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<recommendedContent xmlns="http://api.mspoke.com">
    <recommendedItem id="20100101_19_412"
                     title="Depression During Pregnancy Linked to Kids&apos; Behavior Problems (CME/CE)"
                     score="0.013"
                     href="http://www.medpagetoday.com/Psychiatry/Depression/tb/18321?impressionId=1265789721800"
                     
      &lt;p&gt;Children born to mothers who were depressed during pregnancy were more than twice as likely to display antisocial behavior by age 16 as children whose mothers had not been depressed, researchers found.&lt;/p&gt;
&lt;p&gt;Of 120 mothers from South London who were followed from pregnancy through their children&apos;s teen years, 31% had depression during pregnancy, according to Dale Hay, PhD, of Cardiff University in Wales, and colleagues.&lt;/p&gt;
&lt;p&gt;Children born to these women were significantly more likely to display antisocial behavior (OR 2.46, 95% CI 1.10 to 5.48) and commit violent acts (OR 4.36, 95% CI 1.54 to 12.41) before age 16, the researchers reported in the January/February issue of &lt;em&gt;Child Development&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;The associations were magnified in women who also had a history of behavior problems when they were children.&lt;/p&gt;
&lt;p&gt;&quot;A focus on mothers&apos; history of conduct problems and depression during pregnancy, as opposed to broader measures of the social environment, would hold promise for more targeted early interventions to prevent the development of serious antisocial behavior,&quot; Hay&apos;s group wrote.&lt;/p&gt;
&lt;p&gt;Previous studies have linked mothers&apos; mental health problems in pregnancy with disruptive behaviors in their children, but it&apos;s unclear what explains the relationship, according to the researchers.&lt;/p&gt;
&lt;p&gt;To explore the issue, they turned to the South London Child Development Study, which prospectively followed 120 pregnant women and their children into the teenage years.&lt;/p&gt;
&lt;p&gt;All families came from a relatively disadvantaged urban area. These families were more likely to belong to the working class and to be from ethnic minority groups than the general U.K. population.&lt;/p&gt;
&lt;p&gt;One-third of the children had been arrested or diagnosed with a conduct disorder by age 16. Of these 88.9% had been arrested and 45% had committed violent acts, including theft from a person, violent disorder, fighting, carrying a weapon, and assault.&lt;/p&gt;
&lt;p&gt;The association between maternal depression during pregnancy and risk of antisocial behavior remained relatively constant in analyses controlling for family environment, a child&apos;s exposure to maternal depression after birth, mothers&apos; substance use during pregnancy, and parental antisocial behavior.&lt;/p&gt;
&lt;p&gt;None of the factors fully explained the relationship. Neither did the arrest history of the biological father.&lt;/p&gt;
&lt;p&gt;But, the researchers wrote in the paper, &quot;it would be unwise to conclude that paternal risk factors are unimportant, given that we did not have more detailed information about the father&apos;s own history of conduct disorders.&quot;&lt;/p&gt;
&lt;p&gt;They explored several potential mechanisms for the link between maternal depression and a child&apos;s behavior problems: &lt;ul&gt; &lt;li&gt;Direct effects on the fetus from biological correlates of the mothers&apos; depressive symptoms&lt;/li&gt; &lt;li&gt;Depression in pregnancy as a sign of environmental adversity&lt;/li&gt; &lt;li&gt;Re-exposure to maternal depression after birth&lt;/li&gt; &lt;li&gt;Indirect effects of depression on the developing fetus driven by mothers&apos; smoking, drinking, and drug taking during pregnancy &lt;/li&gt; &lt;li&gt;A genetic explanation whereby women who experience depression in pregnancy may also have a greater genetic risk for antisocial behavior, which they pass on to their offspring &lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;Hay and her colleagues noted that these explanations are not necessarily mutually exclusive.&lt;/p&gt;
&lt;p&gt;They also acknowledged some limitations of the study, including the lack of information about fetal growth and neuroendocrine measures on the mother and child and the relatively small sample size.&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 SLCDS has been funded by U.K. project grants from the Medical Research Council, by the Psychiatric Research Trust, and by the South West G.P. Trust. The current analysis was partially supported by an Economic and Social Research Council studentship to one of Hay&apos;s co-authors and by a Medical Research Council U.K. Program Grant.&lt;/p&gt;&lt;p&gt;The authors did not report any 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_384"
