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<recommendedContent xmlns="http://api.mspoke.com">
    <recommendedItem id="20100101_19_391"
                     title="Rare Genetic Deletion Linked to Morbid Obesity (CME/CE)"
                     score="0.009"
                     href="http://www.medpagetoday.com/Genetics/GeneralGenetics/tb/18286?impressionId=1265783499603"
                     
      &lt;p&gt;Missing sections of DNA may have a powerful impact on weight for a small segment of the population, researchers said.&lt;/p&gt;
&lt;p&gt;Nearly all teens and adults found to have a particular deletion of roughly 30-genes on chromosome 16p11.2 were obese  --  most morbidly so  --  with a body mass index of at least 40 kg/m&lt;sup&gt;2&lt;/sup&gt;, Philippe Froguel, MD, PhD, of Imperial College London, and colleagues reported in &lt;em&gt;Nature&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;While the variant appeared to explain only a small proportion of morbid obesity  --  0.7% in the study population  --  it was never present in healthy, normal-weight controls.&lt;/p&gt;
&lt;p&gt;&quot;Although the recent rise in obesity in the developed world is down to an unhealthy environment, with an abundance of unhealthy food and many people taking very little exercise, the difference in the way people respond to this environment is often genetic,&quot; Froguel said in a prepared statement.&lt;/p&gt;
&lt;p&gt;But with further findings like these, it may be possible to identify such individuals through genetic testing, he said.&lt;/p&gt;
&lt;p&gt;If so, &quot;We can then offer them appropriate support and medical interventions, such as the option of weight-loss surgery, to improve their long-term health,&quot; Froguel declared.&lt;/p&gt;
&lt;p&gt;Although researchers speculate that one in 20 cases of obesity may have a genetic cause, the genetic component remains largely elusive.&lt;/p&gt;
&lt;p&gt;Even accounting for such a small fraction of cases, the newly discovered 16p11.2 variant would be the second most frequent known genetic cause of obesity, Froguel&apos;s group said.&lt;/p&gt;
&lt;p&gt;Extensive genome-wide association studies have linked numerous single nucleotide polymorphisms (SNPs) to obesity, but added all together they account for only a small fraction of the known heritable component, the researchers said.&lt;/p&gt;
&lt;p&gt;&quot;The &apos;common disease, common variant&apos; hypothesis is increasingly coming under challenge,&quot; they wrote.&lt;/p&gt;
&lt;p&gt;Their team first identified the genetic deletion in teen and adults with learning difficulties or delayed development.&lt;/p&gt;
&lt;p&gt;Because the 31 individuals who had the nearly identical deletions of at least 593 kilobases at chromosome 16p11.2 in one copy of their DNA all had a BMI of over 30 kg/m&lt;sup&gt;2&lt;/sup&gt;, the researchers decided to dig a little deeper.&lt;/p&gt;
&lt;p&gt;&quot;Cohorts with extreme phenotypes that include obesity may be enriched for rare but very potent risk variants,&quot; making them easier to discover, they wrote.&lt;/p&gt;
&lt;p&gt;So they undertook a case-control study among 312 patients at three centers in Britain and France who presented with congenital malformations, developmental delay, or both, in addition to obesity.&lt;/p&gt;
&lt;p&gt;The same deletions were seen in 2.9% of these individuals.&lt;/p&gt;
&lt;p&gt;The function of the missing genes are not well known, but some have previously been associated with delayed development, autism, and schizophrenia.&lt;/p&gt;
&lt;p&gt;Notably, though, the frequency of deletion of these genes in the obese case-control cohort was &quot;appreciably higher&quot; than the less than 1% seen in the autism and other studies that didn&apos;t include obesity as an inclusion criteria, the researchers said.&lt;/p&gt;
&lt;p&gt;A second independent survey of genetic data at eight cytogenetic centers in France, Switzerland, and Estonia turned up a 0.6% rate among 3,947 people with developmental delay, malformations, or both, but who were not selected for obesity (&lt;em&gt;P&lt;/em&gt;=0.00022 versus the cohort selected for obesity).&lt;/p&gt;
