Cardiovascular Implications of Calcitonin Therapy: A Narrative Review of Mechanisms, Clinical Risks, and Safety Considerations

Calcitonin, a peptide hormone produced by thyroid parafollicular cells, is used clinically for acute hypercalcemia, Paget’s disease of bone, and, less commonly, postmenopausal osteoporosis. It also has recognized analgesic utility in select pain syndromes. Although its skeletal actions are well established, concerns remain regarding potential cardiovascular adverse effects, particularly in susceptible patients and with parenteral administration. A narrative literature review was conducted using databases including PubMed and Google Scholar to identify publications evaluating the cardiovascular effects of calcitonin therapy. Clinical trials, observational studies, mechanistic investigations, case reports, and pharmacovigilance data were reviewed to summarize reported cardiovascular complications and potential underlying mechanisms. Cardiovascular events associated with calcitonin therapy appear uncommon in clinical trials but have been reported in post-marketing surveillance and case reports. Documented manifestations include palpitations, arrhythmias, transient hypertension, chest discomfort, and peripheral edema. Proposed mechanisms include calcitonin-induced hypocalcemia, electrolyte disturbances such as hypokalemia, renal dysfunction, neuroendocrine activation, and altered vascular smooth muscle calcium signaling. Drug-drug interactions may further increase risk, particularly with medications sensitive to electrolyte shifts or those affecting cardiac conduction. Regulatory restrictions on certain formulations, especially intranasal calcitonin, reflect broader safety concerns, including potential malignancy signals. Calcitonin remains clinically useful for selected indications, including acute hypercalcemia and refractory Paget’s disease. However, clinicians should be aware of potential cardiovascular risks, particularly in older adults and patients with renal impairment, electrolyte abnormalities, or concomitant arrhythmogenic medications. Baseline electrocardiography, electrolyte assessment, early follow-up monitoring, and patient education may be considered to mitigate potential risks. Further prospective studies and pharmacovigilance data are needed to better define the incidence and mechanisms of cardiovascular complications associated with calcitonin therapy.