                     title="Few Surprises in Warning Signs for Infections in Kids (CME/CE)"
                     score="0.012"
                     href="http://www.medpagetoday.com/InfectiousDisease/GeneralInfectiousDisease/tb/18276?impressionId=1265789721800"
                     
      &lt;p&gt;Cyanosis, rapid breathing, poor peripheral perfusion, and petechial rash are red flags for serious childhood infection, a systematic review affirmed.&lt;/p&gt;
&lt;p&gt;Parental concern and physician instinct were also strong warning signs of serious illness in children in developed countries, but only in the primary care setting, Ann Van den Bruel, MD, of Katholieke Universiteit Leuven, Belgium, and colleagues reported online in &lt;em&gt;The Lancet&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;The researchers also looked for &quot;rule-out&quot; signs, with a negative likelihood ratio of less than 0.2, but found none, highlighting the difficulties facing clinicians.&lt;/p&gt;
&lt;p&gt;Nor were any of the red flags consistent at presentation in serious cases, suggesting that effective safeguards are needed, they said.&lt;/p&gt;
&lt;p&gt;&quot;There should be more emphasis on parental concern in the diagnostic process,&quot; they wrote. &quot;However, we now need to identify the level of risk at which clinical action should be taken.&quot;&lt;/p&gt;
&lt;p&gt;While the warning signs will be no surprise to most physicians, the poor evidence base should be shocking, Martin Dawes, MBBS, MD, of McGill University in Montreal, wrote in an accompanying editorial.&lt;/p&gt;
&lt;p&gt;Only one of the 30 studies included in the review was conducted in a primary setting, but that&apos;s the most common environment in which sick children are seen, he said.&lt;/p&gt;
&lt;p&gt;&quot;What is clear is that in 2010 we do not know how to effectively recognize or rule out severe disease in ill children and, what is more, we do not even have a cohesive national or even global research strategy to address this problem,&quot; he wrote.&lt;/p&gt;
&lt;p&gt;The World Health Organization has sponsored large scale studies to address these issues in resource-poor countries, Van den Bruel&apos;s group noted, but the range of diseases is different in developed countries, so that evidence doesn&apos;t generalize.&lt;/p&gt;
&lt;p&gt;The investigators reviewed studies of diagnostic accuracy or prediction rules for serious infection (mostly sepsis, bacteremia, meningitis, pneumonia, or urinary tract infection) in otherwise healthy children ages 1 month to 18 years, using features assessable in an ambulatory care setting.&lt;/p&gt;
&lt;p&gt;The studies had generally modest quality and were predominantly conducted in emergency departments.&lt;/p&gt;
&lt;p&gt;Fever of 104&amp;#176;F or more increased the likelihood of serious infection from 0.8% to 5.0% in the lowest prevalence setting.&lt;/p&gt;
&lt;p&gt;In the one primary care study where there was a low prevalence of disease (under 5%), a parent&apos;s concern that her child&apos;s illness was different from prior illnesses had a positive likelihood ratio of 14.40 for serious infection, while the clinician&apos;s instinct that something is wrong had a 23.50 positive likelihood ratio.&lt;/p&gt;
&lt;p&gt;Other predictors of the presence of serious infection and their positive likelihood ratios were: &lt;ul&gt; &lt;li&gt;Turning blue (52.20)&lt;/li&gt; &lt;li&gt;Poor peripheral circulation (4.71 to 38.80 in the low-to-intermediate prevalence setting and 2.39 to 17.70 in the high-prevalence setting)&lt;/li&gt; &lt;li&gt;Rapid breathing (1.26 to 9.78)&lt;/li&gt; &lt;li&gt;Shortness of breath (1.11 to 9.30)&lt;/li&gt; &lt;li&gt;Meningeal irritation (2.57 to 275)&lt;/li&gt; &lt;li&gt;Petechial rash (6.18 to 83.70)&lt;/li&gt; &lt;li&gt;Unconsciousness (19.80 to 155)&lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;Changed crying pattern was a potential red flag in a low prevalence setting with a positive likelihood ratio of 10.50, but actually was associated with reduced probability of serious disease in a high prevalence setting (positive likelihood ratio 0.49 to 0.74).&lt;/p&gt;
&lt;p&gt;Sending all children with a probability of serious infection greater than 5% to the hospital would overwhelm services there, although parents would &quot;probably be unhappy to know that their child was not being referred despite a 1 in 20 risk of serious infection,&quot; the researchers observed.&lt;/p&gt;
