Nutritional rickets: deficiency of vitamin D, calcium, or both?

Abstract

Nutritional rickets remains a public health problem in many countries, despite dramatic declines in the prevalence of the condition in many developed countries since the discoveries of vitamin D and the role of ultraviolet light in prevention. The disease continues to be problematic among infants in many communities, especially among infants who are exclusively breast-fed, infants and children of dark-skinned immigrants living in temperate climates, infants and their mothers in the Middle East, and infants and children in many developing countries in the tropics and subtropics, such as Nigeria, Ethiopia, Yemen, and Bangladesh. Vitamin D deficiency remains the major cause of rickets among young infants in most countries, because breast milk is low in vitamin D and its metabolites and social and religious customs and/or climatic conditions often prevent adequate ultraviolet light exposure. In sunny countries such as Nigeria, South Africa, and Bangladesh, such factors do not apply. Studies indicated that the disease occurs among older toddlers and children and probably is attributable to low dietary calcium intakes, which are characteristic of cereal-based diets with limited variety and little access to dairy products. In such situations, calcium supplements alone result in healing of the bone disease. Studies among Asian children and African American toddlers suggested that low dietary calcium intakes result in increased catabolism of vitamin D and the development of vitamin D deficiency and rickets. Dietary calcium deficiency and vitamin D deficiency represent 2 ends of the spectrum for the pathogenesis of nutritional rickets, with a combination of the 2 in the middle.

Global vitamin D status and determinants of hypovitaminosis D

“…This is in large part explained by limited sun exposure due to cultural practises and prolonged breastfeeding without vitamin D supplementation in the Middle East [85], and by dark skin colour and calcium deficiency, rather than vitamin D deficiency, in several countries in Africa [86]. However, both regions also have a high prevalence for hypovitaminosis D.…”

Comparative study of children with calciopaenic and phosphopaenic rickets seen at Chris Hani Baragwanath Hospital

“…1 As the pathogenesis of various types of rickets became more apparent, the underlying mechanisms were classified into those associated primarily with disturbances in calcium (calciopaenic rickets) and those related to perturbed phosphate homeostasis (phosphopaenic rickets).…”

“…Table II shows the important differences in the biochemical findings between calciopaenic and phosphopaenic rickets. 1,3,4,8 The commonest cause of calciopaenic rickets is vitamin D deficiency which is easily corrected by oral administration of vitamin D. 3 X-linked hypophosphataemic rickets is the most common form of phosphopaenic rickets and is currently treated with calcitriol and phosphate supplements. 9,10 In South Africa, there are little published data on the prevalence and presentation of the different types of rickets in children.…”

Adverse interaction of low-calcium diet and low 25(OH)D levels on lumbar spine mineralization in late-pubertal girls

“…(9,10,(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26) However, a clear understanding of the biologic significance of given concentrations of circulating 25(OH)D is still lacking, and reference ranges for vitamin D are being reassessed on the basis of what constitutes a normal concentration compared with optimal concentrations. (27)(28)(29) Most clinicians agree that serum 25(OH)D levels below 25 to 30 nmol/L (10 to 12 ng/mL) may lead to nutritional rickets, hypocalcemic convulsions, dental problems, and poor growth in children and adolescents. (30)(31)(32)(33)(34)(35)(36) But the lower threshold of optimal vitamin D status for bone health and calcium homeostasis during growth is still under discussion, with cutoff values proposed from 25 to 30 to 70 to 90 nmol/L in children, (9,10,23,36) as in adults.…”