Longitudinal study of vitamin D status in the 1st 6 months of life.

UNLABELLED: Although hypovitaminosis D has been reported in the neonatal period and infancy, there is currently little information on the longitudinal changes in vitamin D status throughout early infancy. AIM: To estimate, in Al Ain, UAE, the prevalence of vitamin D deficiency and longitudinal changes and risk factors in infants between birth and 6 months of age. METHODS: Serum 25-OH-vitamin-D levels were measured after birth and 6 months later in 27 infants of mothers of Middle Eastern or Asian origin who were pregnant between the months of September and November 2007. RESULTS: At delivery, mean (SD) maternal serum 25-OH-vitamin-D level was 35.5 nmol/L (24.7); five mothers (22%, 95% CI 0.7-43) had adequate serum levels (>50 mmol/L), 11 (48%, 95% CI 27-70) insufficient levels (25-50 nmol/L) and seven (30%, 95% CI 13-53) deficient (<25 nmol/L) levels. Serum 25-OH-vitamin-D levels were adequate in eight infants (30%, CI 14-50%), insufficient in 13 (48%, CI 28-60%) and deficient in six (22%, CI 8.5-42%). Despite recommendations, none had received any vitamin D supplementation since birth. Despite the high prevalence of hypovitaminosis D at birth and the lack of pharmacological supplementation, the number of infants with adequate levels at 6 months of age rose to 20 (87%, CI 66-97%). No infant had deficiency (CI 0-21%) and three (13%, CI 27-33%) had insufficiency. Adequate levels were detected in four infants who were partially breastfed [mean (SD) 108.5 (20.7) nmol/L] and in only 84% of the 19 exclusively breastfed infants [mean (SD) 96.2 (44.5) nmol/L] but the difference was not statistically significant. Although serum levels improved at 6 months, it occurred more slowly in exclusively breastfed infants. CONCLUSION: In the absence of vitamin D supplementation, guidelines for vitamin D supplementation in infancy still need to be followed because the mechanisms for normalisation are not clearly understood.

Dilated cardiomyopathy secondary to nutritional rickets.

Two 9-month-old breastfed infants presented with congestive heart failure secondary to dilated cardiomyopathy. No underlying aetiology was found, except for the presence of advanced rickets. Following treatment with vitamin D and calcium supplements, both infants quickly recovered normal myocardial function.

Symptomatic rickets in adolescence.

AIM: To describe 21 cases of symptomatic rickets in adolescents. METHODS: The setting was a primary and secondary care hospital in Saudi Arabia providing medical care to Saudi Arab company employees and their families. Cases of symptomatic rickets diagnosed between January 1996 and December 1997 in adolescents aged 10 to 15 years were assessed with respect to clinical presentation, biochemical and radiological evaluation, dietary assessment, and estimation of sun exposure. RESULTS: Symptomatic rickets developed in 21 adolescents (20 females), with a prevalence rate of 68 per 100 000 children years. Presentation included carpopedal spasms (n = 12), diffuse limb pains (n = 6), lower limbs deformities (n = 2), and generalised weakness (n = 1). Biochemical findings included hypocalcaemia (n = 19), hypophosphoraemia (n = 9), raised serum alkaline phosphatase (n = 21) and parathormone (n = 7), and reduced 25-hydroxyvitamin D concentrations (n = 7). Radiological studies were suggestive of rickets in only eight children. All children had an inadequate dietary calcium and vitamin D intake. All but one had less than 60 minutes sun exposure per day. CONCLUSION: Even in sunny climates, adolescents, especially females, can be at risk of rickets. Hypocalcaemic tetany and limb pains were the most common presenting symptoms. Radiological evidence was not present in every case.

Rickets as an unusual initial presentation of abetalipoproteinemia and hypobetalipoproteinemia.

OBJECTIVE: Description of rickets as an unexpected initial manifestation in two children with abetalipoproteinemia and hypobetalipoproteinemia, and elucidation of its pathophysiology in these conditions. METHODOLOGY: Two infants aged two and six months with abetalipoproteinemia and hypobetalipoproteinemia respectively had clinical rickets at presentation, confirmed radiologically and biochemically. Vitamin D intake and serum levels were measured and other causes of rickets were looked for. RESULTS: Vitamin D intake and laboratory studies levels were suggestive of rickets due to calcium deficiency instead of vitamin D deficiency. Healing of rickets occurred with dietary treatment of the malabsorption, without any dietary calcium or significant vitamin D supplementation. CONCLUSION: Steatorrhea-induced calcium malabsorption seems to be the most likely cause of rickets in this entity.

Case-control study of diet and sun exposure in adolescents with symptomatic rickets.

Dietary intake and sun exposure were compared in a case-control study of 14 adolescent girls diagnosed to have symptomatic nutritional rickets with hypocalcaemia, hypophosphoraemia, elevated serum alkaline phosphatase and serum parathormone and reduced 25-hydroxy vitamin D levels and 20 controls without clinical rickets (ten girls) of the same age group and socio-economic background. In the control group, calorie intake was reduced in seven boys and eight girls, dietary calcium in seven boys and seven girls and vitamin D in six boys and eight girls. All 20 adolescents of both sexes were exposed to the sun for more than 60 min a day. In the group with rickets, calorie intake was reduced in 11 girls, calcium in 14 girls and vitamin D in nine girls). Sun exposure was significantly less in girls with rickets than in controls (p < 0.001). Adolescents in our population, especially females, are at high risk of developing nutritional rickets. Prevention by longer exposure to the sun is simple and cheap but when not practical for social or cultural reasons routine vitamin D supplementation might be indicated.

Maternal sickle cell anemia and neonatal isoimmunization.

OBJECTIVE: To study the risk of alloimmunization in pregnant women with sickle cell disease (SCD) and of isoimmunization in their offspring. METHOD: Thirty mothers with SCD were studied and their 35 neonates (group 1) were compared with 538 infants of mothers without hemoglobinopathies (group 2). RESULT: Six mothers with SCD developed alloantibodies. There was no correlation with maternal age (P = 0.6), parity (P = 0.18) or blood transfusions (P = 0.4). The risk of alloimmunization by transfusion was 20%. Six neonates were isoimmunized, a higher incidence than in group 2 (P = 0.02; relative risk 3.07). Five had ABO incompatibility and only one had anti-c isoimmunization. All had reticulocytosis, jaundice and required phototherapy, one developed anemia but none required blood transfusion. CONCLUSION: Although alloimmunization was common in mothers with SCD and isoimmunization in their offspring, it was rarely due to non-ABO alloantibody. There was no significant neonatal morbidity.