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    <recommendedItem id="20100101_19_352"
                     title="ICAO: Future Chronic Disease Risk Goes Beyond BMI (CME/CE)"
                     score="0.011"
                     href="http://www.medpagetoday.com/Endocrinology/Diabetes/tb/18233?impressionId=1265756266842"
                     
      When it comes to predicting chronic disease, body mass index doesn&apos;t tell the whole story, according to a population-based study that found elevated risk with obesity and other metabolic risk factors independently.&lt;br&gt;
&lt;br&gt;Metabolically-healthy obese people tended toward being at least twice as likely to develop multiple metabolic risk factors and diabetes as healthy, normal weight individuals over the subsequent 3.5 years of a study led by Sarah Appleton, a postgraduate student at the University of Adelaide, Australia.&lt;br&gt;
&lt;br&gt;However, normal weight individuals with metabolic risk factors  --  a group the researchers called &quot;metabolically obese&quot;  --  were at greater risk, she told attendees at the International Congress on Abdominal Obesity in Hong Kong, a conference sponsored by the International Chair on Cardiometabolic Risk.&lt;br&gt;
&lt;br&gt;Overall, just 4.1% of the 3,743 adults in the population-based, North West Adelaide Health Study were in the normal body mass index range at baseline but had at least two of the following metabolic risk factors:&lt;ul&gt; &lt;li&gt;Triglyceride levels of 1.7 mmol/L or greater&lt;/li&gt; &lt;li&gt;HDL cholesterol under 1.0mmol/L for men or 1.3 mmol/L for women&lt;/li&gt; &lt;li&gt;Blood pressure of 130/85 mm Hg or higher&lt;/li&gt; &lt;li&gt;A fasting plasma glucose of at least 5.6mmol/L or self-reported diabetes&lt;/li&gt; &lt;li&gt;Treatment for any of these disorders &lt;/li&gt; &lt;/ul&gt;
&lt;p&gt;Although free of cardiovascular disease when they entered the study through a random population sample of the northwest region of Adelaide, after a mean of 3.5 years of follow-up, this group was 2.48 times at risk of incident cardiovascular disease or stroke events (95% CI 1.1 to 5.4).&lt;/p&gt;
&lt;p&gt;Compared with metabolically-healthy, normal weight individuals, those with metabolic risk factors tended to be&lt;strong&gt; &lt;/strong&gt;3.27 times as likely to develop diabetes (&lt;em&gt;P&lt;/em&gt;=0.07).&lt;/p&gt;
&lt;p&gt;Identifying these individuals for prevention efforts may require less emphasis on BMI and increased surveillance of central obesity in primary care, the researchers told the congress.&lt;/p&gt;
&lt;p&gt;&quot;The problem with BMI is it doesn&apos;t tell you where the fat is,&quot; Appleton added in an interview. &quot;Visceral fat is really bad for you.&quot;&lt;/p&gt;
&lt;p&gt;Obese individuals without multiple metabolic risk factors at baseline comprised a larger group (12.1%).&lt;/p&gt;
&lt;p&gt;They were more likely to be middle age, live in a disadvantaged neighborhood, have smoked at some point, and get less exercise than their metabolically similar, but slimmer peers.&lt;/p&gt;
&lt;p&gt;Over the subsequent 3.5 years, they were 2.82 times more likely to develop more than one metabolic risk factor than metabolically-healthy, normal weight individuals (95% CI 2.0 to 4.0).&lt;/p&gt;
&lt;p&gt;The metabolically-normal obese also tended to be 2.36 times more likely to develop diabetes (95% CI 0.8 to 7.1). On the other hand, their risk of cardiovascular disease wasn&apos;t elevated, &quot;which likely related to the younger age of that group,&quot; Appleton told &lt;em&gt;MedPage Today&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Notably, abdominal obesity as determined by a waist circumference of 80 cm and over for men or 95 cm and greater for women was 6.1 times more likely among metabolically healthy individuals if their BMI was in the obese versus normal range.&lt;/p&gt;
&lt;p&gt;But those who were in the normal BMI range were 2.2-fold more likely to be overweight or obese according to waist circumference if they had metabolic risk factors, which was statistically significant as well and likely contributed to the health risks they faced over the short-term future, Appleton said.&lt;/p&gt;
