Urate changes in lean and obese boys during pubertal development.

Uric acid metabolism is not uniform throughout puberty. Serum urate increases progressively in obese boys as puberty advances, but it increases significantly only at the end of puberty in lean subjects. Urate filtered per unit of body weight increases in all subjects at the end of puberty when fractional excretion is diminished. Urate clearance decreases a the beginning of puberty in obese boys and at the end of puberty in lean subjects. Urate excretion corrected for body weight and the urinary uric acid to creatinine ratio do not change over the course of pubertal development in both lean and obese boys. These results suggest the following hypotheses: (1) renal retention of urate may represent the first mechanism by which uricemia is enhanced at puberty; (2) the kidney may finely modulate serum uric acid concentration through different mechanisms of urate handling, presumably occurring at different tubular sites; and (3) obesity may evoke sooner the urate changes that in lean boys are observed at the end of puberty.

Uric acid homeostasis in lean and obese girls during pubertal development.

Serum uric acid concentration and fractional excretion were evaluated in lean (n = 67) and obese (n = 56) girls before and during pubertal development. In both lean and obese girls, uricemia gradually increased as puberty advanced. Obese girls were hyperuricemic compared with lean controls (prepubertal: 184 +/- 83 v 130 +/- 29 mumol/L, P = .007; Tanner stage II-III: 190 +/- 53 v 178 +/- 47 mumol/L, NS; Tanner stage IV-V: 232 +/- 53 v 191 +/- 53 mumol/L, P = .02). Fractional excretion of urate decreased with puberty in lean girls (6.46% +/- 2.29%, 4.61% +/- 2.48%, and 3.54% +/- 1.84%), but not in obese subjects (3.74% +/- 2.27%, 4.01% +/- 1.90%, and 4.26% +/- 2.26%). Urate homeostasis was similar in prepubertal obese girls and in adolescent lean controls. We conclude that an increased serum urate concentration occurring at puberty may be due to decreased renal clearance of urate in lean girls, and at least in part to urate overproduction in obese subjects. Obesity may prematurely evoke changes in urate metabolism usually observed at puberty.

Changes in lipid profile observed in children over the course of infectious disease.

Lipid profile was evaluated prospectively in 23 consecutive children, aged 3.2-14.9 years, admitted to the hospital with a febrile illness (pneumonia, upper respiratory tract infection, diarrhea, pyelonephritis, mononucleosis, appendicitis). The degree of dyslipidemia associated with fever was assessed using each child as his/her own control and by comparison with 93 non-febrile children who had no evidence of fever during the past six months. Total cholesterol decreased during the symptomatic phase of the disease. The magnitude and duration of its decrease appeared to be related to the degree and duration of fever. Low HDL-cholesterol and hypertriglyceridemia were observed during the late stage of the febrile disease and were still detected in the convalescent phase. This study suggests that in children, transient and sometimes prolonged lipid changes may occur in association with an infectious febrile disease. This effect is important for defining the appropriate timing for screening for dyslipidemias.

Serum digoxin-like immunoreactive factor in children and its relation to sodium metabolism.

Serum digoxin-like immunoreactive factor (DLIF), an endogenous substance that cross-reacts with antidigoxin antibodies, was assessed (fluorescence polarization immunoassay) in children (n = 134) aged 5-16 y, who had never been treated with cardiac glycosides. DLIF was found in 50% of serum samples at a mean concentration of 0.16 +/- 0.06 ng/ml (range 0.03-0.35 ng/ml). Although the study population as a whole was apparently homogeneous with regard to serum sodium content, and none had clinical signs of sodium imbalance, children with DLIF showed significantly lower natraemia (p = 0.0002), higher urinary concentration (p = 0.001) and fractional excretion (p = 0.001) of sodium, and increased systolic blood pressure (p = 0.009) compared with children without DLIF. Inverse correlations were found between DLIF concentration and serum sodium (p < 0.01), urine sodium content (p < 0.001), 24-h sodium excretion (p < 0.001), systolic (p < 0.001) and diastolic (p < 0.01) blood pressure. These findings suggest that sodium handling is different in children with and without DLIF, since this material seems to be released preferably in subjects who show a trend towards negative sodium balance. Such an association suggests that DLIF may be a physiologically relevant material involved in sodium homeostasis.

pH dependence of the water solubility of bilirubin photo-derivatives and its relevance to phototherapy.

Deoxygenated chloroform solutions of bilirubin were irradiated with visible light and continuously extracted with aqueous solutions at different pHs in the range of 7.20-8.20. The aqueous solutions became yellow rapidly and progressively: the higher their pH, the more intense their coloration. The water soluble E-isomers of bilirubin may not represent the only photoproducts transferred into water. It clearly appears from visible absorption measurements that the photopigment formed in our experiments can be partitioned from chloroform into water at pH as low as 7.2-7.4. Although the water solubility of the photopigment cannot be exactly calculated from experimental data, a direct relationship between water partitioning and water solubility can be reasonably assumed. The fact that the water solubility of the photopigment sharply increases in inverse proportion to the hydrogen ion concentration can be of great relevance to the treatment of jaundiced infants with phototherapy.