Division of Endocrinology and Metabolism, Departments of Medicine (R.R., P.W.L.) and Radiology (N.J.B.), Johns Hopkins University, Baltimore, Maryland 21287-0003
Address all correspondence and requests for reprints to: Paul W. Ladenson, M.D., Department of Medicine, Division of Endocrinology and Metabolism, The Johns Hopkins University, 1830 East Monument Street, Suite 333, Baltimore, Maryland 21287-0003.
An 80-yr-old man with a more than 60-yr history of postsurgical hypoparathyroidism was evaluated for hypocalcemia detected during hospitalization after a fall. The patient had long-standing intermittent paresthesias in his distal extremities, but denied muscle cramps, tetany, or seizures. His past medical history was remarkable for an episode of nephrolithiasis in his 20s. He had been taking up to 4000 mg calcium carbonate (oral, daily) before admission. On examination, Chvostek and Trousseau signs, tremor, and rigidity were absent. Laboratory studies included: 5.9 mg/dl serum calcium (normal range, 8.410.5), 0.78 mmol/liter ionized calcium (normal range, 1.131.32), 6.7 mg/dl phosphate (normal range, 2.74.5), 3.2 g/dl albumin (normal range, 3.55.3), and 1 pg/ml intact PTH (normal range, 1065). In Fig. 1, brain computed tomography showed diffuse, symmetric parenchymal calcifications involving the dentate nuclei (A), thalami (B, curved arrow), globus palladi (B, arrowhead), caudate heads (B, straight arrow), and deep cerebral white matter (C). The patient was treated with 0.5 µg calcitriol and 1000 mg calcium carbonate (oral, daily). After 1 week, his chronic paresthesias resolved and serum calcium rose to 9.2 mg/dl.
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Received November 15, 2002.
Accepted January 6, 2003.
References
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