, the Netherlands) and colleagues in the June 3, 2009 issue of the Journal of the American Medical Association, "is more detrimental than slow weight gain. More studies are required to investigate which factors determine rapid weight gain in early infancy, because those results might lead to interventions that could decrease the risk for development of cardiovascular disease and type 2 diabetes later in life."
The data on birth weight and growth early in life is mixed. Some studies have shown that low birth weight is associated with cardiovascular disease and type 2 diabetes later in life, while others suggested that rapid growth patterns in infancy and childhood were an important determinant of risk later in life. Other data have shown that poor growth early in life, followed by catch-up growth after age two, is related to an increased risk of cardiovascular disease later in life.
In this study, Leunissen and colleagues wanted to determine which period in the first year of life is related to determinants of cardiovascular risk. They collected observational data from 217 participants aged 18 to 24 years participating in the Programming Factors for Growth and Metabolism (PROGRAM) study.
Weight gain in the first three months was inversely associated with insulin sensitivity and HDL-cholesterol levels. There were positive associations between weight gain during these months and waist circumference, acute insulin response, ratio of total cholesterol to HDL cholesterol, and triglyceride levels. Acute insulin response was positively associated with weight gain in months 3 to 6 after birth, but no other association was observed, including in months 6 to 9 and 9 months to one year.
A subgroup analysis was performed in 87 subjects who gained weight rapidly in the first year to assess possible relationships between the "tempo" of weight gain and determinants of cardiovascular disease and type 2 diabetes.
Individuals who gained weight rapidly during the first three months had more body fat, central adiposity, and reduced insulin sensitivity in early adulthood than those with slower growth. Rapid weight gain was defined as >0.67 standard deviation from the mean.
"This indicates that having a low birth weight for gestational age is not directly related with an unfavorable cardiovascular and metabolic profile, but increased weight gain during early childhood is," write Leunissen and colleagues, adding that the tempo of weight gain might even be more important than the timing.
The group said that the reasons for the increased cardiovascular risk are unknown, but that nutrient-enriched diets that contribute to rapid weight gain might have adverse effects of cardiovascular risk factors later in life. Formula-fed infants, for example, grow at a faster rate than breast-fed infants but are more likely to be overweight later in life. Their study, however, is limited, in that there are no nutritional data available. Future studies need to confirm these findings and to determine which factors determine weight gain, as well as to investigate associations with parental factors, such as genetics and maternal health during pregnancy.
Clinical Implications
Weight gain in the first 3 months of life is linked with reduced insulin sensitivity and serum HDL level and greater waist circumference, acute insulin response, ratio of total cholesterol to HDL cholesterol level, and triglyceride level in early adulthood.
Rapid weight gain in the first 3 months of life is linked with greater body fat percentage and central adiposity and reduced insulin sensitivity in early adulthood.
source: http://cme.medscape.com/viewarticle/704321?sssdmh=dm1.486011&src=nldne
by Michael O’Riordan & Penny Murata
Medscape News
June 12, 2009 — Important determinants of cardiovascular disease and type 2 diabetes mellitus in adulthood are increased in infants who gain weight rapidly early in life, a new study has shown. Increased weight gain relative to height in early infancy is associated with reduced insulin sensitivity and serum high-density lipoprotein (HDL)-cholesterol levels, as well as increased waist circumference and serum triglyceride levels, report investigators.
"Rapid weight gain in the first three months of life," write Dr Ralph Leunissen (Erasmus Medical Center, Rotterdam, the Netherlands) and colleagues in the June 3, 2009 issue of the Journal of the American Medical Association, "is more detrimental than slow weight gain. More studies are required to investigate which factors determine rapid weight gain in early infancy, because those results might lead to interventions that could decrease the risk for development of cardiovascular disease and type 2 diabetes later in life."
The data on birth weight and growth early in life is mixed. Some studies have shown that low birth weight is associated with cardiovascular disease and type 2 diabetes later in life, while others suggested that rapid growth patterns in infancy and childhood were an important determinant of risk later in life. Other data have shown that poor growth early in life, followed by catch-up growth after age two, is related to an increased risk of cardiovascular disease later in life.
In this study, Leunissen and colleagues wanted to determine which period in the first year of life is related to determinants of cardiovascular risk. They collected observational data from 217 participants aged 18 to 24 years participating in the Programming Factors for Growth and Metabolism (PROGRAM) study.
Weight gain in the first three months was inversely associated with insulin sensitivity and HDL-cholesterol levels. There were positive associations between weight gain during these months and waist circumference, acute insulin response, ratio of total cholesterol to HDL cholesterol, and triglyceride levels. Acute insulin response was positively associated with weight gain in months 3 to 6 after birth, but no other association was observed, including in months 6 to 9 and 9 months to one year.
A subgroup analysis was performed in 87 subjects who gained weight rapidly in the first year to assess possible relationships between the "tempo" of weight gain and determinants of cardiovascular disease and type 2 diabetes.
Individuals who gained weight rapidly during the first three months had more body fat, central adiposity, and reduced insulin sensitivity in early adulthood than those with slower growth. Rapid weight gain was defined as >0.67 standard deviation from the mean.
"This indicates that having a low birth weight for gestational age is not directly related with an unfavorable cardiovascular and metabolic profile, but increased weight gain during early childhood is," write Leunissen and colleagues, adding that the tempo of weight gain might even be more important than the timing.
