Sickle cell anemia (HbSS) is characterized by hypermetabolism, chronic inflammation, and increased oxidative stress, but the relationship between these factors is undefined. In this study, we examined indicators of inflammatory process and markers of oxidative damage and their impact on resting energy expenditure (REE) in stable HbSS adolescents (n ϭ 35) and healthy controls carrying normal hemoglobin genotype (HbAA) (n ϭ 39). C-reactive protein (CRP), white blood cell (WBC) count, and proinflammatory cytokines were measured as markers of inflammation and 2,3-dinor-5,6-dihydro-15-F 2t -isoprostane (F2-IsoPM) as a marker of oxidative stress. REE was measured by indirect calorimetry. WBC counts (11.90 Ϯ 5.3 ϫ10 3 /L versus 5.6 Ϯ 1.9 ϫ10 3 /L; p Ͻ 0.001), serum CRP (9.1 Ϯ 11.0 g/mL versus 0.4 Ϯ 0.7 g/mL; p Ͻ 0.001) and serum IL-8 (7.5 Ϯ 4.4 pg/mL versus 5.5 Ϯ 4.8 pg/mL; p ϭ 0.

Background Previous studies of children with homozygous sickle cell anemia (SCA) show impaired growth and maturation. The correlation of this suboptimal growth with metabolic and hematological factors during puberty is poorly understood. Procedure We studied a group of pre-adolescent children with SCA (19 males, 14 females) and healthy controls (16 males, 15 females) matched for race, sex, body size, and pubertal development. Height, weight, body mass index (BMI), and body composition changes were longitudinally assessed over a 2-year period and compared between the groups and with Z scores based on US growth charts. These changes were correlated with hemoglobin concentration and with energy expenditure measured using indirect whole-room calorimetry. Results Children with SCA progressed through puberty slower than control children. While, after 2 years, pubertal males with SCA were shorter, their annual increases in weight were not different from controls. The mean fat free mass (FFM) increments were significantly less in males and females with SCA than in control children. In males with SCA, growth in height declined over time and was significantly slower than in matched controls (p<0.05). Conclusion Growth delays were present during puberty in children with SCA. Decreased growth velocity in children with SCA was independently associated with decreased hemoglobin concentration and increased total energy expenditure.

EE estimated using SWA was significantly higher than EE measured using IRC in African American children ages 10-14 yr. Bias in individual EE estimated using SWA could be improved by an adjustment for the body weight of a child. The SWA manufacturer should work with researchers on improving existing algorithms for children.

To investigate the influence of vitamin A intake on the contribution of chylomicrons vs. holo retinol-binding protein to milk vitamin A, female rats were fed diets containing either 10 (n = 6) or 50 micromol vitamin A/kg body (n = 4) during pregnancy and through d 13 of lactation. [3H]Vitamin A was incorporated into each diet beginning on d 6 of lactation. Vitamin A concentrations on d 13 were significantly higher in dam liver (x 3), pup liver (x 2.6), milk (x 2.5) and mammary tissue (x 1.3) in rats consuming the higher level of vitamin A. In both groups, vitamin A specific activities in plasma and milk reached apparent plateaus by 2.33 d after addition of [3H]vitamin A to the diets. Vitamin A specific activity in milk was higher than in plasma at all times in both groups. The estimated minimum contribution of chylomicrons to milk vitamin A was 32 +/- 3% in rats fed the lower level of vitamin A vs. 52 +/- 10% at the higher level (P = 0.014). We concluded that dietary vitamin A, like triglycerides, may be directed to mammary tissue during lactation for preferential secretion into milk; thus, increasing vitamin A intakes will increase the contribution of dietary vitamin A to milk. In contrast to milk, mammary tissue vitamin A turns over very slowly.