Varying Role of Vitamin D Deficiency in the Etiology of Rickets in Young Children vs. Adolescents in Northern India

Abstract

The relative importance of calcium vs. vitamin D deficiency in the etiology of nutritional rickets in the tropics may be different in children compared with adolescents. We studied calcium intake, sun exposure, serum alkaline phosphatase, and 25 hydroxyvitamin D in 24 children and 16 adolescents with rickets/osteomalacia. The values were compared with those obtained in control subjects (34 children and 19 adolescents). We found that young children with rickets had lower calcium intake compared with controls (285 +/- 113 vs. 404 +/- 149 mg/day, p < 0.01), but similar sun exposure (55 +/- 28 vs. 56 +/- 23 min x m2/day) and 25 hydroxyvitamin D (49 +/- 38 vs. 61 +/- 36 nmol/l). Sixteen of 24 children with rickets had 25 hydroxyvitamin D above the rachitic range (> 25 nmol/l), in contrast to one of 16 adolescents. Adolescent patients had low calcium intake vs. controls (305 +/- 196 vs. 762 +/- 183 mg, p < 0.001), and lower sunshine exposure (16 +/- 15 vs. 27 +/- 17 min x m2/day, p < 0.01) and serum 25 hydroxyvitamin D (12.6 +/- 7.1 vs. 46 +/- 45.4 nmol/l, p < 0.001). The odds ratio for developing rickets with a daily calcium intake below 300 mg was 4.8 (95 per cent CI, 1.9 - 12.4, p = 0.001). Subjects with rickets were randomized to receive 1 g calcium daily, with or without vitamin D. Children showed complete healing in 3 months, whether they received calcium alone or with vitamin D. Adolescents showed no response to calcium alone, but had complete healing with calcium and vitamin D in 3-9 months (mean 5.3 months). Thus deficient calcium intake is universal among children and adolescents with rickets/osteomalacia. Inadequate sun exposure and vitamin D deficiency are important in the etiology of adolescent osteomalacia.

Relationship between serum 25-hydroxyvitamin D and parathyroid hormone in the search for a biochemical definition of vitamin D deficiency in children

“…Ideally, the "optimal" 25OHD threshold should separate abnormal bone metabolism from normal bone metabolism. Similar to our study, the majority of published patients with vitamin D deficiency rickets have 25OHD levels < 34 nmol/l (33-36), but nutritional rickets has been reported in children with much greater 25OHD levels (22,37,38). The variability of 25OHD thresholds and guidelines reflects that an influencing factor exists that determines when nutritional rickets occurs and that factor is calcium intake.…”

“…Articles the other hand, deficient calcium supply, through poor intake or malabsorption, can lead to rickets even in the presence of perfectly normal 25OHD levels of up to 140 nmol/l (22,(37)(38)(39). It is well recognized that nutritional rickets has pure calcium deficiency with normal vitamin D on one end of the spectrum and pure vitamin D deficiency with normal calcium intake on the other end (38,39).…”

Vitamin D replacement in pregnant women in rural north India: a pilot study

“…Vitamin D deficiency is highly prevalent in urban and rural India (Balasubramanian et al, 2003;Sahu et al, 2009), and pregnant women and newborns are vulnerable groups (Sachan et al, 2005;Balasubramanian et al, 2006). Data regarding appropriate doses of vitamin D during pregnancy are scant (Brooke et al, 1980;Marya et al, 1988;Madelenat et al, 2001;Datta et al, 2002).…”

Vitamin D status in children with cerebral palsy

“…There are studies from both north India and south India. [19][20][21] These studies clearly state the fact that approximately 75 to 85% of the groups studied have varying degrees of vitamin D deficiency or insufficiency (hypovitaminosis D). Also the latitude, solar zenith angle, ultraviolet radiation, amount of cloud cover, time duration of exposure to sunlight, body surface area exposed to sunlight is different among different parts of the world and also different in various areas of our own country and therefore comparisons between the different groups are not possible.…”