The group said that the reasons for the increased cardiovascular risk are unknown, but that nutrient-enriched diets that contribute to rapid weight gain might have adverse effects of cardiovascular risk factors later in life. Formula-fed infants, for example, grow at a faster rate than breast-fed infants but are more likely to be overweight later in life. Their study, however, is limited, in that there are no nutritional data available. Future studies need to confirm these findings and to determine which factors determine weight gain, as well as to investigate associations with parental factors, such as genetics and maternal health during pregnancy.
Clinical Implications
Weight gain in the first 3 months of life is linked with reduced insulin sensitivity and serum HDL level and greater waist circumference, acute insulin response, ratio of total cholesterol to HDL cholesterol level, and triglyceride level in early adulthood.
Rapid weight gain in the first 3 months of life is linked with greater body fat percentage and central adiposity and reduced insulin sensitivity in early adulthood.
source: http://cme.medscape.com/viewarticle/704321?sssdmh=dm1.486011&src=nldne
Sunday, June 14, 2009
Excessive Soft Drink Consumption - Avoid
From Reuters Health Information
High Daily Consumption of Cola Soft Drinks Can Cause Hypokalemic Myopathy
NEW YORK (Reuters Health) Jun 05 - Drinking several liters of cola-containing soft drinks per day can cause chronic hypokalemia leading to muscle weakness and even paralysis, according to a review article in the International Journal of Clinical Practice for June.
While one might argue that "excessive soft drink consumption at this level is so rare that it is not a public health issue," the author of an accompanying editorial writes, "the problem is that we have every reason to think that it is not rare."
In a search of PubMed, Dr. Moses Elisaf and associates at the University of Ioannina, Greece, identified six reports of cola-induced hypokalemia published since 1994. Quantities of cola consumed ranged from 2 to 9 liters/day. Muscle complaints ranged from mild weakness to profound paralysis, and all patients had abnormally low serum potassium levels.
"Fortunately," Dr. Elisaf and colleagues write, "all patients had a rapid and complete recovery after the discontinuation of cola ingestion and the oral or intravenous supplementation of potassium."
The authors suggest that one component with the potential to alter potassium metabolism is high-fructose corn syrup, which can cause chronic osmotic diarrhea and potassium depletion. Glucose -- by inducing osmotic diuresis and hyperinsulinemia - or caffeine - by causing potassium redistribution into cells and/or increased renal potassium excretion - may also be responsible.
Dr. Elisaf's team cautions that "the cola-induced chronic hypokalemia clearly predisposes to the development of potentially fatal complications such as cardiac arrhythmias."
In his editorial, Dr. Clifford D. Packer at the Louis Stokes Cleveland VA Medical Center in Cleveland, Ohio, comments that "with aggressive mass marketing, super-sizing of soft drinks, and the effects of caffeine tolerance and dependence, there is very little doubt that tens of millions of people in industrialized countries drink at least 2-3 L of cola per day."
The resulting drop in serum potassium levels increases the risk of cardiac ischemia, heart failure, or left ventricular hypertrophy. He also notes that sugar-sweetened soft drinks have been linked to osteoporosis, gout, GERD, chronic kidney disease, secondary hyperparathyroidism, esophageal perforation, hematuria, tongue erosions, and gastritis.
Dr. Packer advises physicians to start asking their patients about soft drink consumption, and stresses that "the soft drink industry needs to promote safe and moderate use of its products for all age groups, reduce serving sizes, and pay heed to the rising call for healthier drinks."
Int J Clin Pract 2009;63:833-835,900-902.
High Daily Consumption of Cola Soft Drinks Can Cause Hypokalemic Myopathy
NEW YORK (Reuters Health) Jun 05 - Drinking several liters of cola-containing soft drinks per day can cause chronic hypokalemia leading to muscle weakness and even paralysis, according to a review article in the International Journal of Clinical Practice for June.
While one might argue that "excessive soft drink consumption at this level is so rare that it is not a public health issue," the author of an accompanying editorial writes, "the problem is that we have every reason to think that it is not rare."
In a search of PubMed, Dr. Moses Elisaf and associates at the University of Ioannina, Greece, identified six reports of cola-induced hypokalemia published since 1994. Quantities of cola consumed ranged from 2 to 9 liters/day. Muscle complaints ranged from mild weakness to profound paralysis, and all patients had abnormally low serum potassium levels.
"Fortunately," Dr. Elisaf and colleagues write, "all patients had a rapid and complete recovery after the discontinuation of cola ingestion and the oral or intravenous supplementation of potassium."
The authors suggest that one component with the potential to alter potassium metabolism is high-fructose corn syrup, which can cause chronic osmotic diarrhea and potassium depletion. Glucose -- by inducing osmotic diuresis and hyperinsulinemia - or caffeine - by causing potassium redistribution into cells and/or increased renal potassium excretion - may also be responsible.
Dr. Elisaf's team cautions that "the cola-induced chronic hypokalemia clearly predisposes to the development of potentially fatal complications such as cardiac arrhythmias."
In his editorial, Dr. Clifford D. Packer at the Louis Stokes Cleveland VA Medical Center in Cleveland, Ohio, comments that "with aggressive mass marketing, super-sizing of soft drinks, and the effects of caffeine tolerance and dependence, there is very little doubt that tens of millions of people in industrialized countries drink at least 2-3 L of cola per day."
The resulting drop in serum potassium levels increases the risk of cardiac ischemia, heart failure, or left ventricular hypertrophy. He also notes that sugar-sweetened soft drinks have been linked to osteoporosis, gout, GERD, chronic kidney disease, secondary hyperparathyroidism, esophageal perforation, hematuria, tongue erosions, and gastritis.