&lt;p&gt;The most widely studied decision rule, the Yale Observation Scale, had disappointingly little value in confirming the possibility of serious infection, they noted (positive likelihood ratio range 1.10 to 6.70, negative likelihood ratio range 0.16 to 0.97).&lt;/p&gt;
&lt;p&gt;The best performing clinical decision rule for excluding serious infection was a five-stage system with a negative likelihood ratio of 0.04.&lt;/p&gt;
&lt;p&gt;The researchers noted that these findings largely fit with those identified by WHO for developing countries, with the exception of difficulty feeding. The current review found that wasn&apos;t helpful in developed areas.&lt;/p&gt;
&lt;p&gt;They cautioned that their review was only as strong as the studies included and was particularly limited by the paucity of studies in the initial presentation primary care setting and difficulties of knowing how reproducible the findings were.&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 Health Technology Assessment and National Institute for Health Research National School for Primary Care Research. The researchers reported no conflicts of interest.&lt;/p&gt;&lt;p&gt;Dawes reported no 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_393"
                     title="SMFM: Gene Variants Linked to Preterm Labor (CME/CE)"
                     score="0.011"
                     href="http://www.medpagetoday.com/MeetingCoverage/SMFM/tb/18295?impressionId=1265789721800"
                     
      Genetic variants involved in regulating inflammation and the extracellular matrix may increase the risk of preterm birth, researchers say.&lt;br&gt;
&lt;br&gt;A single nucleotide polymorphism (SNP) in fetal interleukin-6 (&lt;em&gt;ILR6&lt;/em&gt;) and another in maternal tissue inhibitor of metalloproteinase 2 (&lt;em&gt;TIMP2&lt;/em&gt;) were each associated with a twofold increased risk of spontaneous preterm birth.&lt;br&gt;
&lt;br&gt;Roberto Romero, MD, of the National Institute of Child Health and Human Development, and colleagues reported the findings at the Society for Maternal-Fetal Medicine meeting in Chicago.&lt;/p&gt;
&lt;p&gt;&quot;The genetic makeup of both mother and fetus can contribute to the risk of premature labor,&quot; Romero told &lt;em&gt;MedPage Today&lt;/em&gt;. &quot;Our discovery . . . helps explain why some mothers have premature labor and delivery despite having optimal prenatal care.&quot;&lt;/p&gt;
&lt;p&gt;Inflammatory hormones have been shown to play a role in the labor process, and previous studies have found that a third of preterm infants are born to mothers with a silent amniotic infection.&lt;/p&gt;
&lt;p&gt;Now, the findings suggest that individual genetic variation involved in that inflammatory response may account for discrepancies in preterm births.&lt;/p&gt;
&lt;p&gt;&quot;We have a large body of evidence that proves silent infections are a frequent and important cause of premature labor,&quot; Romero said. &quot;These infections can also attack the fetus before it is born.&quot;&lt;/p&gt;
&lt;p&gt;He explained that the mother&apos;s hormones initiate the onset of labor to get rid of the infected tissue, and the fetus seeks to exit a hostile intrauterine environment that threatens its survival.&lt;/p&gt;
&lt;p&gt;To look at the mechanisms by which this process occurs, Romero and colleagues conducted a case-control study of mothers in Chile to assess genetic factors that could predispose women to spontaneous preterm labor and delivery.&lt;/p&gt;
&lt;p&gt;Patients who delivered prior to 37 weeks gestation served as cases, while women who delivered a normal neonate at term served as controls. There were 223 mothers and 179 fetuses in the case group, and 599 mothers and 628 fetuses in the control group.&lt;/p&gt;
&lt;p&gt;The researchers subsequently examined 190 candidate genes and 775 SNPs.&lt;/p&gt;
&lt;p&gt;They found that the strongest fetal single-locus association with risk of spontaneous preterm birth was in &lt;em&gt;ILR6&lt;/em&gt;, (OR 2.07, 95% CI 1.42 to 3.02,&lt;em&gt; P&lt;/em&gt;=0.0001).&lt;/p&gt;
&lt;p&gt;The strongest maternal single-locus association with spontaneous preterm labor and delivery was in tissue inhibitor of metalloproteinase &lt;em&gt;TIMP2&lt;/em&gt; (OR 1.98, 95% CI 1.38 to 2.83, &lt;em&gt;P&lt;/em&gt;=0.0002). This gene is involved in regulating the extracellular matrix, which holds cells within tissues.&lt;/p&gt;
