j Virginia Commonwealth University, Richmond, Virginia, USA. Summary. To understand nutritional ... Bazaar District, in southeastern Bangladesh. Rice is the ... Experimental Biology 98, San Francisco, USA, 19 April 1998. Correspondence: ...
Nutritional Rickets Without Vitamin D Deficiency in Bangladesh by P. R. Fischer a A. Rahman,b J. P. Cimma,c T. O. Kyaw-Myint,d A.R.M.L. Kabir,e K. Talukder,e N. Hassan,f B. J. Manaster,j D. B. Staab,g J. M. Duxbury,h R. M. Welch,h C. A. Meisner,i S. Haque,b and G. F. Combs, Jr h a Mayo Clinic, Rochester, Minnesota, USA b Society for Assistance and Rehabilitation of the Physically Vulnerable, Dhaka, Bangladesh c Amis des Enfants du Monde, Grenoble, France d UNICEF, Dhaka, Bangladesh e Institute of Child and Mother Health, Dhaka, Bangladesh f University of Dhaka, Dhaka, Bangladesh g Memorial Christian Hospital, Chakaria, Bangladesh h Cornell University, Ithaca, New York, USA i International Maize and Wheat Improvement Center, Dhaka, Bangladesh j Virginia Commonwealth University, Richmond, Virginia, USA Summary To understand nutritional rickets in Bangladesh better, 14 rachitic and 13 ‘unaffected’ children were evaluated. Seventy per cent of children with active rickets had no evidence of either vitamin D deficiency or familial rickets. Rickets in Bangladesh is probably related to calcium deficiency. Abnormalities in ‘unaffected’ children suggest that subclinical calcium insufficiency is common.
Introduction While nutritional rickets is usually attributed to vitamin D deficiency, recent reports suggest that dietary insufficiency of calcium is a more common cause of rickets in Africa.1,2 Nevertheless, recent discussion in the literature has questioned whether calcium deficiency actually causes rickets3 and whether calcium deficiency, even if it exists, is a significant public health problem.4 Aware that rickets is frequently seen in southeastern Bangladesh and that standard vitamin D treatment is of limited value, we characterized rickets in Bangladeshi children by evaluating rachitic and apparently unaffected individuals. Methods Children were evaluated in the Chakaria thana, Cox’s Bazaar District, in southeastern Bangladesh. Rice is the main agricultural product in this area, and seasonal flooding is common. Elders in local communities report that rickets Acknowledgements These data were presented in part to the 7th Annual Scientific Conference of the International Centre for Diarrhoeal Disease Research, Dhaka, Bangladesh, 14 February 1998 and to Experimental Biology 98, San Francisco, USA, 19 April 1998. Correspondence: Philip R. Fischer, Department of Pediatrics and Adolescent Medicine, Mayo Clinic, 200 First Street, S. W. Rochester, Minnesota, 55905, USA. E-mail: Journal of Tropical Pediatrics
Vol. 45
October 1999
is a relatively new problem with cases becoming prevalent only during the past 16–18 years. Health workers in the area report high prevalences of stunting, micronutrient deficiences, diarrhoeal disease, and parasitoses. Through the contacts of a community rehabilitation programme serving disabled people in Chakaria, 14 children with bony deformities suggestive of rickets were identified. Following explanation of the study, consenting caretakers were asked to present for evaluation with the affected child and another relative or neighbour of similar age who seemed well without any bone problem. Demographic information, historical details, physical findings, knee and wrist radiographic findings, and biochemical data were noted. In addition, breastmilk from two mothers who were actively nursing was sampled and tested for caloric density and calcium content. Results Fourteen presumably rachitic children and 13 apparently unaffected ‘control’ children presented for evaluation as requested. Results are summarized in Table 1. Two of the 10 children with active rickets (i.e. alkaline phosphatase >350 U/l) had low vitamin D levels (7 and 8 ng/ml), and one of these had hypophosphataemia (phosphorus 1.9 mg/dl) and could represent a sporadic case of hereditary hypophosphataemic rickets. The other seven children with active rickets had no evidence of renal disease, anticonvulsant use, vitamin D deficiency, or familial rickets. Only one subject, a rachitic child, had q Oxford University Press 1999
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TABLE 1 Findings in rachitic children and ‘unaffected controls’ Finding Number of children studied Male gender Age in months, mean (range) Islamic family Family member with rickets Symptoms limb pain limb weakness age in months at onset, median (range) Physical findings bowed legs knock knees sabre tibiae widened wrists beaded ribs Radiographic rickets Biochemical data alkaline phosphatase, U/l >350 mean (range) calcium, mg/dl mean (range) phosphorus, mg/dl mean (range) 25 OH vitamin D, pg/ml 55 mean (range) lead, whole blood, mcg/dl mean (range)
Rachitic 14 9 (64%) 69 (36–98) 13 (93%) 4 (29%)
p
13 9 (70%) 70 (10–120) 12 (92%) 13 (100%)
13 (93%) 12 (86%) 24 (0–48) 4 (29%) 10 (71%) 3 (21%) 10 (71%) 10 (71%) 7 (54% of 13 tested) 10 (71%) 492 (198–834)
1 (8%) 1 (8%) 3 (23%) 0 (0% of 6 tested) 0 (0%) 206 (138–331)