Dr. Packer advises physicians to start asking their patients about soft drink consumption, and stresses that "the soft drink industry needs to promote safe and moderate use of its products for all age groups, reduce serving sizes, and pay heed to the rising call for healthier drinks."
Int J Clin Pract 2009;63:833-835,900-902.
Thursday, June 11, 2009
Melatonin May Counter Sleep Disorders in Autistic Children
by Jim Kling
June 10, 2009 (Seattle, Washington) — A pilot study in children with autism spectrum disorders (ASD) suggests that low-dose melatonin may be an effective treatment for insomnia in these patients. In this study, positive effects of treatment were seen on both sleep and daytime behavior.
Melatonin "does appear to be effective," Beth Malow, MD, professor of neurology at Vanderbilt University, in Nashville, Tennessee, said during her presentation. She emphasized that the study was small and that more work needs to be done.
"Kids with autism who have some sleep problems are candidates for melatonin, and I believe that large, randomized clinical trials of melatonin are well warranted," she concluded.
Dr. Malow presented the findings here at SLEEP 2009: 23rd Annual Meeting of the Associated Professional Sleep Societies.
Increasing Melatonin Use
Children with ASD may experience insomnia, the researchers note, and parents are increasingly turning to melatonin as a sleep aid. However, not much is known about its potential adverse effects. Melatonin also comes in a wide variety of formulations, some with additives such as antihistamines or vitamins.
Parents perceive melatonin as a natural treatment, but the wide variety of formulations makes it difficult for practicing physicians to assess its utility. "I don't know what they're taking," said 1 attendee, referring to his autistic patients.
To better assess melatonin's safety and efficacy in autistic children, the researchers conducted a 17-week study of children with ASD who had trouble falling asleep.
The study enrolled children aged 4 to 10 years diagnosed with ASD who required at least 30 minutes to fall asleep on 3 out of 7 nights of the week. Parents received behavioral sleep education before melatonin treatments began, and this was continued through the study. Parents filled out sleep and behavioral survey forms at the beginning and end of all study procedures. Patients wore actigraphy watches (Respironics) for 17 weeks.
After 3 weeks, patients were given 1-mg melatonin (Natrol). Every 3 weeks thereafter, the dose was escalated to 3 mg, 6 mg, and 9 mg, until the patient fell asleep within 30 minutes at least 5 out of 7 nights per week. Pre- and posttreatment actigraphy measures were analyzed using a Wilcoxon signed-ranks test.
Ten patients completed the study with no adverse effects. Three required a dose of 1 mg, 5 required 3 mg, and 2 required 6 mg to achieve the desired end point. No patients required a 9-mg dose.
Patients started with a mean sleep latency of 38.7 minutes that was reduced to a mean of 21.8 minutes with treatment (P = 0.039).
The Children's Sleep Habits Questionnaire showed improvement in sleep-onset delay (P = 0.008) and sleep duration (P = 0.004), repetitive-behavior scale domains of compulsive (P = 0.002) and ritualistic behavior (P = 0.004), and Parent Interview for Autism domain of affective responses (P = 0.02).
Definite Promise
Asked for perspective on these findings, Judith Owens, MD, professor of pediatrics at Brown Medical School, in Providence, Rhode Island, who moderated the session, said the data support the safety, tolerability, and efficacy of melatonin in this patient population.
"This was open label, so you can't get solid conclusions of efficacy, but it definitely has promise," Dr. Owens told Medscape Neurology.
The project was supported by grants from the Autism Speaks/Dana Foundation, the National Institutes of Health, and Vanderbilt University. Melatonin was provided by Natrol. Dr. Malow and Dr. Owens have disclosed no relevant financial relationships.
SLEEP 2009: 23rd Annual Meeting of the Associated Professional Sleep Societies: Abstract 0189. Presented June 8, 2009.
Jim Kling is a freelance writer for Medscape.
June 10, 2009 (Seattle, Washington) — A pilot study in children with autism spectrum disorders (ASD) suggests that low-dose melatonin may be an effective treatment for insomnia in these patients. In this study, positive effects of treatment were seen on both sleep and daytime behavior.
Melatonin "does appear to be effective," Beth Malow, MD, professor of neurology at Vanderbilt University, in Nashville, Tennessee, said during her presentation. She emphasized that the study was small and that more work needs to be done.
"Kids with autism who have some sleep problems are candidates for melatonin, and I believe that large, randomized clinical trials of melatonin are well warranted," she concluded.
Dr. Malow presented the findings here at SLEEP 2009: 23rd Annual Meeting of the Associated Professional Sleep Societies.
Increasing Melatonin Use
Children with ASD may experience insomnia, the researchers note, and parents are increasingly turning to melatonin as a sleep aid. However, not much is known about its potential adverse effects. Melatonin also comes in a wide variety of formulations, some with additives such as antihistamines or vitamins.
Parents perceive melatonin as a natural treatment, but the wide variety of formulations makes it difficult for practicing physicians to assess its utility. "I don't know what they're taking," said 1 attendee, referring to his autistic patients.
To better assess melatonin's safety and efficacy in autistic children, the researchers conducted a 17-week study of children with ASD who had trouble falling asleep.
The study enrolled children aged 4 to 10 years diagnosed with ASD who required at least 30 minutes to fall asleep on 3 out of 7 nights of the week. Parents received behavioral sleep education before melatonin treatments began, and this was continued through the study. Parents filled out sleep and behavioral survey forms at the beginning and end of all study procedures. Patients wore actigraphy watches (Respironics) for 17 weeks.