&lt;p&gt;The associations remained significant after controlling for multiple comparisons, Romero said.&lt;/p&gt;
&lt;p&gt;Global haplotype analysis also indicated an association between a fetal DNA variant in insulin-like growth factor 2 (&lt;em&gt;P&lt;/em&gt;=0.004) as well as maternal alpha 3 type IV collagen isoform 1 (&lt;em&gt;COL4A3&lt;/em&gt;) (&lt;em&gt;P&lt;/em&gt;=0.007).&lt;/p&gt;
&lt;p&gt;&quot;Some women and fetuses carry gene variants that predispose them to the early onset of labor,&quot; Romero said.&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 researchers reported no 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_366"
                     title="Placental Infection Could Spur Asthma (CME/CE)"
                     score="0.01"
                     href="http://www.medpagetoday.com/Pediatrics/Asthma/tb/18252?impressionId=1265789721800"
                     
      Preterm birth complicated by chorioamnionitis may modestly increase a child&apos;s risk of later asthma, researchers found.&lt;br&gt;
&lt;br&gt;Children born preterm after a pregnancy complicated by the bacterial infection of placenta and amniotic fluid (chorioamnionitis) were significantly more likely to develop asthma by age eight than preemies without such exposure, according to Darios Getahun, MD, MPH, of Kaiser Permanente Department of Research and Evaluation in Pasadena.&lt;br&gt;
&lt;br&gt;Asthma diagnosis was nearly threefold more common among chorioamnionitis-exposed children who had been born preterm than those carried to term, they wrote in the February &lt;em&gt;Archives of Pediatrics &amp;amp; Adolescent Medicine&lt;/em&gt;.&lt;br&gt;
&lt;br&gt;Premature birth may not give an infant&apos;s lungs a chance to fully develop, leading to early infection and inflammation that elevate risk of chronic lung disease, such as asthma.&lt;p&gt;&lt;/p&gt;
&lt;p&gt;However, in utero exposures could be an important contributor as well, Getahun explained in an interview.&lt;/p&gt;
&lt;p&gt;Chorioamnionitis is thought to be associated with more than half of all preterm births.&lt;/p&gt;
&lt;p&gt;Fetal lungs stay in contact with the amniotic fluid which, when infected, may expose the developing lung to microorganisms, toxic substances, and inflammatory mediators, the researchers wrote.&lt;/p&gt;
&lt;p&gt;Animal model evidence suggests the condition may lead to scarring and fibrosis in the lung and damage to other fetal organs &quot;during a very critical time at preterm gestation,&quot; Getahun told &lt;em&gt;MedPage Today&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;So, his group retrospectively studied Kaiser&apos;s matched perinatal records on 510,216 singleton children born at the managed care group&apos;s hospitals in Southern California between 1991 and 2007.&lt;/p&gt;
&lt;p&gt;Physician-diagnosed asthma incidence by age 8 years, as expected, was significantly higher overall for preemies born at 23 to 36 weeks&apos; gestation than for those carried full-term (60.2 versus 40.0 per 1,000 person-years).&lt;/p&gt;
&lt;p&gt;But chorioamnionitis diagnosed during pregnancy substantially boosted this risk.&lt;/p&gt;
&lt;p&gt;Incidence of asthma rose to 100.7 per 1,000 person-years in exposed children born preterm, versus 39.6 per 1,000 among exposed, full-term children (IR 2.9, 95% CI 2.6 to 3.3).&lt;/p&gt;
&lt;p&gt;This association between chorioamnionitis and asthma in preemies persisted (HR 1.68, 95% CI 1.52 to 1.87) after adjustment for important confounding variables, including maternal age, race or ethnicity, smoking during pregnancy, prenatal care, and maternal asthma.&lt;/p&gt;
&lt;p&gt;Although the asthma risk appeared to rise with greater prematurity in exposed children, the elevated risk associated with chorioamnionitis exposure in utero was seen in every category of prematurity: &lt;ul&gt; &lt;li&gt; 1.23 times higher risk in children born at 23 to 28 weeks (95% CI 1.02 to 1.49)&lt;/li&gt; &lt;li&gt; 1.51 times higher risk in children born at 28 to 33 weeks (95% CI 1.26 to 1.80)&lt;/li&gt; &lt;li&gt; 1.20 times higher risk in children born at 34 to 36 weeks (95% CI 1.03 to 1.47)&lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;Additional adjustment for bronchopulmonary dysplasia  --  &quot;one of the mechanisms through which preterm birth is presumably associated with respiratory problems in early childhood&quot;  --  had little impact on the findings.&lt;/p&gt;
&lt;p&gt;Thus, the bacterial infection appeared to be an independent risk factor for asthma in prematurely born children, the researchers concluded.&lt;/p&gt;
