Rickets, the continuing challenge

Article Abstract:

Common rickets has virtually disappeared in most developed countries. Common rickets is a bone disorder that results from a deficiency in vitamin D; most developed nations now fortify milk with this vitamin, eliminating this cause of rickets. The symptoms of rickets may result from other causes, however. Rickets is a defect in the formation of endochondral bone. This is the necessary process by which bones grow longer. Bone is an active tissue and even adult bones are constantly being remodeled. The same processes that lead to deficient endochondral bone formation also lead to defective bone remodeling, resulting in osteomalacia, or softening of bone tissue. Bone mineral is composed of crystals of hydroxyapatite. Since this substance is composed primarily of calcium and phosphate, a deficiency of either may result in abnormal bone growth. Several different genetic disorders may contribute to the same final result - rickets. A genetic defect in a kidney enzyme leads to inadequate synthesis of 1-alpha,25-dihydroxyvitamin D3, or calcitriol. The clinical result is a condition called Type I vitamin D-dependent rickets. Type II vitamin D-dependent rickets results from a defect in a receptor for calcitriol. Type II is more appropriately called hypocalcemic vitamin D-resistant rickets. Both types result in low levels of calcium. Another genetic disorder can result in the symptoms of rickets. This condition results in a decrease in circulating phosphate rather than calcium. The gene for this disorder, called X-linked hypophosphatemic rickets, is sex-linked. Boys carrying the gene are always affected; the severity of the symptoms in girls carrying one copy of the gene is highly variable. Vitamin D alone cannot reverse the effects of this disorder. However, vitamin D and phosphate together improve the condition. In the December 26, 1991 issue of The New England Journal of Medicine, clinicians describe the benefits of this treatment. They also document, however, that the treatment leads to the accumulation of calcium in the kidneys of a majority of patients. This condition, called nephrocalcinosis, can lead to kidney failure. Consequently, combination therapy demands the careful monitoring of treatment among patients with X-linked hypophosphatemic rickets. (Consumer Summary produced by Reliance Medical Information, Inc.)

Causes of, Physiological aspects, Drug therapy, Hypophosphatemia, Metabolism, Inborn errors of, Inborn errors of metabolism, Vitamin D deficiency

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Rickets today -- children still need mild and sunshine

Article Abstract:

Children in some developing countries still develop rickets. Rickets is characterized by short stature and abnormal bone development. It is commonly thought to be caused by vitamin D deficiency. However, a 1999 study found that calcium alone or with vitamin D was more effective than vitamin D alone in treating rickets in a group of Nigerian children. All of the children were exposed to sunlight so it seems likely that their rickets was caused by calcium deficiency. Dairy products are the best sources of calcium, but calcium can also be incorporated into the diet in other ways.

Prevention, Calcium (Nutrient), Calcium, Dietary

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A comparison of calcium, vitamin D, or both for nutritional rickets in Nigerian children

Article Abstract:

Calcium or calcium combined with vitamin D may be more effective in treating children with rickets than vitamin D alone. Rickets is a bone disease caused by inadequate calcium and vitamin D levels. Researchers randomly assigned 123 Nigerian children with rickets to receive calcium only, vitamin D only, or both. Calcium alone and calcium plus vitamin D were more effective in building bone mass than vitamin D alone.

Vitamin D, Calcium, Calcium (Chemical element)

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