학술논문

Drug-related hypercalcemia
Document Type
Article
Source
Endocrinology and Metabolism Clinics of North America; 20210101, Issue: Preprints
Subject
Language
ISSN
08898529
Abstract
This review focuses on the commonly prescribed medicaments that can be responsible for hypercalcemia, considering the prevalence, the predominant pathophysiological mechanisms, and the optimal medical management of each drug-induced hypercalcemia. The use of free over-the-counter vitamin D supplements has considerably increased the prevalence of vitamin D intoxication. Vitamin D supplements and 1α-hydroxylated vitamin D analogues, the later used mainly in patients with hypoparathyroidism and with PTH/PTHrp signaling disorders, increase intestinal calcium absorption, renal calcium reabsorption as well as bone resorption. In patients with hypoparathyroidism receiving recombinant human PTH, transient hypercalcemia can occur because of overtreatment, usually in patients with decreased renal function and dehydration during acute infection. The mechanism responsible for thiazide-induced hypercalcemia includes both stimulation of PTH secretion and enhanced renal proximal calcium reabsorption. Lithium causes hypercalcemia mainly by drug-induced hyperparathyroidism. Worsening of psychiatric symptoms in a lithium-treated patient should always lead to serum calcium measurement.