&lt;p&gt;Maintenance of metabolic health in the obese population was more likely for younger individuals (OR 2.83 for age 40 or younger, 95% CI 1.1 to 7.6) and those who were at least moderately physically active (OR 2.04, 95% CI 1.01 to 4.1).&lt;/p&gt;
&lt;p&gt;Appleton noted that these findings generally fit with data from the U.S. National Health Assessment Survey and Examination.&lt;/p&gt;
&lt;p&gt;Regardless of whether patients have abdominal obesity, BMI obesity, or other metabolic risk factors, the solution is likely similar  --  improved diet and exercise, she 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 study was supported by the University of Adelaide and the South Australian Department of Health.&lt;/p&gt;&lt;p&gt;Appleton 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_325"
                     title="MRI Reveals Risk for Kidney Failure in Diabetic Patients (CME/CE)"
                     score="0.007"
                     href="http://www.medpagetoday.com/Nephrology/Diabetes/tb/18195?impressionId=1265756266842"
                     
      So-called silent strokes, visible on cerebral MRI scans, predict kidney failure in patients with type 2 diabetes, Japanese researchers said.&lt;br&gt;
&lt;br&gt;After an average follow-up of 7.5 years, diabetic patients with evidence of small cerebral infarctions at baseline later suffered death or kidney failure at more than twice the rate seen in patients who had not had silent strokes, reported Takashi Uzu, MD, of Shiga University of Medical Sciences in Shiga, Japan, and colleagues.&lt;br&gt;
&lt;br&gt;Silent strokes are a consequence of cerebral microvascular disease and thus may logically accompany the development of similar abnormalities in renal blood vessels, ultimately leading to kidney failure, the researchers explained online in the &lt;em&gt;Journal of the American Society of Nephrology&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;&quot;It is important to identify individuals who are at risk of progression of diabetic renal disease,&quot; Uzu and colleagues wrote.&lt;/p&gt;
&lt;p&gt;The current standard prognostic test is the albumin-creatinine ratio, but it is not entirely adequate for the purpose, they suggested: &quot;Recent clinical studies have shown that renal insufficiency can occur in the absence of microalbuminuria in patients with type 2 diabetes.&quot;&lt;/p&gt;
&lt;p&gt;But they acknowledged that brain MRI scans would be too expensive and inconvenient for routine prognostic testing.&lt;/p&gt;
&lt;p&gt;&quot;New strategies are needed to determine the presence of renal and/or extrarenal microvascular diseases,&quot; Uzu and colleagues wrote.&lt;/p&gt;
&lt;p&gt;Their study involved 608 patients with type 2 diabetes who had no clinical signs of cerebrovascular or cardiovascular disease or overt nephropathy. Their mean age at baseline was about 60 and the average glycated hemoglobin level was about 8.6%.&lt;/p&gt;
&lt;p&gt;Participants underwent cerebral MRI scans at baseline, with 177 showing evidence of silent cerebral infarctions, defined as focal lesions of at least 3 mm in diameter with low signal intensity on T1-weighted images and high intensity with T2 weighting. Dilated perivascular spaces were distinguished from infarcts with proton density scans. Patients with positive findings who had a history of stroke or transient ischemic attack were excluded.&lt;/p&gt;
&lt;p&gt;Those with silent infarctions at baseline differed significantly from other participants according to several parameters. Not surprisingly, patients with cerebral infarcts on average were somewhat older (63 versus 57), had had diabetes for a longer period of time (9.8 years versus 7.6), had higher blood pressure (146.8 mm Hg systolic versus 136.5 ), and were more likely to have a history of smoking (58% versus 46%). All differences were significant at &lt;em&gt;P&lt;/em&gt;&amp;lt;0.01.&lt;/p&gt;
&lt;p&gt;On the other hand, baseline fasting plasma glucose and glycated hemoglobin levels were both significantly lower in the patients who&apos;d had silent infarctions: mean 163 mg/dL versus 176 for glucose and 8.3% versus 8.7% for HbA1c (&lt;em&gt;P&lt;/em&gt;&amp;#8804;0.01 for both).&lt;/p&gt;
&lt;p&gt;Patients were followed for up to 10 years, with a mean of 7.5. The primary outcome was end-stage renal disease or death, and Uzu and colleagues chose a secondary outcome combining dialysis with doubling of serum creatinine.&lt;/p&gt;
