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Effects of Lithium Therapy on Bone Mineral Metabolism: A Two-Year Prospective Longitudinal Study¹

Departments of Chemical Pathology (T.W.L.M.), Medicine and Therapeutics (C.-C.C.), and Psychiatry (Y.K.W., S.L.), The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, New Territories; and the Department of Pathology, Queen Elizabeth Hospital (C.-C.S.), Kowloon, Hong Kong

Address all correspondence and requests for reprints to: Dr. Tony W. L. Mak, Department of Clinical Pathology, Tuen Mun Hospital, Tuen Mun, Hong Kong. E-mail: makwl{at}ha.org.hk

Many studies showed an increased occurrence of primary hyperparathyroidism during lithium therapy. We studied 53 patients receiving lithium therapy prospectively for 2 yr. Serum PTH levels were unequivocally elevated. The baseline PTH level was 2.8 ± 1.2 pmol/L and increased progressively to 3.9 ± 1.5 pmol/L after 2 yr (P < 0.0005). There was no change in serum calcium, alkaline phosphatase, inorganic phosphate concentrations or tubular reabsorption of phosphate in relation to glomerular filtration rate. Fasting urinary reabsorption of calcium increased significantly (P < 0.0005), which was concordant with the PTH change. Fasting and 24-h urinary excretion of calcium decreased significantly (P < 0.0005), suggesting reduced, rather than enhanced, bone resorption as in primary hyperparathyoidism. This may be the main mechanism in maintaining normocalcemia, despite PTH elevation, during lithium therapy.

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