Selected Summaries

Calcium Deficiency as a Cause of Rickets

[Pfitzner MA, Thackher TD, Pettifor JM, Zoakat AI, Lawson JO, Isichei CO, Fischer PR. Absence of vitamin D deficiency in young Nigerian Children. J Pediatr 1997; 133: 740-744].

Although deficiencies of either calcium or vitamin D can cause nutritional rickets, most cases of nutritional rickets are ascribed to vitamin D deficiency. Some believe that vitamin D and calcium deficiency should coexist to cause rickets. This cross sectional study was carried out to determine background prevalence of vitamin D deficiency in Nigerian children residing in areas of high rickets prevalence.

Children aged 6 to 35 months were selected using randomized cluster sampling technique over a four week period during the end of dry season. Demographic information, a medical history and results of brief physical examinations of signs and symptoms of rickets were recorded. A crude estimate of sunlight exposure was noted during the interview and using a body surface area nanogram amount of skin exposed and amount of time spent by the child outdoors. Approximately 3-5 ml of blood was drawn from each child and sera stored at _20°C. Serum calcium was measured spectrophotometrically and serum alkaline phosphatase was measured by reflectance spectrophotometery. Serum 25 (OH)₂ vitamin D was measured by the INCSTAR¹²⁵I radioimmunoassay kit. Data was analyzed by EPI infosoftware.

Of the 238 children and parents approached, 218 were enrolled for the study. Families were of 48 different ethnic groups of which 63% (n=136) were Christians and remainder were Muslims. No child had 25 (OH)₂ vitamin D concentration less than 10ng/ml (generally held definition for vitamin D deficiency). Children spend an average 8.3 hours per day outside the home and this did not vary with age. No child was receiving exogenous vitamin D in high doses. Clinical signs of rickets were seen in 20 (9.2%) children. These children had significantly lower calcium levels that those without signs of rickets (9.1 vs 9.4 mg/dl), respectively (p=0.01). No such difference was seen in vitamin D levels. Children with physical signs of rickets were more likely to have been weaned (OR 8.33; 95% CI 1.1-50.0) then children without signs of rickets. Gender, months since breast feeding stopped in those no longer nursing, per cent of body clothed and time spent by child in sunlight did not differ in both the groups.

Comments

Calcium deficiency as a cause of rickets is based only on limited studies in a hospital based population and case reports(1-2). Since there was 5-9% prevalence of rickets in the study population, if vitamin D deficiency was the cause of rickets, and even greater prevalence of subclinical vitamin D deficiency would have been detected. But none of the children had vitamin D levels <10 ng/ml. This proves beyond doubt that calcium deficiency was the cause of rickets in the study poplation.

Although low calcium intakes appear to be a major factor in the pathogenesis of the disease, recent studies in Nigeria where dietary calcium intakes in patients have been compared to those of age matched controls have shown no difference(3). But children with rickets were weaned off earlier (as the present study) and hence differences in other dietary constituents like phosphorous, phytate and oxalates may be interfering in absorption of calcium. Further it is possible that those children who develop rickets are less able to adapt to low dietary calcium intakes than their peers through genetic and environmental factors. Polymorphism in vitamin D receptor gene has been suggested to influence intestinal calcium absorption(4).

Knowledge concerning the pathogenesis of rickets in children in developing countries in tropical and subtropical region has considerable public health significance and forms the basis for preventive public health programmes. In a tropical country like ours with plenty of sunlight as source of vitamin D, calcium deficiency may be the only cause of rickets in a number of cases. Whether this is influenced by maternal calcium deficiency or calcium content of breastmilk remains to be investigated. Also interventional studies examining the effect of improving calcium intake by promoting calcium status of mothers, breastfeeding and calcium rich diet are required.

Anju Aggarwal,
Pediatrician,
ESI Hospital,
Basaidarapur, New Delhi,
India.

References

1. Pettifor JM, Ross P, Wang J, Moddley G, Cooper SJ. Rickets in children of rural origin in South Africa. Is low dietary calcium a factor. Pediatrics 1978; 92: 320-324.

2. Thacher T, Ighogboja SI, Fischer PR. Rickets without vitamin D deficiency in NIgerian children. Ambul Child Hlth 1997; 3: 56-64.

3. Pettifor JM. Rickets and calcium metabolism. In: Issues in Tropical Pediatrics, Proceedings of 5th International Congress of Tropical Pediatrics. Jaipur Priners, India 1999; pp 83-88.

4. Wishart JM, Horowitz M, Need AG, Scopacasa F, Morris HA, Clifton PM, et al. Relations between calcium intake, calcitriol, polymorphism in the vitamin D receptor gene and calcium absorption in premenopausal women. Am J Clin Nutr 1997; 65: 798-802.