After 3 weeks, patients were given 1-mg melatonin (Natrol). Every 3 weeks thereafter, the dose was escalated to 3 mg, 6 mg, and 9 mg, until the patient fell asleep within 30 minutes at least 5 out of 7 nights per week. Pre- and posttreatment actigraphy measures were analyzed using a Wilcoxon signed-ranks test.
Ten patients completed the study with no adverse effects. Three required a dose of 1 mg, 5 required 3 mg, and 2 required 6 mg to achieve the desired end point. No patients required a 9-mg dose.
Patients started with a mean sleep latency of 38.7 minutes that was reduced to a mean of 21.8 minutes with treatment (P = 0.039).
The Children's Sleep Habits Questionnaire showed improvement in sleep-onset delay (P = 0.008) and sleep duration (P = 0.004), repetitive-behavior scale domains of compulsive (P = 0.002) and ritualistic behavior (P = 0.004), and Parent Interview for Autism domain of affective responses (P = 0.02).
Definite Promise
Asked for perspective on these findings, Judith Owens, MD, professor of pediatrics at Brown Medical School, in Providence, Rhode Island, who moderated the session, said the data support the safety, tolerability, and efficacy of melatonin in this patient population.
"This was open label, so you can't get solid conclusions of efficacy, but it definitely has promise," Dr. Owens told Medscape Neurology.
The project was supported by grants from the Autism Speaks/Dana Foundation, the National Institutes of Health, and Vanderbilt University. Melatonin was provided by Natrol. Dr. Malow and Dr. Owens have disclosed no relevant financial relationships.
SLEEP 2009: 23rd Annual Meeting of the Associated Professional Sleep Societies: Abstract 0189. Presented June 8, 2009.
Jim Kling is a freelance writer for Medscape.
Saturday, May 30, 2009
Red and Processed Meat Intake Linked to Mortality
News Author: Laurie Barclay, MD
CME Author: Charles Vega, MD, FAAFP
Arch Intern Med. 2009;169:543-545, 562-571
March 26, 2009 — Eating red and processed meat is associated with modest increases in total mortality, cancer mortality, and cardiovascular disease mortality rates, according to the results of a large, prospective study reported in the March 23 issue of the Archives of Internal Medicine.
"High intakes of red or processed meat may increase the risk of mortality," write Rashmi Sinha, PhD, from the National Cancer Institute, National Institutes of Health, Department of Health and Human Services in Rockville, Maryland, and colleagues. "Our objective was to determine the relations of red, white, and processed meat intakes to risk for total and cause-specific mortality."
The National Institutes of Health–AARP Diet and Health Study enrolled approximately half a million people aged 50 to 71 years at baseline. A food frequency questionnaire administered at baseline allowed estimation of meat intake, and Cox proportional hazards regression models allowed calculation of hazard ratios (HRs) and 95% confidence intervals (CIs) within quintiles of meat intake.
Red meat included all types of beef and pork such as bacon, beef, cold cuts, hamburgers, hotdogs, steak, and meats in pizza, lasagna, and stew. White meat included chicken, turkey, and fish along with poultry cold cuts, canned tuna, and low-fat hotdogs. Processed meats could include either red or white meats in the form of sandwich meats or cold cuts as well as bacon, red meat and poultry sausages, and regular hotdogs and low-fat hotdogs made from poultry. The authors note that some of the meats may overlap in the 3 categories, but they were not duplicated or used in the same models in the study analysis.
The models considered covariates of age, education, marital status, presence or absence of family history of cancer (for cancer mortality only), race, body mass index, smoking history, physical activity, energy intake, alcohol drinking, use of vitamin supplements, fruit consumption, vegetable consumption, and use of menopausal hormone therapy in women. Primary endpoints of the study were total mortality and deaths caused by cancer, cardiovascular disease, injury and sudden deaths, and all other causes.
During 10 years of follow-up, 47,976 men and 23,276 women died.
Overall mortality risks were increased for men and women in the highest vs the lowest quintile of red meat intake (HR, 1.31; 95% CI, 1.27 - 1.35; and HR, 1.36; 95% CI, 1.30-1.43, respectively) and processed meat intake (HR, 1.16; 95% CI, 1.12 - 1.20; and HR, 1.25; 95% CI, 1.20 - 1.31, respectively).
Men and women with higher intake also had increased risks for cancer mortality for red meat (HR, 1.22; 95% CI, 1.16 - 1.29; and HR, 1.20; 95% CI, 1.12 - 1.30, respectively) and processed meat (HR, 1.12; 95% CI, 1.06 - 1.19; and HR, 1.11; 95% CI 1.04 - 1.19, respectively).
Cardiovascular disease risk was increased for men and women in the highest quintile of intake of red meat (HR, 1.27; 95% CI, 1.20 - 1.35; and HR, 1.50; 95% CI, 1.37 - 1.65, respectively) and processed meat (HR, 1.09; 95% CI, 1.03 - 1.15; and HR, 1.38; 95% CI, 1.26 - 1.51, respectively).
For the highest vs the lowest quintile of white meat intake for both men and women, there was an inverse association for total mortality, cancer mortality, and mortality from all other causes.
"Red and processed meat intakes were associated with modest increases in total mortality, cancer mortality, and cardiovascular disease mortality," the study authors write. "In contrast, high white meat intake and a low-risk meat diet was associated with a small decrease in total and cancer mortality."
Limitations of this study include possible residual confounding by smoking; possible measurement error; and cohort predominantly non-Hispanic white, more educated, with less smoking, less fat and red meat intake, and more intake of fiber and fruit and vegetables than similarly aged adults in the US population, limiting generalizability.
