A high prevalence of
rickets of unknown aetiology has been reported in Chakaria, Bangladesh. Classically,
rickets is caused by
vitamin D deficiency but increasing evidence from Africa and Asia points towards other
nutritional deficiencies or excessive exposure to some metals. The aim of this study was to investigate the aetiology of
rickets in rural Bangladeshi children.
METHODS: 64 cases with
rickets-like
deformities were recruited at first presentation together with age-sex-village matched controls. Data and sample acquisition included anthropometry, radiographs, fasted plasma and urinary samples, 24 h weighed dietary intake together with a 24 h urine collection, and 13C-breath tests to detect Helicobacter (H.) pylori
infection.
RESULTS: One child had active
rickets and frank hypovitaminosis D (F, n = 1) and one had
deformities with radiological features of
Blount disease (M, n = 1). The remaining cases were grouped into those with active
rickets, defined as a radiographic Thacher score ≥1.5 (Group A, n = 24, 12M, 12F) and
rickets-like bone
deformities but not active
rickets (Group B, n = 38, 28M, 10F). All children had a low
dietary calcium intake, but this was lower in Group A than their controls (mean (SD): 156 (80) versus 323 (249) mg/day, p = 0.005). Plasma
25-hydroxyvitamin D (25OHD) was lower in Group A compared to controls; 63% of Group A and 8% of controls had a concentration <25 nmol/L (p ≤ 0.0001). There was, however, no evidence of differences in skin sunshine exposure. Group A had lower plasma
calcium and
phosphate and higher
1,25-dihydroxyvitamin D (1,25(
OH)2D) and
parathyroid hormone (PTH). 88% of Group A and 0% of controls had undetectable plasma intact
fibroblast growth factor (iFGF23), with c-terminal FGF23 (cFGF23) concentrations in the normal range. Urinary
phosphate and daily outputs of environmental metals relative to
creatinine were higher and tubular maximal
phosphate reabsorption per unit glomerular filtration rate (
TmP/GFR) was lower in Group A compared to controls. Although less pronounced than Group A, Group B had higher
alkaline phosphatase, 1,25(
OH)2D and PTH concentrations than controls but similar
calcium intake,
TmP/GFR, iFGF23 and cFGF23 concentrations. Mean 25OHD concentrations were also similar to controls and there was no significant difference in the percentage <25 nmol/L (Group B: 13%, controls: 5%, p = 0.2) No group differences were seen in prevalence of anaemia,
iron deficiency or H. pylori
infection.
CONCLUSION: