Broadus A E, Hanson T A, Bartter F C, Walton J
Am J Med. 1977 Aug;63(2):298-305. doi: 10.1016/0002-9343(77)90245-5.
A patient presented with the classic features of anticonvulsant-induced osteomalacia. Following discontinuance of diphenylhydantoin therapy and repletion with physiologic quantities of vitamin D, hypercalcemia and persistent biochemical hyperparathyroidism developed, and a parathyroid adenoma was removed. A history of nephrolithiasis and hypercalcemia preceding the institution of drug therapy allowed this patient's underlying parathyroid disease to be defined as primary hyperparathyroidism, which had been obscured by anticonvulsant therapy.