Secondary hyperparathyroidism

PTH functions to maintain calcium homeostasis by acting on the renal tubules, on calcium stores in the skeletal system, and indirectly on the GI tract through activation of vitamin D and enteral absorption. Hypocalcemia will elevate PTH levels and can serve as a cause of secondary hyperparathyroidism.

Classically, this condition is caused by chronic kidney disease, intestinal malabsorption, or chronic inadequate sunlight exposure, which gives rise to characteristic alterations in vitamin D, phosphorus, and calcium.

Inadequate vitamin D stores are common among older patients, particularly those who always use sunblock or are housebound, institutionalized, or hospitalized.

Management includes appropriate treatment of the underlying cause and vitamin D supplementation. Parathyroidectomy is infrequently required to remove irreversibly enlarged parathyroid glands in an effort to restore normal parathyroid physiology.

Untreated, it can result in significant skeletal and cardiovascular complications, which contribute to overall morbidity and mortality.

Any disorder that results in hypocalcemia will elevate parathyroid hormone levels and can serve as a cause of secondary hyperparathyroidism. The most frequent causes of the condition are chronic kidney disease (CKD), malabsorption syndromes, and chronic inadequate sunlight exposure, acting via alterations in vitamin D, phosphorus, and calcium. CKD results in decreased levels of 1,25-dihydroxyvitamin D, hyperphosphatemia, and hypocalcemia. CKD-related mineral bone disorder is a systemic disorder of mineral and bone metabolism caused by CKD. It manifests itself by either one or a combination of the following: abnormalities of calcium, phosphorus, parathyroid hormone (PTH), or vitamin D metabolism; abnormalities in bone turnover, mineralization, volume, linear growth, or strength; vascular or other soft tissue calcification.[1]Moe S, Drüeke T, Cunningham J, et al; Kidney Disease: Improving Global Outcomes (KDIGO). Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int. 2006 Jun;69(11):1945-53. http://www.sciencedirect.com/science/article/pii/S0085253815514154 http://www.ncbi.nlm.nih.gov/pubmed/16641930?tool=bestpractice.com