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Primary hyperparathyroidism presenting as anticonvulsant-induced osteomalacia

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      Abstract

      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.
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      References

        • Kruse R
        Osteopathein bei antiepileptischer langyeitterapie.
        Monatsschr Kinderheilkd. 1968; 116: 378
        • Dent CE
        • Richens A
        • Rowe DJF
        • et al.
        Osteomalacia with long-term anticonvulsant therapy in epilepsy.
        Br Med J. 1970; 4: 69
        • Richens A
        • Rowe DJF
        Disturbance of calcium metabolism by anticonvulsant drugs.
        Br Med J. 1970; 4: 70
        • Hunter J
        • Maxwell JD
        • Stewart DA
        • et al.
        Altered calcium metabolism in epileptic children on anticonvulsants.
        Br Med J. 1971; 4: 202
        • Hahn TJ
        • Hendin BA
        • Scharp CR
        • et al.
        Effect of chronic anticonvulsant therapy on serum 25-hydroxycalciferol levels in adults.
        N Engl J Med. 1972; 287: 900
        • Hahn TJ
        • Avioli LV
        Anticonvulsant osteomalacia.
        Arch Intern Med. 1975; 135: 997
        • Hahn TJ
        • Birge SJ
        • Scharp CR
        • et al.
        Phenobarbital-induced alterations in vitamin D metabolism.
        J Clin Invest. 1972; 51: 741
        • Boonstra CE
        • Jackson CE
        Hyperparathyroidism detected by routine serum calcium analysis: prevalence in a clinic population.
        Ann Intern Med. 1963; 63: 468
        • Purnell DC
        • Smith LH
        • Scholz DA
        • et al.
        Primary hyperparathyroidism: a prospective clinical study.
        Am J Med. 1971; 50: 670
        • Potts JT
        • Deftos U
        Parathyroid hormone, calcitonin, vitamin D, bone and bone mineral metabolism.
        (chap 20)in: Bondy PL Rosenberg LE Duncan's Diseases of Metabolism. W. B. Saunders Co, Philadelphia1974
        • Strott CA
        • Nugent CA
        Laboratory tests in the diagnosis of hyperparathyroidism in hypercalcemic patients.
        Ann Intern Med. 1968; 68: 188
        • Wills MR
        Normocalcemic primary hyperparathyroidism.
        Lancet. 1971; 1: 849
        • Yendt ER
        • Gagne RJA
        Detection of primary hyperparathyroidism, with special reference to its occurrence in hypercalciuric females with normal or borderline serum calcium.
        Can Med Assoc J. 1968; 98: 331
        • Vaishnava H
        • Rizvi SNA
        Primary hyperparathyroidism associated with nutritional osteomalacia.
        Am J Med. 1969; 46: 640
        • Woodhouse NJY
        • Doyle FH
        • Jopkin GF
        Vitamin D deficiency and primary hyperparathyroidism.
        Lancet. 1971; 2: 283
        • Stanbury SW
        • Torkington P
        • Lumb GA
        • et al.
        Asian tickets and osteomalacia: patterns of parathyroid response in vitamin D deficiency.
        in: 3rd ed. Proc Nutr Soc. 34. 1975: 111
        • Keynes WM
        • Caird FI
        Hypocalcemic primary hyperparathyroidism.
        Br Med J. 1970; 1: 208
        • Dent CE
        • Jones PE
        • Mullan DP
        Masked primary (or tertiary) hyperparathyroidism.
        Lancet. 1975; 1: 1161
        • Potts JT
        • Krutzik SR
        Parathyroid hormone radioimmunoassay: clinical applications.
        Nichols Institute Radioimmunoassay Manual. 1975; (3rd ed): 1
      1. Broadus AE, et al.: Nephrogenous cyclic AMP as a parathyroid function test. J Clin Invest (in press).

        • Haddad JG
        • Chyu KJ
        Competitive protein-binding radioassay for 25-hydroxycholecalciferol.
        J Clin Endocrinol Metab. 1971; 33: 992
        • Patten BM
        • Bilezikian JP
        • Mallette LE
        • et al.
        Neuromuscular disease in primary hyperparathyroidism.
        Ann Intern Med. 1974; 80: 182
        • Mallette LE
        • Patten BM
        • Engel WK
        Neuromuscular disease in secondary hyperparathyroidism.
        Ann Intern Med. 1975; 82: 474
        • Broadus AE
        • Bartter FC
        A simple test for diagnosis of patients with hyperparathyroidism and episodic hypercalcemia.
        Clin Res. 1976; 24: 637A
        • Goldsmith RE
        • Gall EA
        • Altemeier WA
        • et al.
        Hyperparathyroidism: therapy and response, with a test for assessment of response.
        Ann Intern Med. 1971; 75: 395
        • Lumb GA
        • Stanbury SW
        Parathyroid function in human vitamin D deficiency and vitamin D deficiency in primary hyperparathyroidism.
        Am J Med. 1974; 56: 833
        • Murray TM
        • Peacock M
        • Powell D
        • et al.
        Non-autonomy of hormone secretion in primary hyperparathyroidism.
        Clin Endocrinol. 1972; 1: 235
        • Deluca HF
        The kidney as an endocrine organ involved in the function of vitamin D.
        Am J Med. 1975; 58: 39
      2. Bordier P, Ryckewart A, Gueris J, et al.: On the pathogenesis of so-called idiopathic hypercalciuria. Am J Med (in press).