Hispanic and black US children's paths to high adolescent obesity prevalence.

OBJECTIVE: The study aims to identify the ages contributing most to the development of higher obesity prevalence in the 8th grade (approximately age 14) among Hispanic and black children than among non-Hispanic white children in the United States. METHODS: Using the nationally representative Early Childhood Longitudinal Study (ECLS-K), a sample of 17,420 children in kindergarten in 1999, followed in 1st, 3rd, 5th and 8th grades through 2007, was analysed. First, 'normal', 'overweight' and 'obese' weight-status categories in each grade were assigned from US Centers for Disease Control body mass index percentiles. Second, probabilities of being in each of the three weight-status categories in kindergarten and of transitioning between categories after kindergarten were estimated by logistic regression. These probabilities were then used as parameters of a weight-status trajectory simulation model from which a decomposition analysis was performed. RESULTS: Obesity prevalence in the 8th grade was equally high among Hispanic (25.0%, 95% confidence interval [CI]: 22.3, 27.8%) and black children (25.1%; 95% CI: 20.9, 29.6%) compared to white children (17.4%; 95% CI: 15.9, 19.0%). As much as 73% of the Hispanic-white 8th grade obesity disparity was generated by 3rd grade and 44% by kindergarten. In contrast, only 15% of the black-white obesity 8th grade disparity was generated by kindergarten, whereas 75% was generated between the 3rd and 8th grades and 53% between the 5th and 8th grades. CONCLUSIONS: Although adolescent obesity is equally prevalent among Hispanic and black children, obesity emerges and is sustained earlier in Hispanic children. Diagnosis and prevention strategies should be designed accordingly.

Ursodeoxycholic acid treatment in patients with primary biliary cirrhosis. A Swedish multicentre, double-blind, randomized controlled study.

BACKGROUND: Ursodeoxycholic acid (UDCA) has been shown to improve serum levels of liver enzymes and bilirubin in primary biliary cirrhosis (PBC). However, it is still uncertain whether UDCA treatment also improves symptoms, liver histology, and survival without liver transplantation. METHODS: We randomized 116 patients with PBC to receive 0.5 g UDCA (n = 60) or placebo (n = 56) daily for 2 years. During the next 2 years, 80% of the UDCA-treated patients and 65% of the placebo-treated patients continued to take UDCA. RESULTS: UDCA improved serum enzyme values but not survival, symptoms, serum bilirubin levels, or liver histology. There was no significant difference in response between initially symptomatic and asymptomatic patients. CONCLUSIONS: UDCA in a dosage of 7.7 mg/kg body weight is of little benefit in PBC. This does not exclude the possibility that larger doses have beneficial effects.

Protracted cholestasis probably induced by oral contraceptive.

The case of a patient with intrahepatic cholestasis, probably induced by an oral contraceptive agent, is reported. Initially, early primary biliary cirrhosis was suspected, but this diagnosis could not be verified either clinically or by immunological tests. Re-examination and re-evaluation of the liver biopsy revealed some eosinophilia and sinusoidal dilatation, changes indicative of drug-induced liver injury. The cholestasis gradually disappeared as indicated both biochemically and histologically, but the elevation of serum alkaline phosphatase levels persisted for some 10 years after termination of drug therapy. Oral contraceptive agent-induced jaundice or cholestasis is generally reported to disappear when the drug is stopped, and we are unaware of similar cases in the literature with a protracted course such as that described here. Still, the circumstances of this patient suggest that a correlation between the oral contraceptive agent and the hepatic reaction is most likely, and we consider it important that colleagues pay attention to this possibility.