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.
637tecting deterioration but a separate evaluation by the research team showed that at least 74% of the patients who had been deemed to have relapsed had an increase of florid symptoms. Though one-third of the patients in our sample had florid symptoms when they entered the trial their condition was stabilized at the time. When switched to placebo 83 % of these increased the number of florid symptoms (table VII). The social behaviour of many patients on placebo deteriorated and put additional strain on their relatives (Stevens, 1973), but in most cases it was associated with an exacerbation of schizophrenic symptoms. We therefore conclude that fluphenazine decanoate has a powerful effect in preventing and ameliorating both schizophrenic symptoms and deterioration of behaviour and social functioning.We have stated that we cannot accept the 8% relapse rate of our experimental group at face value. Ninety-five per cent. of our sample had been established on treatment more than three months and most more than a year, so that patients who had been negative responders, relapsed or lapsed from treatment would have been omitted from the sample. Thus the proportion of chronic schizophrenics who relapsed and began treatment with fluphenazine decanoate but were unlikely to remain well-controlled for a year might be expected to be more than 30%, in contrast to patients well established on treatment, of whom only 8% relapsed during nine months in this trial.It is noteworthy that 89% of patients entering our trial received just one 25-mg injection of fluphenazine decanoate monthly. Some centres give much higher doses, but these findings suggest that low doses are effective in most cases.This study has not touched on the problems of the chronic disabilities of these patients. With the greater control of florid symptoms which treatment provides the management of residual disability will become an increasing problem, because of the growing number of chronic patients returning to live in the community. Summary Investigation of 20 patients with skeletal fluorosis showed that five had clear evidence of secondary hyperparathyroidism. The hyperactivity of the parathyroid glands in skeletal fluorosis in the presence of decreased solubility of the bone mineral (fluoroapatite) strongly suggests that it is a compensatory attempt to maintain a normal extraceElular ionized calcium equilibrium. Further study of the parathyroid glands and of bone lesions in skeletal fluorosis is in progress.
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.
. Endemic skeletal fluorosis. Endemic skeletal fluorosis is described in 6 children aged 11 or over. Four cases were crippled with severe deformities in the spine, hips, and knees. All showed positive phosphorus, magnesium, and nitrogen balances and excessively positive calcium balances. The skeletal x-rays, histology, and chemical composition of the bones revealed diagnostic changes in each case.Endemic fluorosis as manifested by mottled dental enamel and by diffuse osteosclerosis of the skeleton was first described in India from the State of Madras by Shortt et al. (1937). Subsequently cases have been described from other parts of India (Pandit et al
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.
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