Endocrine Abstracts

Background: Lithium salts have been widely known to induce thyroid dysfunction, however, parathyroid dysfunction due to lithium use is uncommonly encountered. Hypercalcemia is a relatively common consequence of lithium therapy presenting with nonspecific symptoms that may be overlooked. Although cerebral infarction may be an independent event from psychiatric disorders, it can also be a rare complication that must be recognized particularly in patients on lithium therapy.

Case: A 64-year old female diagnosed with bipolar disorder and maintained on Lithium for 25 years, noted to have multiple recurrent cerebral infarctions presenting as dizziness, headache and vomiting. She had a multinodular nontoxic goiter and osteoporosis. Work-up showed elevated ionized calcium and intact PTH, with evidence of bilateral renal parenchymal calcifications and the parathyroid scintigraphy revealed two Sestamibi-avid nodules.

Discussion: Hypercalcemia and hyperparathyroidism are common but often unrecognized consequences of lithium therapy. Lithium causes a shift in the inhibitory set point for PTH secretion to a higher serum calcium concentration and, although rare, complications include cerebral infarction due to hypercalcemia and should be watched out for in these patients. Single as well as multigland involvement may be seen in patients with LAH and preoperative localization studies should be done in patients with surgical indications. The low incidence of lithium-associated hyperparathyroidism limits acquisition of enough information for formulation of clinical guidelines for diagnosis and management, hence documentation and reporting of cases are important contribution for a larger pool of data.