&lt;p&gt;Analysis of those with the missing genes revealed an age-dependent link to weight: All four teens and adults were obese. Children were often obese (four of 15) or overweight (two of 15). Children under 2 years all had normal weight.&lt;/p&gt;
&lt;p&gt;So to see whether the deletion was independent of neurodevelopmental problems, Froguel&apos;s group examined genome-wide association study data from general population cohorts totaling 11,856 individuals along with 2,772 from childhood obesity and adult morbid obesity case-control studies, 931 in an extreme early-onset obesity study, and 141 who had bariatric weight-loss surgery.&lt;/p&gt;
&lt;p&gt;All adult carriers of the deletion were obese with the exception of one who was apparently diabetic. Each of the seven children and adolescents who carried the variant had a BMI in the top 0.1% for their age and gender.&lt;/p&gt;
&lt;p&gt;None had any reported developmental or cognitive problems. Four had reported hyperphagia with excessive hunger and food intake.&lt;/p&gt;
&lt;p&gt;Altogether, the 16p11.2 deletions predicted 29.8-fold elevated risk of obesity (&lt;em&gt;P&lt;/em&gt;=0.00000058) and 43.0-fold elevated risk of morbid obesity (&lt;em&gt;P&lt;/em&gt;=0.000000064) compared with lean or normal weight.&lt;/p&gt;
&lt;p&gt;By extrapolation, the researchers extrapolated that about 0.4% of all morbidly obese cases are attributable to an inherited 16p11.2 deletion, with 0.3% arising from a de novo deletion in the same genetic region.&lt;/p&gt;
&lt;p&gt;&quot;Although they may be heterogeneous in nature, these deletions are highly likely to be the causal variants,&quot; they wrote.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was supported by &quot;Le Conseil Regional Nord Pas de Calais/FEDER&quot; along with various governmental and industry supporters for the various component studies.&lt;/p&gt;&lt;p&gt;The researchers reported no financial conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_301"
                     title="Tight Glucose Control Fails in Septic Shock (CME/CE)"
                     score="0.003"
                     href="http://www.medpagetoday.com/CriticalCare/Sepsis/tb/18160?impressionId=1265783499603"
                     
      Septic shock patients treated with a corticosteroid get no survival advantage from tight glucose control or addition of a second corticosteroid to provide more mineralocorticoid activity, according to results of a randomized trial.&lt;br&gt;
&lt;br&gt;Aiming for normoglycemia at 80 to 110 mg/dL rather than the standard 150 mg/dL had no impact on inhospital mortality rates (45.9% versus 42.9%, &lt;em&gt;P&lt;/em&gt;=0.50), Djillali Annane, MD, of H&amp;#244;pital Raymond Poincar&amp;#233; in Garches, France, and colleagues found.&lt;br&gt;
&lt;br&gt;Inhospital mortality was likewise similar whether patients got hydrocortisone (Solu-Cortef) alone or with the addition of fludrocortisone ([Florinef] 42.9% versus 45.8%, &lt;em&gt;P&lt;/em&gt;=0.50), they reported in the Jan. 27 issue of the &lt;em&gt;Journal of the American Medical Association&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;This aggressive treatment strategy should not be routine, the researchers recommended.&lt;/p&gt;
&lt;p&gt;These findings largely match the general lack of benefit seen with tight glycemic control in recent studies with ICU patients overall.&lt;/p&gt;
&lt;p&gt;The prematurely terminated &lt;a href=&quot;http://www.medpagetoday.com/MeetingCoverage/SCCM/5096&quot; mce_href=&quot;http://www.medpagetoday.com/MeetingCoverage/SCCM/5096&quot; target=&quot;_blank&quot;&gt;European Glucontrol Trial&lt;/a&gt; found no mortality benefit but a seven-fold higher risk of hypoglycemia with an 80 to 110 mg/dL target in the ICU.&lt;/p&gt;
