The clinical consequences of secondary hyperparathyroidism: focus on clinical outcomes.
Secondary hyperparathyroidism (SHPT) is a common occurrence in patients with chronic renal failure and is characterized by excessive serum parathyroid hormone ( PTH) levels, parathyroid hyperplasia and imbalances in calcium and phosphorus metabolism. PTH acts as a uraemic toxin and it may be responsible for the following long-term consequences: renal osteodystrophy; non-skeletal abnormalities, including severe vascular and heart valve calcification; alterations in cardiovascular structure and function; immune dysfunction; and renal anaemia. The risk of developing SHPT is not the same for all uraemic patients. Black patients appear to have a higher risk of developing SHPT than Caucasian patients, and patients with diabetes have a lower risk than non-diabetic patients. Current treatments include dietary phosphate restriction, oral phosphate binders, vitamin D and its analogues, and, in severe cases, parathyroidectomy. These treatments do not provide optimal treatment for many patients, and compounds that directly inhibit PTH secretion may prove a major step forward in the treatment of SHPT.[1]References
- The clinical consequences of secondary hyperparathyroidism: focus on clinical outcomes. Hörl, W.H. Nephrol. Dial. Transplant. (2004) [Pubmed]
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