The relationship of the parathyroid gland to calcium metabolism had been known for many years, but it was not realized until 1926 that widespread decalcification of the skeleton can be produced by a functioning parathyroid tumor. This discovery provided a wealth of new information relative to the abnormal metabolism of bone and also furnished the clue to successful treatment of hyperparathyroidism by surgical extirpation of the tumor. In certain cases, however, the clinical picture was not entirely typical of hyperparathyroidism.1 The bony lesions developed in childhood and were spotty or disseminated rather than generalized2 and sometimes were predominantly unilateral.3 Extraskeletal abnormalities, such as large areas of cutaneous pigmentation, were noted, and in females precocious puberty was an outstanding feature.4 Three seemingly dissociated manifestations, namely, disseminated fibrosis of bone, cutaneous pigmentation and precocious puberty among females, completed a syndrome which Albright and his co-workers5 described in
DOCKERTY MB, GHORMLEY RK, KENNEDY RLJ, PUGH DG. ALBRIGHT'S SYNDROME: (POLYOSTOTIC FIBROUS DYSPLASIA WITH CUTANEOUS PIGMENTATION IN BOTH SEXES AND GONADAL DYSFUNCTION IN FEMALES). Arch Intern Med (Chic). 1945;75(6):357–375. doi:10.1001/archinte.1945.00210300003001
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