&lt;p&gt;In the &lt;a href=&quot;http://www.medpagetoday.com/CriticalCare/Intensivists/13397&quot; mce_href=&quot;http://www.medpagetoday.com/CriticalCare/Intensivists/13397&quot; target=&quot;_blank&quot;&gt;NICE-SUGAR&lt;/a&gt; study, 90-day mortality was actually higher in the tight glucose control group (27.9% versus 24.9%, &lt;em&gt;P&lt;/em&gt;=0.02), although there was a trend for benefit in patients who got corticosteroids (&lt;em&gt;P&lt;/em&gt;=0.06).&lt;/p&gt;
&lt;p&gt;Glucose targets are being re-evaluated across medicine as the &quot;lower is better&quot; paradigm has had a safety asterisk added everywhere from diabetes care to the ICU, noted Richard Bergenstal, MD, American Diabetes Association president for medicine and science.&lt;/p&gt;
&lt;p&gt;&quot;All of a sudden it&apos;s becoming more than a single number,&quot; he told &lt;em&gt;MedPage Today&lt;/em&gt;. &quot;Now be it inpatient or outpatient, we&apos;re realizing that ... you have to do it while you&apos;re minimizing hypoglycemia.&quot;&lt;/p&gt;
&lt;p&gt;A more nuanced and &lt;a href=&quot;http://www.medpagetoday.com/Cardiology/Diabetes/13818&quot; mce_href=&quot;http://www.medpagetoday.com/Cardiology/Diabetes/13818&quot; target=&quot;_blank&quot;&gt;individualized&lt;/a&gt; strategy is prudent, Bergenstal agreed.&lt;/p&gt;
&lt;p&gt;The current clinical uncertainty underscores the need for large-scale international cooperation to get adequately powered trials, according to an accompanying editorial.&lt;/p&gt;
&lt;p&gt;In it, Greet Van den Berghe, MD, PhD, of the Catholic University of Leuven, Belgium, cautioned that Annane&apos;s Corticosteroids and Intensive Insulin Therapy for Septic Shock (COIITSS) study was grossly underpowered.&lt;/p&gt;
&lt;p&gt;The initial studies that led to rapid adoption of intensive insulin therapy in ICUs around the world had suggested an absolute reduction in mortality of only 3%, whereas the COIITSS study projected a 12.5% absolute benefit.&lt;/p&gt;
&lt;p&gt;More importantly, the study achieved mean glucose levels of only between 120 and 130 mg/dL in the intervention group for whom the aim was 80 to 110 mg/dL, which resulted in considerable overlap with the standard care group for whom mean levels were about 145 mg/dL.&lt;/p&gt;
&lt;p&gt;This could account for the lack of difference in outcome, Van den Berghe said.&lt;/p&gt;
&lt;p&gt;But the intensive insulin group did have &quot;markedly&quot; lower blood glucose levels for the duration of their ICU stay and spent more time in the 80 to 110 mg/dL range compared with the standard care group (both &lt;em&gt;P&lt;/em&gt;&amp;lt;0.00001), the researchers noted.&lt;/p&gt;
&lt;p&gt;Because corticosteroids further aggravate the &quot;diabetes of injury&quot; seen with septic shock, Annane&apos;s group undertook a multicenter trial of 509 adults treated for septic shock with multiple organ dysfunction over a three year period at 11 ICUs in France.&lt;/p&gt;
&lt;p&gt;Patients were randomly assigned to tight glucose control using continuous intravenous insulin infusion to target a glucose level of 80 to 110 mg/dL or conventional insulin therapy targeted to guidelines-recommended 150 mg/dL or under. They were additionally randomized to receive hydrocortisone alone (50-mg bolus every six hours) or in combination with fludrocortisone (50-&amp;#956;g tablets once daily) for seven days.&lt;/p&gt;
&lt;p&gt;Aside from the lack of inhospital mortality advantage, tight glucose control also failed to produce a benefit for the following secondary endpoints: &lt;ul&gt; &lt;li&gt;Overall survival (hazard ratio 1.04, &lt;em&gt;P&lt;/em&gt;=0.78) &lt;/li&gt; &lt;li&gt; ICU length of stay for survivors (median 10 versus nine days, &lt;em&gt;P&lt;/em&gt;=0.68)&lt;/li&gt; &lt;li&gt;Duration of hospital stay overall (24 versus 22 days, &lt;em&gt;P&lt;/em&gt;=0.87)&lt;/li&gt; &lt;li&gt;Median vasopressor-free days (four for both, P=0.58)&lt;/li&gt; &lt;li&gt;Median mechanical ventilation-free days (10 versus 13, &lt;em&gt;P&lt;/em&gt;=0.51)&lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;Nor was there evidence for interaction with fludrocortisone in the primary endpoint (relative risk 0.89 versus 0.91 hydrocortisone alone, &lt;em&gt;P&lt;/em&gt;=0.31) or benefit in any other endpoint.&lt;/p&gt;
