Identification and treatment of obesity as a standard of care for all patients in children's hospitals.

Obese children and adolescents have unique needs for specialized medical equipment while hospitalized and might require special diets and physical activity options as part of their medical treatment. It is important that patients with a diagnosis of obesity be identified on admission so that appropriate equipment and resources can be provided. We examined what components a healthy hospital environment should include and sought to determine if children's hospitals provide a healthy hospital environment that offers these components. In addition, we sought to determine if children's hospitals have policies in place to identify children with obesity so that appropriate resources and services can be offered to treat that diagnosis. We surveyed National Association of Children's Hospitals and Related Institutions member hospitals via a Web-based questionnaire and found that the majority of them do not have policies in place to identify patients with obesity. We did find that the majority of hospitals reported innovative programs or services to provide a healthy hospital environment for their patients, visitors, and staff but acknowledged limitations in providing some services. Specifically, children's hospitals can and should improve on their identification and management of obese pediatric patients.

Building capacity for childhood obesity prevention and treatment in the medical community: call to action.

Large gaps exist in the capacity of the US medical system to participate meaningfully in childhood obesity-prevention efforts and to meet the treatment needs of obese children. Current primary care practice for the prevention and treatment of childhood obesity often varies from evidence-based recommendations. Childhood obesity specialists have partnered successfully with schools of medicine, professional societies, and other organizations to collaboratively engage with primary care providers in quality improvement for obesity prevention and treatment. This review and commentary targets 2 audiences. For childhood obesity experts and their organizational partners, methods to support change in primary practice and the evidence supporting their use are outlined. For primary care providers and non-obesity specialists, effective strategies for changing practice and the potential benefits of addressing childhood obesity systematically are discussed.

Increased risk of Blount disease in obese children and adolescents with vitamin D deficiency.

BACKGROUND: Poor dietary habits and decreased outdoor activity has led to an epidemic of obese children and vitamin D deficiency. The lack of vitamin D alters bone development and mineralization by diminishing physiological levels of calcium and phosphorus. Given vitamin D's role in bone and growth plate mineralization and regulation, we hypothesized that vitamin D deficiency would lead to higher rates of fractures, slipped capital femoral epiphysis (SCFE), and Blount disease in obese youth. METHODS: A retrospective review was performed at the obesity clinic using the obesity database (890 patients). Data obtained included body mass index (BMI), vitamin D levels (25-vitamin D), history of fractures, Blount disease, and/or SCFE. The chart review identified 2 populations of obese patients, those with vitamin D deficiency, <16 ng/mL (198 patients) and those not vitamin D deficient >16 ng/mL (692 patients). Fisher exact, χ², and 2-sample t tests along with logistic regression were used for statistical analysis. A P value ≤0.05 was considered statistically significant. RESULTS: Blount disease was found to have a statistically significant (P<0.05) positive association with patient's sex, BMI, and vitamin D level. Specifically, males were 8.16 times more likely than females to be observed with Blount disease (P=0.01). Patients with very low vitamin D levels were 7.33 times more likely to have Blount disease than patients with higher levels (P=0.002). Each whole number increase in BMI increases the likelihood of Blount disease by 3% (P=0.01). There was no association between increased number of fractures or SCFE with vitamin D deficiency in these obese patients. CONCLUSION: As our findings indicate, BMI and vitamin D levels have a strong association with Blount disease, which may be especially important among males. Ours is the first study to show a relationship between vitamin D deficiency and Blount disease, but further prospective studies are needed with larger numbers to confirm this independent association of vitamin D deficiency with Blount disease. LEVEL OF EVIDENCE: Level III retrospective study.

Forensic laboratory evidence in sexually abused children and adolescents.

OBJECTIVES: To determine if forensic laboratory evidence could be recovered from alleged sexual abuse victims more than 24 hours after the event and to determine if age or historical factors could be used to determine the need for forensic evidence collections. DESIGN: Retrospective study of hospital records matched with forensic evidence reports from the Arkansas State Crime Laboratory, Little Rock. SETTING: The emergency department at Arkansas Children's Hospital, Little Rock. PARTICIPANTS: Eighty children (aged <12 years) and adolescents (aged > or =12 years) who presented to the emergency department within 72 hours of an alleged event of sexual abuse or assault with genital contact. MAIN OUTCOME MEASURES: Cases positive for semen were correlated with age of the victim and post-event length of time to presentation to the emergency department. RESULTS: Of the 80 subjects, 16 had positive findings for semen. All 16 subjects who tested positive for semen presented to the emergency department less than 24 hours after the alleged abuse or assault event (P<.001). Of the 16 subjects who tested positive, 13 (81%) were adolescents. None of the prepubertal children had semen recovered from any body site; semen was recovered only from clothing or linen in those 3 children. CONCLUSIONS: Forensic evidence collections from body sites in child and adolescent rape patients are unlikely to yield positive results for semen (1) more than 24 hours after the event and (2) when taken from prepubertal patients. Consideration should be given to amending guidelines regarding forensic evidence collections in child and adolescent sexual abuse or assault victims.

