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FGF23 is elevated in Gambian children with rickets
Ann Prentice1, Mustapha Ceesay, Shailja Nigdikar
1MRC Keneba, The Gambia. ann.prentice@mrc-hnr.cam.ac.uk
Insights
Elevated Fibroblast Growth Factor 23 (FGF23) and low phosphate levels suggest a role in African rickets. These findings highlight potential FGF23 and phosphate regulation issues in calcium-deficiency rickets.
Area of Science:
- Pediatric Endocrinology
- Mineral Metabolism
- Nutritional Rickets
Background:
- Fibroblast Growth Factor 23 (FGF23) is a key regulator of phosphate homeostasis.
- Rickets, particularly in the absence of vitamin D deficiency, is observed in populations with low calcium intake, but risk factors remain unclear.
- Previous studies have indicated elevated FGF23 in certain hypophosphatemic conditions.
Purpose of the Study:
- To investigate the biochemical profile, including FGF23 levels, in Gambian children with rickets of unknown etiology.
- To compare FGF23 concentrations in these patients with those of healthy local children.
- To explore potential associations between FGF23, phosphate, and rickets severity.
Main Methods:
- A cohort of 46 Gambian children with rickets and plasma 25-hydroxyvitamin D above 20 nmol/l were studied.
- Plasma FGF23, phosphate, alkaline phosphatase, and other biochemical markers were measured.
- Patient samples were compared to those from a control group of local children.
Main Results:
- Rickets patients exhibited lower plasma phosphate and 25-hydroxyvitamin D, and higher alkaline phosphatase compared to controls.
- Significantly elevated FGF23 concentrations were observed in rickets patients (mean 367 RU/ml) versus controls (mean 51 RU/ml).
- Plasma phosphate showed a significant inverse correlation with FGF23 levels.
Conclusions:
- The findings suggest that dysregulation of phosphate and FGF23 may contribute to the development of calcium-deficiency rickets in African and Asian populations.
- Elevated FGF23 levels, despite adequate vitamin D status, point towards alternative pathogenic mechanisms in certain forms of rickets.
- Further research into FGF23 and phosphate metabolism is warranted for understanding and managing rickets in these regions.
Objectives:
Fibroblast growth factor 23 (FGF23) is a phosphaturic factor that is elevated in several diseases associated with hypophosphatemia and rickets. Rickets in the absence of vitamin D deficiency has been reported in African and Asian populations with a low calcium intake but the definition of risk factors has proved elusive. The aim of the study was to characterize the biochemical profile and measure FGF23 in a series of Gambian children who had presented with rickets of unknown etiology and a plasma 25-hydroxyvitamin D (25OHD) above the range typical of vitamin D-deficiency rickets.
Methods:
The 46 patients (30 males, 16 females) had bone deformities typical of rickets and were 1.1-16.4 years old (geometric mean, 3.4 years). Active rickets (on radiographs and/or elevated plasma alkaline phosphatase) was present in 28%. Plasma 25-hydroxyvitamin D was above 20 nmol/l in all patients. Concentrations of plasma FGF23, phosphate and other relevant biochemical analytes were measured in stored samples of fasting, early morning plasma and compared with those measured in samples collected from local children and stored under similar conditions.
Results:
The rickets patients had lower plasma phosphate, lower 25-hydroxyvitamin D, higher 1,25-dihydroxyvitamin D and elevated total alkaline phosphatase than local children. Those with active rickets had raised parathyroid hormone concentration. The patients had significantly higher FGF23 concentration than local children (geometric mean (-1SD, +1SD, range) RU/ml: 367 (87, 1552, 46-7052, n=39) vs 51 (23, 112, 3-130, n=30), p
Conclusions:
These data suggest that perturbations of phosphate and FGF23 regulation may be implicated in the pathogenesis of calcium-deficiency rickets in Africa and Asia.
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