&lt;p&gt;The one effect of intensive insulin appeared to be an increase in episodes of severe hypoglycemia, defined by glucose falling below 40 mg/dL (mean 0.29 versus 0.14 episodes per patient, &lt;em&gt;P&lt;/em&gt;=0.003).&lt;/p&gt;
&lt;p&gt;However, having hypoglycemia did not increase the risk of death in intervention group patients compared with controls (45.2% versus 50%).&lt;/p&gt;
&lt;p&gt;The researchers cautioned that the study did not rule out a benefit from some degree of glucose control compared with none.&lt;/p&gt;
&lt;p&gt;They also noted that healthcare providers were not blinded to administration of fludrocortisone, for which no placebo was available.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was funded by the Assistance Publique&amp;#8211;H&amp;#244;pitaux de Paris. The researchers reported no conflicts of interest.&lt;/p&gt;&lt;p&gt;Van den Berghe, through the Catholic University of Leuven, reported receiving structural research financing from the Methusalem program, funded by the Flemish government.&lt;/p&gt;&lt;p&gt;Bergenstal reported receiving research funding and serving on advisory boards for various pharmaceutical companies related to novel diabetes drugs but without any personal financial compensation.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_291"
                     title="Obese Kids at Risk for Adult CVD (CME/CE)"
                     score="0.002"
                     href="http://www.medpagetoday.com/Endocrinology/MetabolicSyndrome/tb/18153?impressionId=1265783499603"
                     
      Obesity in children as young as 7 years old may put them at higher risk of heart disease and stroke later in life, even if they lack other cardiovascular risk factors such as high blood pressure, a new study found.&lt;br&gt;
&lt;br&gt;Obese children had higher levels of biomarkers for inflammation and prothrombosis than thin children. These included 10 times higher concentrations of high sensitivity C-reactive protein, a marker associated with increased risk of developing heart disease, cardiovascular disease, or other processes involving inflammation (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.01), according to an online report published Jan. 26 in the &lt;em&gt;Journal of Clinical Endocrinology and Metabolism&lt;/em&gt;.&lt;br&gt;
&lt;br&gt;Fibrinogen, interleukin-6 (IL-6) and plasminogen activator inhibitor 1 (PAI-1), other markers associated with inflammation and elevated blood clotting risk, were also elevated in obese children (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.01).&lt;p&gt;&lt;/p&gt;
&lt;p&gt;&quot;These observations reflect the unhealthy status of many youth at risk for adult cardiovascular disease in our catchment area in the southeastern U.S.,&quot; Nelly Mauras, MD, of Nemours Children&apos;s Clinic in Jacksonville, Fla., and colleagues wrote.&lt;/p&gt;
&lt;p&gt;The number of overweight children in the U.S. has tripled in the last 30 years, and more than 17% of children between the ages of 6 and 19 are overweight, according to the authors.&lt;/p&gt;
&lt;p&gt;Overweight children often develop metabolic syndrome, a collection of findings that includes abdominal obesity, elevated triglyceride and decreased HDL concentrations, hypertension, and impaired glucose tolerance. These put the youngsters at risk for early adult cardiovascular disease. Yet the exact definition of metabolic syndrome is a matter of ongoing debate.&lt;/p&gt;
&lt;p&gt;While children are typically considered to be at low risk of tissue damage if they show no signs of carbohydrate intolerance, hypertension, and dyslipidemia, Mauras and colleagues theorized that obese children without other risk factors for metabolic syndrome could still be at risk for later cardiovascular disease.&lt;/p&gt;
&lt;p&gt;To test this, they compared markers for inflammation and prothrombosis in 115 obese children and 88 lean children between the ages of 7 and 18 years. The study was conducted at Wolfson Children&apos;s Hospital, in Jacksonville, Fla.&lt;/p&gt;
