Lean body mass may explain apparent racial differences in carotid intima-media thickness in obese children.

BACKGROUND: Racial differences in carotid intima-media thickness (cIMT) have been suggested to be associated with the disproportionally high prevalence of cardiovascular disease in black adults. The objective of this study was to evaluate the effects of cardiovascular risk factors on the racial differences seen in cIMT in obese children. METHODS: Obese subjects aged 4 to 21 years were recruited prospectively. Height, weight, blood pressure, fasting insulin, glucose, lipid panel, high-sensitivity C-reactive protein, and body composition by dual-energy x-ray absorptiometry were obtained. B-mode carotid imaging was analyzed by a single blinded physician. RESULTS: A total of 120 subjects (46 white, 74 black) were enrolled. Black subjects exhibited greater cIMT (0.45 ± 0.03 vs 0.43 ± 0.02 cm, P < .01) and higher lean body mass index (19.3 ± 3.4 vs 17.3 ± 3.2 kg/m², P = .02) than white subjects. Simple linear regression revealed modest associations between mean cIMT and race (R = 0.52, P < .01), systolic blood pressure (R = 0.47, P < .01), and lean body mass (R = 0.51, P < .01). On multivariate regression analysis, lean body mass remained the only measure to maintain a statistically significant relationship with mean cIMT (P < .01). CONCLUSIONS: Black subjects demonstrated greater cIMT than white subjects. The relationship between race and cIMT disappeared when lean body mass was accounted for. Future studies assessing the association of cardiovascular disease risk factors to cIMT in obese children should include lean body mass in the analysis.

Secondary surfactant deficiency in neonates.

Surfactant treatment has become the standard of care in premature infants with respiratory distress syndrome (RDS). Pulmonary hemorrhage, pulmonary edema, pneumonia, and atelectasis have been shown to liberate inflammatory mediators and plasma proteins, which damage type II pneumocytes and inactivate surfactant. These disease processes may, therefore, lead to a secondary surfactant inactivation or deficiency, which can be an unrecognized cause of respiratory decompensation after initial recovery from RDS in this vulnerable population. This is a descriptive report of three cases, which had acute respiratory decompensation between 1 and 3 weeks of age. All three infants demonstrated a response to secondary doses of surfactant. We submit that the diagnosis and treatment of secondary surfactant deficiency in the critically ill premature neonate warrants further study.