Treating overweight children and adolescents in the clinic.

The increasing prevalence of pediatric overweight has caused the medical community to begin searching for ways to deal with this new pediatric medical problem. The Centers for Disease Control developed the Body Mass Index (BMI) growth charts, which came into use in 2000. Primary care providers are seeking education on this relatively new topic. This article provides fundamental information based on the medical evidence for pediatricians to learn how to care for their overweight pediatric patients in the office setting.

Severe obesity in children and adolescents: implications for treatment.

The prevalence of clinically severe obesity in adults has been rising rapidly. We completed a needs assessment that examined the prevalence of severe obesity in a tertiary pediatric weight management clinic. The Arkansas Children's Hospital (ACH) Fitness Clinic, a specialty clinic treating overweight children and adolescents, is offered in partnership with the University of Arkansas for Medical Sciences Child and Adolescent Bariatrics Center. Our hypothesis is that the ACH Fitness Clinic has a large proportion of severely overweight children and that these patients are in need of more aggressive adjuvant therapies to improve their health status. The study reported here is part of an ongoing feasibility study regarding the need for pharmacologic and surgical options for Fitness patients who are morbidly overweight and are not responding well to a behavior treatment program alone. Of the 701 overweight (BMI >95th percentile for age and gender) children and adolescents seen in Fitness Clinic over a 29-month period, 72% had a Body Mass Index (BMI) >35, which is considered severe obesity in adults.

The effects of lovastatin on proteasome activities in highly purified rabbit 20 S proteasome preparations and mouse MC3T3-E1 osteoblastic cells.

A number of clinical studies suggest that the use of the lipid-lowering agents collectively referred to as statins (hydroxymethyl glutaryl coenzyme A [HMG-CoA] reductase inhibitors) is associated with increased bone density, reduced fracture risk, and net bone anabolism. Statins (< or =5 micromol/L) stimulate rodent bone formation, but the mechanistic basis remains unclear. Since statins and the proteasome inhibitor lactacystin are structurally similar, and high doses (> or =40 micromol/L) of statins can inhibit the chymotryptic activity of the proteasome, it has been hypothesized that statins exert their anabolic effects on bone, in part, by inhibiting the proteasome, the major eukaryotic intracellular regulatory protease. This hypothesis conflicts with reports that statins stimulate proteasome activity and that proteasome-catalyzed degradation of specific substrates is required for cell proliferation, differentiation, and survival. Our chief objective was to determine the effects of statins (< or =10 micromol/L) on the chymotryptic activity of the proteasome in the 20 S proteasome and intact murine MC3T3-E1 cells cultured to low density (preosteoblasts) or high density (differentiated osteoblasts). Lovastatin (0.001 micromol/L to 5.0 micromol/L) stimulated the chymotryptic activity of the highly purified 20 S proteasome. Preosteoblasts and differentiated osteoblasts treated with 1, 5, or 10 micromol/L lovastatin for 1 hour exhibited morphologic abnormalities that were ameliorated by preincubation and treatment with 20 micromol/L mevalonate. The chymotryptic activity of the preosteoblast proteasome increased after 2 days of 1.0 micromol/L or 5.0 micromol/L lovastatin treatment. In addition, the DNA and protein contents of 1.0 micromol/L or 5.0 micromol/L lovastatin-treated preosteoblast cultures were lower those that observed in vehicle-, 0.01 micromol/L lovastatin-, or 0.10 micromol/L lovastatin-treated cultures. The chymotryptic activity of the proteasome was much lower in differentiated osteoblasts than in preosteoblasts. Two days of treatment with 1 micromol/L lovastatin modestly stimulated the chymotryptic activity of the proteasome in differentiated osteoblasts, but had no effects on total protein or DNA, compared to cultures treated with vehicle or lower doses of lovastatin. Thus, the data support the hypothesis that statins stimulate proteasome activities in highly purified proteasome preparations and preosteoblastic cells. Treating preosteoblastic or differentiated MC3T3-E1 cells with lovastatin concentrations > or = 1 micromol/L resulted in abnormal morphology and reduced the DNA and protein levels in preosteoblastic cultures, confirming the adverse effects of statins previously reported for other cells. In conclusion, the hypothesis that lovastatin exerts its anabolic effects on bone by inhibiting the proteasome activity of the osteoblast was refuted, and the effects of lovastatin on MC3T3-E1 cells were found to be highly dose- and development-dependent.