&lt;p&gt;&quot;Children with obesity show a marked increase in the concentrations of hsCRP, 351 fibrinogen, IL-6 and PAI-1, reflective of a proinflammatory and prothrombotic state, even before the comorbidities of the Metabolic Syndrome are present, and even before the onset of puberty,&quot; they wrote.&lt;/p&gt;
&lt;p&gt;&quot;These data support the need for more aggressive interventions in very young children with obesity regardless of the absence of associated comorbidities.&quot;&lt;/p&gt;
&lt;p&gt;They also found that elevated levels of hsCRP and fibrinogen correlated with a wider waist circumference (R=0.73 and 0.40, respectively) and the percent of fat mass (r= 0.76 and 0.47) (&lt;em&gt;P&lt;/em&gt;=0.0001). Prepubertal obese children were taller than their lean counterparts (&lt;em&gt;P&lt;/em&gt;=0.005) and had higher systolic blood pressure.&lt;/p&gt;
&lt;p&gt;The authors noted that their study did not address whether the abnormalities they found are reversible with early therapeutic interventions.&lt;/p&gt;
&lt;p&gt;&quot;Weight reduction (or weight maintenance in many growing children) remains the cornerstone of any intervention in childhood obesity,&quot; they wrote.&lt;/p&gt;
&lt;p&gt;&quot;However, further longitudinal studies adding pharmacological interventions, in addition to lifestyle changes, will soon offer much needed insight as to whether a decrease in the proinflammatory and prothrombotic state will improve long-term cardiovascular risk of obese children, even in preadolescence and before the development of the Metabolic Syndrome.&quot;&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The authors reported no sources of funding for the study and no financial conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_288"
                     title="SSRIs Affect Breast Milk Production (CME/CE)"
                     score="0.002"
                     href="http://www.medpagetoday.com/Endocrinology/GeneralEndocrinology/tb/18149?impressionId=1265783499603"
                     
      &lt;p&gt;Women taking selective serotonin reuptake inhibitor (SSRI) antidepressants may experience delays in postpartum breast milk production, researchers said.&lt;/p&gt;
&lt;p&gt;Delayed secretory activation occurred in 87.5% of a small group of women taking SSRIs, compared with 43.5% of those not taking the drugs (RR 2, 95% CI 1.51 to 2.67, &lt;em&gt;P&lt;/em&gt;=0.02), according to Aaron M. Marshall, PhD, of the University of Cincinnati.&lt;/p&gt;
&lt;p&gt;The relative risk of delayed activation remained significantly higher (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.05) among SSRI users after adjustment for maternal age, obesity, cesarean delivery, infant gestational age, and infant breastfeeding behavior, the researchers reported online in the &lt;em&gt;Journal of Clinical Endocrinology and Metabolism&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;An early breastfeeding difficulty faced by many women, particularly those who are primiparous, is milk secretion delayed beyond 72 hours postpartum.&lt;/p&gt;
&lt;p&gt;These women also are at risk of early cessation of breastfeeding. In fact, only 11% of mothers in the U.S. breastfeed exclusively for the recommended six months.&lt;/p&gt;
&lt;p&gt;Studies in animal models and cell cultures suggested that serotonin (5-HT) is an important local regulator of lactation homeostasis, and the 5-HT transporter is expressed in mammary tissue at the apical membrane of epithelial cells.&lt;/p&gt;
&lt;p&gt;Serotonin is controlled intracellularly by a balance between synthesis and degradation, while extracellularly its availability is controlled through recycling by the 5-HT transporter.&lt;/p&gt;
&lt;p&gt;The 5-HT transporter also is the target for the most commonly prescribed class of antidepressants in the U.S. and other developed countries. These SSRI antidepressants are typically used to treat postpartum depression.&lt;/p&gt;
