Title:Hyperparathyroidism and Peripheral Arterial Disease
Volume: 22
Issue: 2
Author(s): Pier Luigi Antignani*, Mateja K Jezovnik, Ales Blinc, Dimitri P. Mikhailidis, Panagiotis Anagnostis, Gerit-Holger Schernthaner, Mojca Jensterle, Katica Bajuk Studen, Miso Sabovic and Pavel Poredos
Affiliation:
- Vascular Centre Nuova Villa Claudia, Rome, Italy
Keywords:
Parathyroid hormone, chronic hypercalcaemia, vascular calcifications, peripheral arterial disease, parathyroidectomy, hyperparathyroidism.
Abstract:
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.