&lt;p&gt;The risks were particularly high for children born to African-American women who developed chorioamnionitis, suggesting this may be an at-risk group to single out for attention clinically, they suggested.&lt;/p&gt;
&lt;p&gt;Getahun cautioned, though, that his group&apos;s study could not prove causality. The researchers also noted that the study was limited by lack of data on parental atopy and smoking.&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 Kaiser Permanente Direct Community Benefit funds. The researchers reported no 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_355"
                     title="Obesity Delays Puberty in Boys (CME/CE)"
                     score="0.009"
                     href="http://www.medpagetoday.com/Pediatrics/Obesity/tb/18235?impressionId=1265789721800"
                     
      &lt;p&gt;Unlike overweight girls, who tend to enter puberty early, overweight and obese boys in the U.S. may begin puberty later than thin boys, according to one of the first longitudinal studies of weight and timing of puberty in males.&lt;/p&gt;
&lt;p&gt;At 11.5 years, boys with the highest body mass index (mean BMI z score=1.84) were 165% more likely to be prepubertal than the thinnest boys (95% CI 1.05 to 6.61; &lt;em&gt;P&lt;/em&gt;=0.04), researchers reported online in the Feb. 1 &lt;em&gt;Archives of Pediatrics and Adolescent Medicine&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;&quot;This longitudinal study provides further evidence that higher BMI during early and middle childhood is not associated with earlier pubertal onset in boys, contrary to what is seen in girls,&quot; Joyce M. Lee, MD, MPH, of the University of Michigan, and colleagues wrote.&lt;/p&gt;
&lt;p&gt;&quot;In fact, higher BMI in earlier childhood may be associated with and precede later onset of puberty among a population-based sample of U.S. boys.&quot;&lt;/p&gt;
&lt;p&gt;Rates of obesity among American girls and boys have nearly tripled since the 1960s, prompting concerns about the effect of excess weight on growth and development. Most research has focused on obese girls, who appear to reach puberty earlier than thin girls. A recent cross-sectional study suggested that, unlike their female counterparts, overweight boys may develop later.&lt;/p&gt;
&lt;p&gt;To further explore this relationship, Lee and colleagues analyzed the records of 401 boys from diverse socioeconomic backgrounds in ten regions of the U.S., using data from the National Institute of Child Health and Human Development Study of Early Child Care and Youth Development. The participants were full-term, only children born in 1991.&lt;/p&gt;
&lt;p&gt;The data included height and weight measurements of the children from ages 2 to 12 years and a visual assessment of whether the children had begun puberty, using Tanner genitalia staging, at 9.5, 10.5, and 11.5 years. Boys were defined as prepubertal if they were Tanner stage 1 at 11.5 years old and were otherwise categorized as pubertal.&lt;/p&gt;
&lt;p&gt;Among the participants, 14.4% were overweight (BMI &amp;#8805; 85th and &amp;lt;95th percentiles) and 19.4% were obese (BMI&amp;#8805;95th percentile) at age 11.5. Overall, 49 boys (12.2%) were prepubertal at age 11.5 years by Tanner genitalia staging.&lt;/p&gt;
&lt;p&gt;The authors wrote that their findings have important implications for understanding sex differences in physiological mechanisms of puberty.&lt;/p&gt;
&lt;p&gt;They noted that puberty is regulated by the gonadotropin-releasing hormone axis for both girls and boys, but it&apos;s unclear why such different associations between body fat and the timing of pubertal onset would exist between the sexes.&lt;/p&gt;
&lt;p&gt;&quot;Given the recent childhood obesity epidemic, additional studies are needed to further investigate the epidemiological link between body fat and pubertal initiation and progression in boys as well as the physiological mechanisms responsible,&quot; they concluded.&lt;/p&gt;
&lt;p&gt;The authors were unable to analyze the data based on race, because most of the children in the study were white. They also noted that BMI is a surrogate measure of overall body fat, and that study has found that the relationship between body fat and BMI varies depending on race. They also recommended that future studies use multiple methods of determining whether children have entered puberty.&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 National Institute of Child Health and Human Development and the American Heart Association.&lt;/p&gt;&lt;p&gt;The authors reported no financial conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
</recommendedContent>