&lt;p&gt;The investigators conducted in vitro and animal studies to establish that the 5-HT transporter is expressed in breast tissue, particularly in the apical membranes of mammary epithelial cells, and that pharmacologic inhibition of the transporter disrupts tight junctures leading to a local involution-like effect.&lt;/p&gt;
&lt;p&gt;To examine the potential effect of SSRI inhibition on milk production in women, Marshall and colleagues enrolled 431 mothers as part of a longitudinal cohort study examining barriers to early lactation success.&lt;/p&gt;
&lt;p&gt;All were expecting their first live-born infants, had no known absolute contraindication to breastfeeding, and were at least 19 years old.&lt;/p&gt;
&lt;p&gt;Women taking SSRIs were more likely to have scored higher on a depressive symptom scale (as expected), and were somewhat more likely to be obese or to have had a cesarean delivery.&lt;/p&gt;
&lt;p&gt;Participating mothers were visited between 72 and 96 hours after giving birth to assess their breastfeeding experience and to determine the timing of secretory activation, and then seen again one week later.&lt;/p&gt;
&lt;p&gt;Delayed secretory activation was defined as initiation more than 72 hours postpartum.&lt;/p&gt;
&lt;p&gt;Median onset of secretory activation among the SSRI-treated mothers was 85.8 hours compared with 69.1 hours in mothers not using the drugs (&lt;em&gt;P&lt;/em&gt;=0.004).&lt;/p&gt;
&lt;p&gt;Eight women reported regular use of an SSRI medication. Seven experienced definite delayed secretory activation, and the eighth reported activation at 72 hours and therefore did not meet the defined cutoff for delayed activation.&lt;/p&gt;
&lt;p&gt;All women taking SSRIs had experienced secretory activation by their second visit a week after the first interview.&lt;/p&gt;
&lt;p&gt;The researchers noted that most studies on the effects of SSRI use during pregnancy and lactation have focused on the risks for developmental defects or whether the drugs passed into milk during lactation.&lt;/p&gt;
&lt;p&gt;This study, they said, is the first to report data on another important aspect of SSRI use during the peripartum, the effect on milk production.&lt;/p&gt;
&lt;p&gt;They concluded that the risk of delayed secretory activation was twice as great among primiparous women using an SSRI medication, and although the fraction of women taking the drugs was small, the risk was significant and remained so after adjustment for potential confounding factors.&lt;/p&gt;
&lt;p&gt;Further examination of this relationship is needed in larger groups of mothers, the researchers said, and in studies to determine if there are differences among the antidepressant medications.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;This work was supported by the National Institutes of Health, the USDA Cooperative State Research, Education, and Extension Service, and the Department of Health and Human Services.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_261"
                     title="Scrubbing Away Germs Can Backfire on Backsides (CME/CE)"
                     score="0"
                     href="http://www.medpagetoday.com/Pediatrics/GeneralPediatrics/tb/18121?impressionId=1265783499603"
                     
      Rashes from toilet seats are once again afflicting American children, and the rare condition is often misdiagnosed, which may delay proper treatment.&lt;br&gt;
&lt;br&gt;That&apos;s the conclusion from a report based of five-cases of toilet-seat contact dermatitis investigated by researchers at Johns Hopkins University School of Medicine and reported in the Jan. 25 issue of &lt;em&gt;Pediatrics&lt;/em&gt;.&lt;br&gt;
&lt;br&gt;While toilet-seat dermatitis is commonly thought to result from allergies to wooden seats, the report concludes that another source is plastic toilet seats cleaned with harsh detergents.&lt;/p&gt;
&lt;p&gt;&quot;This case series and previous reports have documented that toilet-seat dermatitis is much more common than previously recognized in the U.S. and around the world,&quot; Bernard A. Cohen, MD, and colleagues wrote.&lt;/p&gt;