&lt;p&gt;Kaplan-Meier curves for the patients with and without silent infarctions at baseline indicated that the primary outcome occurred at equal rates through the first four years of follow-up, but then the curves diverged abruptly.&lt;/p&gt;
&lt;p&gt;At year eight, approximately 6% of the noninfarcted group had experienced the primary outcome, compared with 21% of those who&apos;d had silent strokes (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.0001), according to Uzu and colleagues.&lt;/p&gt;
&lt;p&gt;Curves for the secondary outcome began diverging by year three. At year eight, about 6% of the noninfarct participants had gone to dialysis or had serum creatinine levels double, whereas these endpoints occurred in nearly 30% of the infarct group (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.0001).&lt;/p&gt;
&lt;p&gt;Overall, the hazard ratio associated with baseline silent cerebral infarctions for the primary outcome during follow-up was 2.44 (95% CI 1.36 to 4.38).&lt;/p&gt;
&lt;p&gt;The hazard ratio for death alone was somewhat smaller (1.61, 95% CI 0.71 to 3.62), indicating that most of the risk measured by the primary outcome was actually in end-stage renal disease.&lt;/p&gt;
&lt;p&gt;For the secondary outcome, the hazard ratio was 4.79 (95% CI 2.72 to 8.46).&lt;/p&gt;
&lt;p&gt;All the hazard ratios reflected adjustments for age, sex, duration of diabetes, body mass index, smoking status, HbA1c, blood pressure, serum lipids, and standard lab indices of kidney function at baseline.&lt;/p&gt;
&lt;p&gt;Estimated glomerular filtration rate (eGFR) during follow-up also decreased faster in patients with silent strokes. After five years, mean eGFR had fallen by 8 ml/min/m&lt;sup&gt;2&lt;/sup&gt; in the patients without silent infarcts at baseline compared with 10.5 ml/min/m&lt;sup&gt;2&lt;/sup&gt; in those with cerebral microvascular disease.&lt;/p&gt;
&lt;p&gt;The researchers noted that the study was conducted at two clinical sites, which used somewhat different MRI procedures. But they also indicated that the prevalence of silent infarctions did not differ between the sites.&lt;/p&gt;
&lt;p&gt;Other limitations included use of an older creatinine assay, inclusion of larger silent infarcts which could reflect macrovascular disease, and more patients in the cerebral infarct group who were taking renin-angiotensin system blocking drugs, which have renal impairment as an adverse effect.&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;External funding for the study was not reported.&lt;/p&gt;&lt;p&gt;No potential conflicts of interest were reported.&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="0.005"
                     href="http://www.medpagetoday.com/Endocrinology/MetabolicSyndrome/tb/18153?impressionId=1265756266842"
                     
      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_235"
                     title="Congenital Anomalies Linked to Mom&apos;s Diabetes (CME/CE)"
                     score="0"
                     href="http://www.medpagetoday.com/OBGYN/Pregnancy/tb/18065?impressionId=1265756266842"
                     
      &lt;p&gt;Pregestational maternal diabetes was associated with an increased risk of a major congenital anomaly, but obesity itself was not, a cross-sectional study found.&lt;/p&gt;
&lt;p&gt;In a multivariable logistic model, the major contributor to a rising rate of congenital anomalies was maternal pregestational diabetes (OR 3.8, 95% CI 2.1 to 6.6), according to Joseph R. Biggio, Jr., MD, and colleagues from the University of Alabama at Birmingham.&lt;/p&gt;
&lt;p&gt;&quot;Because hyperglycemia is a major contributor to developmental malformations, interventions to address obesity and identify women at risk for diabetes and hyperglycemia should be considered in efforts to reduce the occurrence of congenital anomalies,&quot; they wrote in the February issue of &lt;em&gt;Obstetrics &amp;amp; Gynecology.&lt;/em&gt;&lt;/p&gt;
&lt;p&gt;Maternal obesity has been linked with numerous problems, including preeclampsia, gestational diabetes, fetal and neonatal death, and birth trauma, but scientists have disagreed over whether it also contributes to the risk of fetal malformations, the researchers noted.&lt;/p&gt;
&lt;p&gt;To help settle the issue, Biggio and colleagues used a perinatal database in their university health system that included all women with singletons delivered between 1991 and 2004.&lt;/p&gt;
