The appearance of nonfamilial rickets in adults is most frequently due to generalized gastrointestinal malabsorption. Recent studies suggest that rickets secondary to a specific gastrointestinal malabsorption of vitamin D and of calcium is now more common in adults and especially in elderly individuals, possibly because of concomitant dietary deficiencies, inadequate exposure to sunlight, and previous gastric surgery.1 Other conditions which commonly cause rickets are chronic renal glomerular insufficiency and renal tubular disorders such as renal tubular acidosis and the Fanconi syndrome.2 On rare occasions, rickets may complicate hypoparathyroidism, hyperthyroidism, ureterosigmoidostomy, the prolonged ingestion of magnesiumaluminum gel antacids, and hypophosphatasia.2,3
Primary hypophosphatemic rickets (phosphate diabetes) unrelated to the conditions enumerated above may be either familial or sporadic.2 The familial variety is transmitted by sex-linked or autosomal inheritance and usually begins in infancy or childhood, whereas the sporadic variety may occur at any age. The biochemical characteristics of
Burnett V, Baker RK, Wallach S. Primary Hypophosphatemic Rickets in an Elderly Woman. Arch Intern Med. 1973;131(4):581–587. doi:10.1001/archinte.1973.00320100109015
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