Vitamin D and Secondary Hyperparathyroid States.

Abstract

The interplay between vitamin D and parathyroid hormone (PTH) represents one of the most important metabolic mechanisms of regulation of the calcium/phosphorus homeostasis. Secondary hyperparathyroidism is therefore a major complication that arises as a result of reduced vitamin D levels, both as primary 25-hydroxy-vitamin D (25[OH]D) and/or 1,25-dihydroxyvitamin D (1,25[OH]2D) reduction. Different metabolic pathways are involved, as well as target organs and tissues, with several clinical complications. The skeleton is primarily involved, but many other extra-skeletal organs expressing the vitamin D and/or PTH receptors may theoretically be affected by vitamin D inadequacy and secondary hyperparathyroidism. Mechanisms associated with low vitamin D (mostly, but not exclusively 1,25[OH]2D deficiency) and high serum PTH also intensify chronic kidney disease (CKD), with further consequences on the mineral metabolism system and development of skeletal and cardiovascular disease. Therapeutic intervention is primarily aimed at enhancing serum 25(OH)D levels and reducing secondary hyperparathyroidism, by employing different strategies and endpoints according to the clinical contest. This chapter reviews the current knowledge on the metabolic pathways involved in the vitamin D/PTH axis regulation in different clinical settings and gives an update on the recommended treatment strategies.