"These results complement the recommendations by the American Institute for Cancer Research and the World Cancer Research Fund to reduce red and processed meat intake to decrease cancer incidence," the study authors write. "Future research should investigate the relation between subtypes of meat and specific causes of mortality."
In an accompanying editorial, Barry M. Popkin, PhD, from the University of North Carolina, Chapel Hill, discusses how the implications of reducing excessive meat intake would relate to several major global concerns.
"Of equal importance is the role of clinicians as public health advocates," Dr. Popkin writes. "Far too few clinicians speak out on topics such as this. What the public hears is the side of the profession that is preaching vegetarian diets and not the side of the profession that is discussing moderation as a healthy option."
The Intramural Research Program of the National Institute of Health, National Cancer Institute supported this study in part. The study authors have disclosed no relevant financial relationships. Dr. Popkin is not a vegetarian and has no financial conflict of interest related to any food product as it affects health.
Clinical Context
Dietary patterns are changing around the globe, and an editorial by Popkin, which accompanies the current article, describes these patterns. Individuals in higher-income countries continue to consume meat and dairy products at 2 to 3 times the rate of lower-income countries. However, meat and dairy products are becoming a more common dietary staple in some developing countries, particularly India, China, and Brazil.
In part, higher consumption of meat is the result of a lower cost of beef vs several decades ago. At the same time, the cost of grains and rice has increased significantly on the world market in the last 6 years. This has important environmental consequences, as the need for water and feedstock is much higher in raising animals vs raising basic crops.
Meat consumption can have significant effects on rates of obesity and overall health as well. The current study examines a large cohort of adults to determine the effect of meat intake on mortality rates.
CME Author: Charles Vega, MD, FAAFP
Arch Intern Med. 2009;169:543-545, 562-571
March 26, 2009 — Eating red and processed meat is associated with modest increases in total mortality, cancer mortality, and cardiovascular disease mortality rates, according to the results of a large, prospective study reported in the March 23 issue of the Archives of Internal Medicine.
"High intakes of red or processed meat may increase the risk of mortality," write Rashmi Sinha, PhD, from the National Cancer Institute, National Institutes of Health, Department of Health and Human Services in Rockville, Maryland, and colleagues. "Our objective was to determine the relations of red, white, and processed meat intakes to risk for total and cause-specific mortality."
The National Institutes of Health–AARP Diet and Health Study enrolled approximately half a million people aged 50 to 71 years at baseline. A food frequency questionnaire administered at baseline allowed estimation of meat intake, and Cox proportional hazards regression models allowed calculation of hazard ratios (HRs) and 95% confidence intervals (CIs) within quintiles of meat intake.
Red meat included all types of beef and pork such as bacon, beef, cold cuts, hamburgers, hotdogs, steak, and meats in pizza, lasagna, and stew. White meat included chicken, turkey, and fish along with poultry cold cuts, canned tuna, and low-fat hotdogs. Processed meats could include either red or white meats in the form of sandwich meats or cold cuts as well as bacon, red meat and poultry sausages, and regular hotdogs and low-fat hotdogs made from poultry. The authors note that some of the meats may overlap in the 3 categories, but they were not duplicated or used in the same models in the study analysis.
The models considered covariates of age, education, marital status, presence or absence of family history of cancer (for cancer mortality only), race, body mass index, smoking history, physical activity, energy intake, alcohol drinking, use of vitamin supplements, fruit consumption, vegetable consumption, and use of menopausal hormone therapy in women. Primary endpoints of the study were total mortality and deaths caused by cancer, cardiovascular disease, injury and sudden deaths, and all other causes.
During 10 years of follow-up, 47,976 men and 23,276 women died.
Overall mortality risks were increased for men and women in the highest vs the lowest quintile of red meat intake (HR, 1.31; 95% CI, 1.27 - 1.35; and HR, 1.36; 95% CI, 1.30-1.43, respectively) and processed meat intake (HR, 1.16; 95% CI, 1.12 - 1.20; and HR, 1.25; 95% CI, 1.20 - 1.31, respectively).
Men and women with higher intake also had increased risks for cancer mortality for red meat (HR, 1.22; 95% CI, 1.16 - 1.29; and HR, 1.20; 95% CI, 1.12 - 1.30, respectively) and processed meat (HR, 1.12; 95% CI, 1.06 - 1.19; and HR, 1.11; 95% CI 1.04 - 1.19, respectively).
Cardiovascular disease risk was increased for men and women in the highest quintile of intake of red meat (HR, 1.27; 95% CI, 1.20 - 1.35; and HR, 1.50; 95% CI, 1.37 - 1.65, respectively) and processed meat (HR, 1.09; 95% CI, 1.03 - 1.15; and HR, 1.38; 95% CI, 1.26 - 1.51, respectively).
For the highest vs the lowest quintile of white meat intake for both men and women, there was an inverse association for total mortality, cancer mortality, and mortality from all other causes.
"Red and processed meat intakes were associated with modest increases in total mortality, cancer mortality, and cardiovascular disease mortality," the study authors write. "In contrast, high white meat intake and a low-risk meat diet was associated with a small decrease in total and cancer mortality."
Limitations of this study include possible residual confounding by smoking; possible measurement error; and cohort predominantly non-Hispanic white, more educated, with less smoking, less fat and red meat intake, and more intake of fiber and fruit and vegetables than similarly aged adults in the US population, limiting generalizability.
