PEDIATRICS Vol. 66 No. 3 September 1980, pp. 359-365
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Rickets

Robert D. Lovinger MD1

1 Departments of Pediatrics and Pathology, Medical College of Virginia, Richmond

Rickets is a disease of growing children. Historically, its winter prevalence and its occurrence among children confined to sunless sweat shops and smog-ridden cities during the industrial revolution implicated insufficient exposure to sunlight in its etiology.1-3 Despite the discovery of the anti-rachitic action of cod-liver oil more than 200 years ago, rickets remained a serious health problem until the early part of the 20th century when the identification, isolation, and finally almost ubiquitous addition of vitamin D to our food supply soon rendered conventional rickets a disorder of mere academic interest. Recently, however, a slow increase in the incidence of rickets in children with a variety of medical problems including renal tubular disorders, illness requiring chronic hemodialysis, cystic fibrosis, and as a complication of anticonvulsant therapy has been noted. Thus, the reappearance of rickets in new, more subtle forms, necessitates increased physician awareness of its incidence and its pathogenesis.

CALCIUM AND PHOSPHORUS HOMEOSTASES

Fundamental to the pathophysiology of rickets are calcium and phosphorus homeostases.4 Calcium plays a central role in many body functions and is an important cofactor in muscle contraction, neural transmission, enzyme activity, blood clotting, and other cellular processes. Calcium exists in a number of body pools of varying exchangeability or availability for immediate use. The nonexchangeable calcium pool includes the bones, which contain approximately 99% of the body's calcium, and certain body proteins to which it is tightly complexed. The rapidly exchangeable pool is made up of either ionized or loosely complexed calcium, present both in the body fluids and within individual cells.

Submitted on December 21, 1979
Accepted on February 11, 1980




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