Sickle cell bone disease: response to vitamin D and calcium.

Bone disease with osteoporosis and osteomalacia are common in sickle cell disease (SCD). Some patients have vitamin D deficiency and low bone mineral density (BMD). The role of vitamin D and calcium supplementation to restore bone health in SCD has not been well studied. In 14 adults with SCD, we measured 25(OH)D (25-hydroxyvitamin D) and BMD at the femoral neck, lumbar spine, and distal third of the ulna plus radius, along with markers of bone resorption (CTx; C-terminal component of pro-collagen type I) and bone formation (osteocalcin) before and after 12 months of vitamin D(2) and calcium carbonate treatment. Pretreatment, all patients were vitamin D deficient with a mean 25(OH)D level of 11.6 [corrected] +/- 4 [corrected] ng/ml, had low BMD at the lumbar spine (L-spine), 0.87 +/- 0.11 g/cm(2) (mean Z-score of -2.6 3 +/- 0.71 SD and T score of -2.31 +/- 0.75 SD), femoral neck, 0.8 +/- 0.18 g/cm(2) (mean Z-score -1.36 +/- 0.84, T-score -1.14 +/- 0.75), and the distal radius and ulna, 0.6 +/- 0.17 g/cm(2) (mean Z-score -1.18 +/- 0.79, T-score -1.01 +/- 0.74) and had elevated CTx (0.87 +/- 0.5 ng/ml) and osteocalcin levels (12.3 +/- 3.7 ng/mul). After treatment, all patients corrected their 25(OH)D level (34.6 [corrected] +/- 11 [corrected] ng/ml) (P < 0.001) with a 3.6% +/- 3.9% increase in BMD at the L-spine (P = 0.009), 4.6% +/- 8.5% increase at the femoral neck (P = 0.05) and 6.5% +/- 12.6% increase at the distal radius plus ulna (P = 0.09). CTx, osteocalcin, and PTH(i) levels were unchanged. Treatment of adult SCD with vitamin D and calcium can restore 25(OH)D levels to normal and improve BMD, but, markers of bone resorption remained unchanged. Screening for vitamin D deficiency and BMD in SCD patients seems warranted.

Vitamin D status among 4-month-old infants in New England: a prospective cohort study.

BACKGROUND: Concerns over vitamin D deficiency in infants and children recently prompted the American Academy of Pediatrics to recommend increased supplementation. Few studies have examined vitamin D status in the same infants over time. Also, while many researchers label "breastfeeding" as a risk factor for vitamin D deficiency, few differentiate between any breastfeeding, exclusive breastfeeding, and supplemented or unsupplemented breastfeeders. OBJECTIVE: To determine predictors of 25(OH)D deficiency at 4 months in a group of children previously tested at birth. METHODS: We enrolled newborns from 2005 to 2007 at an urban Boston hospital. Maternal and infant blood samples were collected within 72 hours of birth. At 4 months, we obtained a second infant blood sample. RESULTS: At 4 months, 11.9% of the 177 infants were vitamin D deficient compared to 37.5% at birth (25(OH)D <20 ng/mL). Median 25(OH)D was 35.2 ng/mL (range, 5-100.8; 95% confidence interval [CI], 32.8-37.6). At 4 months, 40% of unsupplemented infants were deficient. Lack of supplementation was significantly associated with increased risk of deficiency (adjusted odds ratio [AOR], 19.3; 95% CI, 4.80-77.2). Being outside at least 10 minutes a day, once per week, was protective (AOR, 0.12; 95% CI, 0.02-0.66), as was increasing gestational age (AOR, 0.36; 95% CI, 0.19-0.69). In 48.4% of patients, physicians failed to prescribe vitamin D at 2 months. CONCLUSIONS: Despite inconsistent supplementation, a smaller proportion of infants were vitamin D deficient at 4 months than at birth. While supplemented breastfed infants were not at risk of deficiency, unsupplemented exclusively breastfed infants were at high risk of severe deficiency.