"These results complement the recommendations by the American Institute for Cancer Research and the World Cancer Research Fund to reduce red and processed meat intake to decrease cancer incidence," the study authors write. "Future research should investigate the relation between subtypes of meat and specific causes of mortality."
In an accompanying editorial, Barry M. Popkin, PhD, from the University of North Carolina, Chapel Hill, discusses how the implications of reducing excessive meat intake would relate to several major global concerns.
"Of equal importance is the role of clinicians as public health advocates," Dr. Popkin writes. "Far too few clinicians speak out on topics such as this. What the public hears is the side of the profession that is preaching vegetarian diets and not the side of the profession that is discussing moderation as a healthy option."
The Intramural Research Program of the National Institute of Health, National Cancer Institute supported this study in part. The study authors have disclosed no relevant financial relationships. Dr. Popkin is not a vegetarian and has no financial conflict of interest related to any food product as it affects health.
Clinical Context
Dietary patterns are changing around the globe, and an editorial by Popkin, which accompanies the current article, describes these patterns. Individuals in higher-income countries continue to consume meat and dairy products at 2 to 3 times the rate of lower-income countries. However, meat and dairy products are becoming a more common dietary staple in some developing countries, particularly India, China, and Brazil.
In part, higher consumption of meat is the result of a lower cost of beef vs several decades ago. At the same time, the cost of grains and rice has increased significantly on the world market in the last 6 years. This has important environmental consequences, as the need for water and feedstock is much higher in raising animals vs raising basic crops.
Meat consumption can have significant effects on rates of obesity and overall health as well. The current study examines a large cohort of adults to determine the effect of meat intake on mortality rates.
Sunday, May 24, 2009
Melamine & kidney damage
Melamine Nephrotoxicity: An Emerging Epidemic in an Era of Globalization: Global Impact of the Milk Contamination in China
Vivek Bhalla,1 Paul C. Grimm,2 Glenn M. Chertow,1 Alan C. Pao 1
Division of Nephrology, Department of Medicine, Stanford University, Stanford, California
Global Impact of the Milk Contamination in China
Melamine contamination of foodstuffs produced in China is an international public health crisis, and the full repercussions of this scandal may not be known for many years. A recent report by the World Health Organization (WHO) estimated that 51,900 children in the People's Republic of China have been affected and six deaths have resulted due to melamine contamination.[1] After initial reports of nephrolithiasis among Chinese infants who drank milk-based formula surfaced in the summer of 2008, a systematic search by the Chinese Administration of Quality Supervision, Inspection, and Quarantine (AQSIQ) revealed 22 commercial brands of milk powder (69 batches out of 491 tested) with detectable levels of melamine.[2] Thirteen of the batches contained > 2.5 parts per million (p.p.m.) (2.5 mg/kg), the level of melamine above which the United States Food and Drug Agency (USFDA) had conservatively concluded would exceed the tolerable daily intake of 0.063 mg/kg of body weight/day in humans.[3] The culprit powder with the highest melamine concentration, produced by the Shijiazhuang-based San Lu company, the largest national distributor and exporter of milk powder, contained samples with 2563 p.p.m. of melamine, more than 1000-fold higher than the USFDA tolerable daily intake.[2] As of 12 September 2008, 66 of 175 infant formula manufacturers across China had halted production, and the remaining 109 manufacturers were undergoing investigation. This controversy required reaction from the highest levels of the Chinese government. The chief of the AQSIQ, Li Changjang, resigned, and Premier Wen Jiabao recently apologized publicly and promised reform of current safety regulations.[4]
Children outside of mainland China in Taiwan, Hong Kong, and Macau have also been affected.[1] Reports of detectable melamine in foodstuffs from around the globe continue to document the widespread nature of this epidemic. Sixty-eight countries (see Figure 1) have already taken decisive action to limit the dissemination of contaminated products,[4] which include Chinese-made milk-based infant formula and milk-based products, such as cookies and chocolates (see Table 1). Other nations are now monitoring the incidence of nephrolithiasis as a surrogate for melamine intoxication in their respective populations.[5] Several international agencies including the World Health Organization (WHO), the Food and Agriculture Organization (FAO), the European Food Safety Association (EFSA), and the International Food Safety Authorities Network (INFOSAN) are working together to characterize and control this outbreak.[1] The USFDA has twice amended its assessment of melamine toxicity for infants, and concluded that only foods with less than 1 p.p.m. of melamine are safe for infants.[3] The USFDA has also announced the establishment of an office in Beijing, China to oversee exports shipped to the United States.[3]
Additional Melamine Contamination in Animal Feed
Two international incidents in 2004 and 2007 showed that pet food containing a wheat gluten exported from China was responsible for kidney failure and death in domesticated cats and dogs in the United States and Europe.[3] Pet food scraps in the United States from the 2007 outbreak revealed similar levels of melamine as the infant formulas recently produced in China, ranging from 9.4 to 1952 p.p.m.[3] as well as another compound, cyanuric acid.[3] The 2004 pet food outbreak is presumed to have been due to melamine because autopsy reports from 2004 are comparable with those of animals that died in 2007. In October 2008, hundreds of raccoon dogs in China died from kidney failure after the ingestion of melamine-contaminated animal feed. Reports from Hong Kong and other nations state that chicken eggs and fish (fit for human consumption) recently imported from China contain melamine,[4] providing circumstantial evidence that the food supply is now contaminated and demonstrating that this epidemic is pervasive. The WHO has criticized the Chinese government for not effectively eliminating melamine from the animal feed supply despite a ban imposed in June 2007.[4] Milk-based products, animals, and animal by-products are all believed to be potential sources of melamine exposure for humans.
