Aetiology of Gambian rickets
|ING Staff:||Ann Prentice, Landing Jarjou, Vickie Braithwaite, Kerry Jones, Gail Goldberg|
We have previously reported on a case-series of 46 children with suspected calcium-deficiency rickets who presented in The Gambia with rickets-like bone deformities. Biochemical analyses discounted vitamin D-deficiency as an aetiological factor but indicated a perturbation of Ca-P metabolism involving low plasma phosphate and high circulating fibroblast growth factor-23 (FGF23) concentrations. This finding led us to a novel hypothesis linking chronically low dietary calcium supply to urinary phosphate-wasting and rickets.
Our ongoing studies in cases, healthy controls and reference children are designed to test our hypothesis that Gambian rickets is linked to derangements of phosphate metabolism through chronically elevated 1,25(OH)2D and FGF23 and to consider other potential aetiological factors. These include urinary phosphate-wasting, calcium and other mineral deficiencies, iron status, dietary and environmental factors, biochemical abnormalities, genetic predisposition, intestinal absorption, 25OHD turnover and the response to calcium loading.
These Gambian studies are complemented by our studies of the aetiology of rickets in Bangladesh.