&lt;p&gt;&quot;Furthermore, the incidence of this condition is rising in North America because of a resurgent popularity of exotic-wood toilet seats and frequent use of detergents that contain highly irritant/sensitizing compounds such as quaternary ammonium compounds, phenol, formaldehyde, etc. in public restrooms.&quot;&lt;/p&gt;
&lt;p&gt;Of the cases analyzed by the authors, two occurred in the U.S. and the other three occurred in India.&lt;/p&gt;
&lt;p&gt;Both U.S. cases were girls, a 6-year-old who had a rash for over two years before it was correctly diagnosed and a 10-year-old whose rash lasted for a year. In both cases, the rashes seemed to worsen during the school year when the girls were using school restrooms. The younger girl&apos;s dermatitis twice became infected with methicillin-resistant &lt;em&gt;Staphylococcus aureus &lt;/em&gt;and required treatment with antibiotics.&lt;/p&gt;
&lt;p&gt;After doctors determined the rashes were the result of contact with toilet seats and instructed the girls to use toilet-seat covers and apply moisturizers and topical steroids to the affected areas, the eruptions cleared up within a few weeks.&lt;/p&gt;
&lt;p&gt;The cases in India included a 14-month old boy and two girls, 12 and 10.&lt;/p&gt;
&lt;p&gt;The boy and the 12-year-old girl were both initially misdiagnosed with ringworm and unsuccessfully treated with clotrimazole cream. The other girl was unsuccessfully treated with ayurvedic and homeopathic topical medications before doctors diagnosed toilet-seat dermatitis. Two of the children were instructed to use soaps that only exacerbated the problem.&lt;/p&gt;
&lt;p&gt;In all three cases, the rashes cleared up with some combination of topical steroids, using toilet-seat covers, replacing the household toilet seat, and limiting time on the toilet.&lt;/p&gt;
&lt;p&gt;The authors distinguished between two types of toilet-seat dermatitis: allergic contact dermatitis, the better described form of the condition, in which a patient develops allergy to wooden toilet seats, and irritant contact dermatitis, in which the rashes result from contact with harsh detergents used on plastic toilet seats.&lt;/p&gt;
&lt;p&gt;They noted that detergents used in public restrooms and in hospitals are potentially more irritating to the skin than those used at home and that alkaline detergents are more likely to cause skin irritation than acidic detergents, because they perturb the body&apos;s natural acidic environment.&lt;/p&gt;
&lt;p&gt;Toilet-seat dermatitis was first identified as an external skin rash in 1927. Exposure to wooden toilet seats and associated varnish, lacquers, and paints led to sensitization and development of an allergic contact dermatitis.&lt;/p&gt;
&lt;p&gt;The condition nearly disappeared in the U.S. in 1980s and 1990s, after public facilities and homeowners in the U.S. changed from wooden to plastic toilet seats and sanitary seat covers became readily available.&lt;/p&gt;
&lt;p&gt;However, in recent years the number of cases has grown as a result of homeowners installing toilet seats made of exotic woods and the increased use of harsh toilet seat detergents.&lt;/p&gt;
&lt;p&gt;Most reports have focused on adults with rashes, but little previous attention has focused on the condition in children. &quot;In this case series we describe toilet-seat contact dermatitis in children and underscore a typical history and physical findings that we hope will aid clinicians in recognizing this disease,&quot; the authors wrote.&lt;/p&gt;
&lt;p&gt;&quot;It is important to underscore that regular use of toilet-seat covers is the key to success in treatment,&quot; the authors wrote. &quot;Such seat covers can be purchased at any major retailer such as Walmart or online.&lt;/p&gt;
&lt;p&gt;As an alternative, newspaper cutouts could be used to provide barrier protection. Although it is possible to develop an allergy to toilet-seat covers, none have been reported thus far in the literature.&quot;&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The authors reported no sources of funding or financial conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
</recommendedContent>