Environmental Exposures and Kidney Disease
This Chinese milk controversy and emerging cases of kidney disease in infants is another reminder of how nephrology and the environment are intertwined. Many environmental and/or occupational kidney diseases have been described since the industrial revolution of the nineteenth century. Various toxins have been associated with AKI, CKD, and ESRD, whereas others have caused non-renal complications in persons with pre-existing kidney disease. Similar to melamine nephrotoxicity, most of these diseases have a known etiologic agent and yet, despite years of national and international safety regulations, are still with us today.
As organs responsible for much of the body's waste management, with extensive exposure to blood-borne toxins, the kidneys often bear the burden of clearing the bloodstream of materials to which humans are parenterally or enterally exposed. The recent recognition of acute phosphate nephropathy following exposure to phosphate-containing bowel preparations is a good example of this vulnerability.[14]
Just as melamine has emerged in the past few months, in an era of free trade and globalization, new toxins will certainly surface, and tools designed to rapidly identify cases and their etiology will be necessary. The prospect of earlier detection of AKI with novel biomarkers has gained traction over the past several years. Newer biomarkers could facilitate diagnosis of AKI in hospitalized patients and may also identify potentially nephrotoxic pharmaceuticals or food additives in preclinical studies.[15]
Several CKDs have been ascribed to occupational or environmental exposures. Occupational kidney diseases, including chronic lead nephropathy, cadmium nephrotoxicity, and nephropathy due to other heavy metals or solvents, have been described for decades,[13] but lead, for example, is still encountered today as a progression factor for CKD.[16] Analgesic nephropathy is caused by well-recognized, over-the-counter 'toxins,' particularly in Europe and Australia.[17] Aristolochic acid, which has been used as a component of weight loss regimens and is probably the etiologic agent of endemic Balkan nephropathy,[18] is an example of a toxin that was used therapeutically and/or was present in the environment and caused kidney disease for many years before being identified as such.
Several other toxic exposures have affected patients with pre-existing kidney disease by virtue of poor solute clearance. Itai-itai byo or 'ouch-ouch' disease in post-World War II Japan caused by cadmium contamination of rice fields downstream of metal mining operations - caused Fanconi syndrome and osteomalacia in many individuals, but those with decreased glomerular filtration rate were among the most severely affected.[13] Infants with CKD whose organ systems are still developing may be most sensitive and therefore act as 'sentinel canaries' for the detection of environmental toxins, where the effects may be amplified compared with those effects in adults. In pediatric patients with CKD, aluminum binders were often prescribed at the same time as citrate-containing base supplements to treat metabolic acidosis in CKD. This combination markedly increased the absorption of aluminum by the gastrointestinal tract further aggravating the neurotoxic effects of aluminum in the developing brain.[19] It is an important lesson that this interaction had been recognized in the early 1980s, but these therapies continued to be used by physicians for many years after. More recent concerns have centered on the use of gadolinium-chelating agents for contrast enhancement on magnetic resonance imaging. While epidemiologists eventually identified gadolinium as the culprit etiologic agent of nephrogenic systemic fibrosis, the insidious onset and relatively low incidence rate delayed recognition of the association for many years.[20]
These examples highlight the challenges facing nephrologists and other health providers in establishing links between hazardous environmental exposures, the development or progression of kidney disease, and/or complications of CKD. Particularly in view of the high prevalence of CKD, with a large fraction of the disease burden unexplained by known risk factors, we should probably adopt a high index of suspicion for environmental and/or occupational exposures as potential contributing causes.
for complete article:http://www.medscape.com/viewarticle/702630_6
Vivek Bhalla,1 Paul C. Grimm,2 Glenn M. Chertow,1 Alan C. Pao 1
Division of Nephrology, Department of Medicine, Stanford University, Stanford, California
Global Impact of the Milk Contamination in China
Melamine contamination of foodstuffs produced in China is an international public health crisis, and the full repercussions of this scandal may not be known for many years. A recent report by the World Health Organization (WHO) estimated that 51,900 children in the People's Republic of China have been affected and six deaths have resulted due to melamine contamination.[1] After initial reports of nephrolithiasis among Chinese infants who drank milk-based formula surfaced in the summer of 2008, a systematic search by the Chinese Administration of Quality Supervision, Inspection, and Quarantine (AQSIQ) revealed 22 commercial brands of milk powder (69 batches out of 491 tested) with detectable levels of melamine.[2] Thirteen of the batches contained > 2.5 parts per million (p.p.m.) (2.5 mg/kg), the level of melamine above which the United States Food and Drug Agency (USFDA) had conservatively concluded would exceed the tolerable daily intake of 0.063 mg/kg of body weight/day in humans.[3] The culprit powder with the highest melamine concentration, produced by the Shijiazhuang-based San Lu company, the largest national distributor and exporter of milk powder, contained samples with 2563 p.p.m. of melamine, more than 1000-fold higher than the USFDA tolerable daily intake.[2] As of 12 September 2008, 66 of 175 infant formula manufacturers across China had halted production, and the remaining 109 manufacturers were undergoing investigation. This controversy required reaction from the highest levels of the Chinese government. The chief of the AQSIQ, Li Changjang, resigned, and Premier Wen Jiabao recently apologized publicly and promised reform of current safety regulations.[4]
