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A 53-year-old woman presented to her general practitioner with a 3-month history of lethargy. She was taking lithium carbonate (900 mg daily for 9 years) and carbamezepine (400 mg daily for 3 years) for manic depressive illness, and thyroxine (50 μg daily for 4 years) for primary hypothyroidism. She smoked 20 cigarettes a day. There was no abnormal...
Citations
... Lithium directly stimulates the secretion of parathyroid hormone. 5 Lithium also decreases intracellular calcium uptake, thus reducing parathyroid sensitivity to circulating calcium levels. Reduction of the parathyroid gland sensitivity to the circulating calcium will lead to an increase in PTH concentration. ...
... Reduction of the parathyroid gland sensitivity to the circulating calcium will lead to an increase in PTH concentration. 5 Furthermore, in vitro studies suggests that lithium may stimulate PTH secretion through inhibition of action of glycogen synthase kinase 3b,which inhibits PTH gene transcription. 6 PTH transcription thereby proceeds after suppression of this inhibitor enzyme, leading to an overproduction of PTH. 7 Lithium therapy may accentuate the set-point error in patients with primary hyperparathyroidism and unmask preexisting hyper-plastic or adenomatous changes in the parathyroid glands. ...
Our objective was to evaluate whether lithium-induced hyperparathyroidism (LIHPT) is caused by single-gland versus multigland disease.
Medical records of 7 patients who underwent parathyroidectomy for LIHPT were reviewed.
The mean preoperative calcium was 11.1 ± 0.7 mg/dL. Six of 7 patients were rendered eucalcemic with surgery. Of the 6 patients successfully treated with surgery, 4 had single-gland disease, 1 had double adenomas, and 1 had 4-gland hyperplasia. Intraoperative intact serum parathyroid hormone (iPTH) accurately predicted resolution of hyperparathyroidism in 6 of 7 patients. One patient then subsequently developed persistent hyperparathyroidism refractory to further surgery. Localization studies defined the extent of disease in 5 of 7 patients.
LIHPT presents with a spectrum of disease ranging from single-gland to multigland disease. The utility of preoperative localization studies and intraoperative iPTH in this population is uncertain. Bilateral exploration may be best to achieve a resolution of LIHPT.
This chapter discusses several case studies explaining the adverse effects of lithium on cardiovascular systems; respiratory system; ear, nose, throat; nervous system; endocrine system; metabolism; gastrointestinal system; urinary tract; and other parts of human body. The teratogenic effects of lithium are also reviewed. The chapter also describes drug interactions with lithium, focusing on interactions in the elderly. The interaction of non-steroidal anti-inflammatory drugs (NSAIDs) with lithium is also described. Both celecoxib and naproxen, non-selective cyclo-oxygenase inhibitors, reduce renal clearance of endogenous lithium (used as a measure of proximal tubular sodium reabsorption). The clinical implications are unclear, because the US package insert for celecoxib describes a study in which 200 mg bd caused a mean increase in serum lithium concentration of only 17% in 24 subjects taking lithium carbonate 450 mg bd. The chapter also discusses the interference of lithium with diagnostic tests.