&lt;p&gt;They divided the cohort into three time periods  --  1991 to 1994, 1995 to 1999, and 2000 to 2004, with a total of 41,902 pregnancies.&lt;/p&gt;
&lt;p&gt;For their primary analysis, they defined maternal obesity as a first prenatal visit weight greater than 200 lb, because during the earlier epochs many women did not have body mass index (BMI) calculated. For their secondary analyses they used BMI greater than 29 kg/m&lt;sup&gt;2&lt;/sup&gt; as the criterion for obesity.&lt;/p&gt;
&lt;p&gt;In each epoch, there were increases in mean maternal weight, mean BMI, the proportion of women weighing more than 200 lb, the proportion with a BMI greater than 29 kg/m&lt;sup&gt;2&lt;/sup&gt;, and the prevalence of pregestational diabetes (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001 for all).&lt;/p&gt;
&lt;p&gt;Univariable analysis determined that the rate of major anomalies, particularly involving the cardiac and pulmonary systems, also increased during each time period.&lt;/p&gt;
&lt;p&gt;But there was no independent association between congenital anomalies and maternal obesity using either definition, during any of the three time periods or during the study overall.&lt;/p&gt;
&lt;p&gt;Although no direct association was seen between congenital malformations and maternal obesity, the investigators reported that the proportion of anomalies that could be attributed to obesity increased from 0% to 23% during the overall study period.&lt;/p&gt;
&lt;p&gt;The proportion of anomalies that could be attributed to diabetes ranged from 58% to 76%.&lt;/p&gt;
&lt;p&gt;Moreover, for obese women with diabetes the proportion of anomalies attributed to diabetes increased sharply, from 48% in the first epoch to 74% in the third epoch.&lt;/p&gt;
&lt;p&gt;In contrast, for the obstetric population as a whole, the population-attributable risk of congenital malformation related to obesity rose from near zero in the first epoch to 6.1% in the third epoch, while that related to diabetes increased from 3.3% to 9.2%, the investigators reported.&lt;/p&gt;
&lt;p&gt;During the course of the study there was a nearly 15-lb increase in maternal weight and a 30% increase in the proportion of women whose BMI exceeded 29 kg/m&lt;sup&gt;2&lt;/sup&gt;.&lt;/p&gt;
&lt;p&gt;There also was a nearly twofold increase in the rate of major anomalies  --  and a 250% increase in the prevalence of diabetes.&lt;/p&gt;
&lt;p&gt;The authors observed that there has been much interest in the effects of maternal obesity on birth defects.&lt;/p&gt;
&lt;p&gt;Although the pathophysiologic basis for this possible association have not been identified, hypotheses have included increased serum insulin, lower levels of folic acid, chronic hypoxia, and increased inflammatory mediators.&lt;/p&gt;
&lt;p&gt;&quot;Our study provides evidence that the defects may not be due solely to the maternal obesity per se but may be due to undiagnosed diabetes,&quot; the investigators wrote.&lt;/p&gt;
&lt;p&gt;From a public health standpoint, the study findings suggest that efforts to reduce the prevalence of congenital anomalies should be focused less on obesity and aimed more closely at correcting hyperglycemia.&lt;/p&gt;
&lt;p&gt;&quot;If euglycemia could be achieved before pregnancy, or at least embryogenesis and organogenesis, the majority of these anomalies could potentially be avoided,&quot; they observed.&lt;/p&gt;
&lt;p&gt;They also suggested that even women of normal weight, but with other diabetes risk factors, could benefit from closer attention to glycemic control.&lt;/p&gt;
&lt;p&gt;A weakness of the study was the fact that detailed data on glycemic control was not available in the perinatal database, &quot;and therefore we cannot comment on the association between glycemic control and anomaly rates,&quot; the investigators 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 in part by the National Institute of Child Health and Human Development.&lt;/p&gt;&lt;p&gt;The authors did not report any potential conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20090101_3_757"
                     title="High-Dose Statins Lower Risks in Coronary Patients with Metabolic Syndrome"
                     score="-0.005"
                     href="