Congenital rickets in 3 newborns of mothers with advanced nutritional osteomalacia, healed with maternal breast milk feeding when mothers alone were given calcium supplements and 7.5 mg of intravenous D2 and the mother baby pair protected from sunlight. Maternal plasma biochemistry indicated more severe vitamin D deficiency compared to their newborns (intrauterine foetal priority). The first dose of 7.5 mg of vitamin D3 and calcium supplements to mother healed osteomalacia but did not appear to heal the rickets of their breast fed infants (extrauterine maternal priority for vitamin D). A second dose given at 3 months interval healed the rickets in their infants and the biochemistry of the mother and baby returned towards normal. Congenital rickets developed when maternal bone mineral and vitamin D stores had been completely exhausted. Raised IPTH levels in the newborn suggested that foetal parathyroids were responsive to hypocalcaemic stimulus.

Adult↗

PubMedDate not supplied

Nutritional and metabolic rickets.

Nutritional rickets is caused by vitamin D deficiency due to lack of exposure to sunlight. Neonatal rickets occurs only in infants born to mothers with very severe osteomalacia. Calcium deficiency alone does not cause mineralisation defects. It only causes osteoporosis and secondary hyperparathyroidism with raised plasma, 1,25 (OH)2D and osteocalcin. Low 25-OHD, increased IPTH, increased alkaline phosphatase in plasma and decreased calcium and increased hydroxyproline in urine are diagnostic of rickets. Low or undetectable plasma levels of 25-OHD, in presence of high plasma 1,25(OH)2D and IPTH are often observed during treatment with vitamin D. Even the marginal intakes of fluoride (> 2.5 mg/day) cause rickets in calcium deficient children. Indian children often need high dose of vitamin D due to severely depleted D stores, high IPTH and severe bone disease (radiologic and histomorphometric) for treatment.

Calcium, Dietary↗

PubMedDate not supplied

Endemic chronic fluoride toxicity and dietary calcium deficiency interaction syndromes of metabolic bone disease and deformities in India: year 2000.

Epidemiological studies during 1963-1997 were conducted in 45,725 children exposed to high intake of endemic fluoride in the drinking water since their birth. Children with adequate (dietary calcium > 800 mg/d) and inadequate (dietary calcium < 300 mg/d) calcium nutrition and with comparable intakes of fluoride (mean 9.5 +/- 1.9 mg/d) were compared. The toxic-effects of fluoride were severe and more complex and the incidence of metabolic bone disease (rickets, osteoporosis. PTH bone disease) and bony leg deformities (genu valgum, genu varum, bowing, rotational and wind-swept) was greater (> 90%) in children with calcium deficiency as compared to < 25% in children with adequate calcium who largely had osteosclerotic form of skeletal fluorosis with minimal secondary hyperparathyroidism. The syndrome of skeletal fluorosis and associated metabolic bone disease and deformity is a unique clinical entity classified as a variant of osteosclerotic form of skeletal fluorosis. This syndrome chiefly results from the biological impact of excess fluoride, low calcium, high PTH and 1,25 (OH)2D3 separately and through their interactions on bone structure and metabolism as studied by radiology, bone scanning, bone histomorphometry and relevant metabolic and endocrine laboratory investigations. Metabolically active and vascular bones of children accumulate fluoride at faster and greater rate than adults (at the sites of active growth). In calcium deficient children the toxic effects of fluoride manifest even at marginally high (> 2.5 mg/d) exposures to fluoride. Fluoride toxicity also exaggerates the metabolic effects of calcium deficiency on bone. The findings strongly suggest that children with calcium deficiency rickets reported in the literature should be re-investigated for possible fluoride interactions. Deep bore drinking water supply with fluoride < 0.5 ppm and improvement of calcium nutrition provide 100% protection against the toxic effects of fluoride and are recommended as the cost effective and practical public health measures for the prevention and control of endemic fluorosis.

Adolescent↗

PubMedDate not supplied

Ataxia telangiectasia.

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Adolescent↗