Children outside of mainland China in Taiwan, Hong Kong, and Macau have also been affected.[1] Reports of detectable melamine in foodstuffs from around the globe continue to document the widespread nature of this epidemic. Sixty-eight countries (see Figure 1) have already taken decisive action to limit the dissemination of contaminated products,[4] which include Chinese-made milk-based infant formula and milk-based products, such as cookies and chocolates (see Table 1). Other nations are now monitoring the incidence of nephrolithiasis as a surrogate for melamine intoxication in their respective populations.[5] Several international agencies including the World Health Organization (WHO), the Food and Agriculture Organization (FAO), the European Food Safety Association (EFSA), and the International Food Safety Authorities Network (INFOSAN) are working together to characterize and control this outbreak.[1] The USFDA has twice amended its assessment of melamine toxicity for infants, and concluded that only foods with less than 1 p.p.m. of melamine are safe for infants.[3] The USFDA has also announced the establishment of an office in Beijing, China to oversee exports shipped to the United States.[3]
Additional Melamine Contamination in Animal Feed
Two international incidents in 2004 and 2007 showed that pet food containing a wheat gluten exported from China was responsible for kidney failure and death in domesticated cats and dogs in the United States and Europe.[3] Pet food scraps in the United States from the 2007 outbreak revealed similar levels of melamine as the infant formulas recently produced in China, ranging from 9.4 to 1952 p.p.m.[3] as well as another compound, cyanuric acid.[3] The 2004 pet food outbreak is presumed to have been due to melamine because autopsy reports from 2004 are comparable with those of animals that died in 2007. In October 2008, hundreds of raccoon dogs in China died from kidney failure after the ingestion of melamine-contaminated animal feed. Reports from Hong Kong and other nations state that chicken eggs and fish (fit for human consumption) recently imported from China contain melamine,[4] providing circumstantial evidence that the food supply is now contaminated and demonstrating that this epidemic is pervasive. The WHO has criticized the Chinese government for not effectively eliminating melamine from the animal feed supply despite a ban imposed in June 2007.[4] Milk-based products, animals, and animal by-products are all believed to be potential sources of melamine exposure for humans.
Environmental Exposures and Kidney Disease
This Chinese milk controversy and emerging cases of kidney disease in infants is another reminder of how nephrology and the environment are intertwined. Many environmental and/or occupational kidney diseases have been described since the industrial revolution of the nineteenth century. Various toxins have been associated with AKI, CKD, and ESRD, whereas others have caused non-renal complications in persons with pre-existing kidney disease. Similar to melamine nephrotoxicity, most of these diseases have a known etiologic agent and yet, despite years of national and international safety regulations, are still with us today.
As organs responsible for much of the body's waste management, with extensive exposure to blood-borne toxins, the kidneys often bear the burden of clearing the bloodstream of materials to which humans are parenterally or enterally exposed. The recent recognition of acute phosphate nephropathy following exposure to phosphate-containing bowel preparations is a good example of this vulnerability.[14]
Just as melamine has emerged in the past few months, in an era of free trade and globalization, new toxins will certainly surface, and tools designed to rapidly identify cases and their etiology will be necessary. The prospect of earlier detection of AKI with novel biomarkers has gained traction over the past several years. Newer biomarkers could facilitate diagnosis of AKI in hospitalized patients and may also identify potentially nephrotoxic pharmaceuticals or food additives in preclinical studies.[15]
Several CKDs have been ascribed to occupational or environmental exposures. Occupational kidney diseases, including chronic lead nephropathy, cadmium nephrotoxicity, and nephropathy due to other heavy metals or solvents, have been described for decades,[13] but lead, for example, is still encountered today as a progression factor for CKD.[16] Analgesic nephropathy is caused by well-recognized, over-the-counter 'toxins,' particularly in Europe and Australia.[17] Aristolochic acid, which has been used as a component of weight loss regimens and is probably the etiologic agent of endemic Balkan nephropathy,[18] is an example of a toxin that was used therapeutically and/or was present in the environment and caused kidney disease for many years before being identified as such.
Several other toxic exposures have affected patients with pre-existing kidney disease by virtue of poor solute clearance. Itai-itai byo or 'ouch-ouch' disease in post-World War II Japan caused by cadmium contamination of rice fields downstream of metal mining operations - caused Fanconi syndrome and osteomalacia in many individuals, but those with decreased glomerular filtration rate were among the most severely affected.[13] Infants with CKD whose organ systems are still developing may be most sensitive and therefore act as 'sentinel canaries' for the detection of environmental toxins, where the effects may be amplified compared with those effects in adults. In pediatric patients with CKD, aluminum binders were often prescribed at the same time as citrate-containing base supplements to treat metabolic acidosis in CKD. This combination markedly increased the absorption of aluminum by the gastrointestinal tract further aggravating the neurotoxic effects of aluminum in the developing brain.[19] It is an important lesson that this interaction had been recognized in the early 1980s, but these therapies continued to be used by physicians for many years after. More recent concerns have centered on the use of gadolinium-chelating agents for contrast enhancement on magnetic resonance imaging. While epidemiologists eventually identified gadolinium as the culprit etiologic agent of nephrogenic systemic fibrosis, the insidious onset and relatively low incidence rate delayed recognition of the association for many years.[20]
These examples highlight the challenges facing nephrologists and other health providers in establishing links between hazardous environmental exposures, the development or progression of kidney disease, and/or complications of CKD. Particularly in view of the high prevalence of CKD, with a large fraction of the disease burden unexplained by known risk factors, we should probably adopt a high index of suspicion for environmental and/or occupational exposures as potential contributing causes.
for complete article:http://www.medscape.com/viewarticle/702630_6
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