Rickets

Rickets develops in children when growing bones do not mineralize. The bones soften and may cause a variety of deformities including growth retardation, dental abnormalities, and bowed legs, or may result in bone pain and fractures.

Because vitamin D assists in calcium absorption through specific hormone production, any disturbances with the intake of vitamin D, production of its by-products, absorption, or subsequent metabolism may contribute to the development of rickets. Additionally, ultraviolet light assists in the production of vitamin D through exposure to the skin and conversion therein of specific enzymes. Because melanin filters and absorbs solar radiation, darker skinned individuals may actually require more sunlight exposure to produce the same amount of vitamin D.

The most common cause of rickets outside of the United States is a consequence of malnutrition. If there is overall insufficient oral intake, then inadequate nutrition may result, as sometimes seen in countries suffering from famine. However, specific inadequate intake of vitamin D, as sometimes seen in children exclusively breast fed, may also contribute to this lack of nutrition causing rickets. Other etiologies of nutritional rickets include inadequate intake of dietary calcium or phosphorus.

It is important to note that other medical conditions can contribute to rickets. Because further enzyme conversions occur within the liver and the kidney, specific renal diseases or biliary tract diseases can cause disturbances in the regulation of calcium and phosphorus. Other malabsorptive diseases involving the absorption of nutrients in the gastrointestinal tract can also contribute to the development of rickets. Additionally, rickets may occur as a result of malignancy when tumors secrete factors affect the kidney causing phosphate wasting and disregulation of hormones necessary for calcium.

Side effects of specific medications may also be a factor in the development of rickets. Certain alumi-num-containing antacids lead to hypophosphatemia, while loop diuretics and corticosteroids can lead to calcium and phosphorus deficiency. One anticonvulsant, phenytoin/Dilantin, has been found to react with the lack of target organ ability to absorb a hormone necessary for calcium regulation.

Patterns of inheritance also exist in the development of rickets. Genetic defects have been found that [Page 1497]do not allow vitamin D to be absorbed (receptor abnormalities), as well as mutations causing renal wasting of phosphorus resulting in hypophosphatemia.

Treatment is based upon the etiology. Although physical examination and laboratory evaluation are necessary for diagnosis, management is based upon correction of the nutritional abnormalities. The bony abnormalities may require surgical intervention, but the underlying cause must be discerned so that optimal bone healing may occur.