Related Experiment Videos
Rickets in Nigerian children: a consequence of calcium malnutrition
F Okonofua1, D S Gill, Z O Alabi
1Department of Obstetrics and Gynaecology, University of Ile-Ife, Nigeria.
Insights
Nigerian children
Area of Science:
- Pediatric Endocrinology
- Nutritional Biochemistry
- Bone Metabolism
Background:
- Rickets is a significant pediatric skeletal disorder.
- Vitamin D deficiency is a common cause of rickets globally.
- The etiology of rickets in some tropical regions remains unclear.
Purpose of the Study:
- To investigate the biochemical and etiological factors of rickets in Nigerian children.
- To differentiate between vitamin D deficiency and calcium deficiency as causes of rickets.
- To inform targeted treatment and prevention strategies for rickets in Nigeria.
Main Methods:
- Biochemical assessment of calcium, phosphate, alkaline phosphatase (ALP), 25-hydroxyvitamin D (25-OHD), 1,25-dihydroxyvitamin D (1,25-(OH)2D), parathyroid hormone (PTH), and osteocalcin in rachitic children and controls.
- Histological examination of bone biopsy.
- Dietary calcium intake assessment.
- Clinical and biochemical monitoring during calcium supplementation treatment.
Main Results:
- Rickets in Nigerian children presented with low calcium, elevated ALP, but normal phosphate and vitamin D levels.
- Elevated 1,25-dihydroxyvitamin D (1,25-(OH)2D) to 25-hydroxyvitamin D (25-OHD) ratio and increased parathyroid hormone (PTH) were observed.
- All affected children had critically low daily calcium intake (<150 mg).
- Treatment with calcium supplementation (calcium gluconate) resulted in complete healing of rickets.
Conclusions:
- Rickets in this cohort of Nigerian children is primarily caused by calcium deficiency, not vitamin D deficiency.
- This finding challenges the conventional understanding of rickets etiology in tropical regions.
- Adequate calcium intake is crucial for preventing and treating rickets/osteomalacia in Nigeria and potentially other tropical countries.
Abstract:
Eleven Nigerian children with clinically and radiologically proven rickets were assessed biochemically. The children had low or low normal concentrations of total and corrected calcium, and elevated plasma alkaline phosphatase (ALP) activity, but normal plasma phosphate concentrations. Their serum 25-hydroxyvitamin D (25-OHD) and 1,25-dihydroxyvitamin D (1,25-(OH)2D) concentrations were not significantly different from those in controls, but the ratio of 1,25-(OH)2D to 25-OHD was significantly greater than that in controls. Parathyroid hormone (PTH) concentrations were greater in rachitic children, and there was a significant correlation between 1,25-(OH)2D and PTH concentrations. Osteocalcin concentrations in rachitic children were not significantly different from those in controls, but they were markedly elevated in the three patients with the highest 1,25-(OH)2D and PTH concentrations. One child, from whom a sample of bone (from a corrective osteotomy) was available for histological examination, showed markedly thickened osteoid seams, characteristic of rickets. All the rachitic children had a calcium intake of less than 150 mg daily. Treatment of these rachitic children with calcium gluconate (1 g/d) led to clinical, radiological, and biochemical healing of rickets. We conclude that rickets in Nigerian children is not due to vitamin D deficiency, but to a lack of calcium. This observation has implications regarding the pathogenesis, treatment, and prevention of rickets/osteomalacia in Nigeria and possibly other African and tropical countries.