This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by BIRNBAUM, J. Articles by HERLE, A. V. Search for Related Content PubMed PubMed Citation Articles by BIRNBAUM, J. Articles by HERLE, A. V. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB CALCIUM COMPOUNDS CALCIUM, ELEMENTAL LITHIUM COMPOUNDS LITHIUM, ELEMENTAL PARATHYROID HORMONE

Lithium Stimulates the Release of Human Parathyroid Hormone in Vitro

Departments of Medicine/Endocrinology and Surgery/Division General Surgery, University of California at Los Angeles School of Medicine Los Angeles, California 90024-1682.

Address requests for reprints to: A. J. Van Herle, M.D., Department of Medicine, Division of Endocrinology, University of California School of Medicine, Los Angeles, California 90024-1682.

The effect of lithium on PTH release from human parathyroid tissue was studied using a perifusion system and an immunoradiometric assay for intact human PTH. Tissue was obtained from three patients undergoing surgery for thyroid disease, three patients with secondary hyperparathyroidism due to chronic renal insufficency, and four patients with primary hyperparathyroidism due to a parathyroid adenoma. Addition of lithium in concentrations equivalent to the therapeutic serum levels normally attained in man (1.3 mmol/L) resulted in a significant (P < 0.05) increase in PTH release under normocalcemic (1.15 mmol/L) conditions from normal and hyperplastic tissues. The magnitude of the lithium-induced response of PTH release ranged from a 1.4- to 5.3-fold increase above basal levels (perifusion with 1.15 mmol/L calcium alone) and was comparable to the response during a low calcium (0.42 mmol/L) perifusion. Although the response to lithium was delayed compared to that of hypocalcemia, PTH returned to basal levels immediately after removal of either stimulator. In contrast, parathyroid adenomas did not respond to either lithium or hypocalcemia in a characteristic manner, but, rather, functioned in an autonomous fashion with repeated pulsatile bursts of PTH release that were not suppressible even under hypercalcemic (1.70 mmol/L) conditions. These in vitro studies suggest that lithium therapy may elevate serum PTH levels in some patients and could, thus, be responsible for hypercalcemia in them.

Received September 1, 1987.

This article has been cited by other articles:

				C. Livingstone and H. Rampes Lithium: a review of its metabolic adverse effects J Psychopharmacol, May 1, 2006; 20(3): 347 - 355. [Abstract] [PDF]

				T. W. L. Mak, C.-C. Shek, C.-C. Chow, Y.-K. Wing, and S. Lee Effects of Lithium Therapy on Bone Mineral Metabolism: A Two-Year Prospective Longitudinal Study J. Clin. Endocrinol. Metab., November 1, 1998; 83(11): 3857 - 3859. [Abstract] [Full Text]

				S. T. Haden, A. L. Stoll, S. McCormick, J. Scott, and G. El-Hajj Fuleihan Alterations in Parathyroid Dynamics in Lithium-Treated Subjects J. Clin. Endocrinol. Metab., September 1, 1997; 82(9): 2844 - 2848. [Abstract] [Full Text] [PDF]

				A. Saxe and G. Gibson Effect of Lithium on Incorporation of Bromodeoxyuridine and Tritiated Thymidine Into Human Parathyroid Cells Arch Surg, August 1, 1993; 128(8): 865 - 869. [Abstract] [PDF]