In a previous study of rachitic children in Jos, Nigeria we concluded that inadequate dietary intake of calcium was the primary contributing factor to the development of their rickets. The objective of the present study was to determine the effect of calcium supplementation in 10 children with radiographically and biochemically proven rickets from the same geographical area. Rachitic children were provided with calcium supplements of 1000 mg/day for a period of 3 months. Serum and urine samples were obtained at baseline and at 24 hours, 1 week, 4 weeks, and 12 weeks after initiation of supplementation. Serum calcium, phosphorus, alkaline phosphatase, intact parathyroid hormone, 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D were measured at each time point. Dietary recalls obtained at two separate times were used to estimate usual daily intakes of calcium and phosphorus. Ten non-rachitic age-matched controls from the same geographical area were recruited for comparison. Nine of 10 rachitic subjects had radiographic evidence of healing after 3 months of calcium therapy. Although serum calcium concentrations returned to control levels, other biochemical data indicated that the rickets of these subjects may have been multifactorial in aetiology, pointing to a possible defect in the synthesis of 25-hydroxyvitamin D.

The Fulani are semi-nomadic pastoralists of the western Sahel whose culture and economy are centered on cattle. We have shown previously that Fulani children and adolescents (5-18 years old) are stunted and underweight. Nutritional status and lung function were studied in Fulani children and adolescents (n = 70), aged 6-18, and compared with a non-Fulani, rural Nigerian control group (n = 153) of the same age. Participants were restricted to healthy individuals with no prior history of respiratory disease and no symptoms of an upper respiratory tract infection within the past 6 weeks. Significant deficits in forced vital capacity (FVC; Fulani males, 1.51 l; non-Fulani males, 1.86 l, p = 0.009; Fulani females, 1.36 l; non-Fulani females, 1.79 l, p < 0.001), forced expiratory volume in one second (FEV1; Fulani males, 1.44 l; non-Fulani males, 1.76 l, p = 0.02; Fulani females, 1.24 l; non-Fulani females, 1.69 l, p < 0.001), and peak expiratory flow rate (PEFR; Fulani males, 2.69 l/s; non-Fulani males, 3.48 l/s, p = 0.002; Fulani females, 2.29 l/s; non-Fulani females, 3.35 l/s, p < 0.001) were found in both the Fulani boys and girls compared with the non-Fulani controls. The diminished lung function in the Fulani group could be attributed to respiratory muscle weakness or an overall deficit in energy.

Generalized aminoaciduria is associated with vitamin D-deficiency rickets in humans, but there is little information regarding aminoaciduria in rickets caused by primary calcium deficiency. In contrast to rickets in other parts of the world, this bone disease in Nigeria is caused primarily by inadequate intake of dietary calcium. We conducted a clinical trial in Jos, Nigeria in 10 children with radiographically and biochemically proven rickets; an equal number of non-rachitic healthy children from the same area served as controls. Serum and 24 h urine samples were obtained at baseline and at 24 h, 1 week, 4 weeks, and 12 weeks after initiation of calcium supplementation (1000 mg/day) and were analysed for their content of amino acids. Serum calcium, phosphorus, intact parathyroid hormone (PTH), 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D were also measured at each time point. In the rachitic subjects urinary amino acid concentrations were elevated from 2- to 16-fold at baseline, while serum amino acid levels increased 1.5- to 3.8-fold compared to controls. After 12 weeks of calcium supplementation, serum and urine amino acids decreased. There was no correlation between the degree of aminoaciduria and serum PTH or 1,25-dihydroxyvitamin D concentrations. We conclude that the aminoaciduria in these rachitic children was related to their calcium status and not to their vitamin D or PTH status.