Hyperparathyroidism and Peripheral Arterial Disease

• Published in: Current vascular pharmacology
• Main Authors: Antignani, Pier Luigi, K Jezovnik, Mateja, Blinc, Ales, P Mikhailidis, Dimitri, Anagnostis, Panagiotis, Schernthaner, Gerit Holger, Jensterle, Mojca, Studen, Katica Bajuk, Sabovic, Miso, Poredos, Pavel
• Format: Journal Article
• Language: English
• Published: United Arab Emirates 01.01.2024
• Subjects: atherosclerosis; parathyroid hormone; vascular calcifications; chronic hypercalcaemia; parathyroidectomy
• ISSN: 1875-6212
• DOI: 10.2174/0115701611280905231227045826

Primary hyperparathyroidism (PHPT) is presented in various forms, including classic PHPT, characterised by increased parathyroid hormone (PTH) secretion, normohormonal PHPT, and normocalcaemic PHPT. Secondary hyperparathyroidism is characterised by increased PTH secretion triggered by factors such as vitamin D deficiency and kidney failure. This review aims to discuss the involvement of hyperparathyroidism (HPT) in atherosclerosis, including peripheral arterial disease (PAD). The increased level of PTH is involved in developing subclinical and overt vascular diseases, encompassing endothelial dysfunction, vascular stiffness, hypertension, and coronary and peripheral arterial diseases. It has been consistently associated with an augmented risk of cardiovascular morbidity and mortality, independent of classical risk factors for atherosclerosis. Chronic hypercalcemia associated with increased levels of PTH contributes to the development of calcification of vessel walls and atherosclerotic plaques. Vascular calcification can occur in the intima or media of the arterial wall and is associated with stiffness of peripheral arteries, which the formation of atherosclerotic plaques and narrowing of the vessel lumen can follow. For treating hyperparathyroidism, particularly SHPT, calcimimetics, novel phosphorus binders and novel vitamin D receptor activators are used. However, they are ineffective in severe PHPT. Therefore, parathyroidectomy remains the primary therapeutic option of PHPT.