2008Clinical Kidney JournalOpen access

Secondary Hyperparathyroidism Disease Stabilization Following Calcimimetic Therapy

João Frazão, Mariano Rodríguez

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Abstract

Standard therapy for secondary hyperparathyroidism (SHPT) includes dietary calcium supplementation, active vitamin D, and phosphate binders; however, these are often insufficient to allow patients to achieve their serum parathyroid hormone (PTH), calcium and calcium-phosphorus product (Ca × P) targets. Recent preclinical studies have demonstrated that treatment with type II calcimimetics that increase the sensitivity of the calcium-sensing receptor (CaR) to calcium can reverse the alterations in CaR and vitamin D receptor expression and parathyroid cell proliferation that are associated with SHPT. These data suggest that calcimimetic treatment could stabilize disease progression and improve maintenance of treatment goals. In clinical trials involving SHPT patients, the calcimimetic cinacalcet has been shown to decrease PTH, calcium, phosphorus and Ca × P. Significant improvements were seen regardless of initial disease severity, and benefits were maintained over the course of long-term therapy (up to 4 years), indicating effective disease stabilization. In conclusion, preclinical and clinical data provide both theoretical and empirical support for the use of calcimimetics in moderate and advanced SHPT to effectively stabilize disease.

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Standard therapy for secondary hyperparathyroidism (SHPT) includes dietary calcium supplementation, active vitamin D, and phosphate binders; however, these are often insufficient to allow patients to achieve their serum parathyroid hormone (PTH), calcium and calcium-phosphorus product (Ca × P) targets. Recent preclinical studies have demonstrated that treatment with type II calcimimetics that increase the sensitivity of the calcium-sensing receptor (CaR) to calcium can reverse the alterations in CaR and vitamin D receptor expression and parathyroid cell proliferation that are associated with SHPT. These data suggest that calcimimetic treatment could stabilize disease progression and improve maintenance of treatment goals. In clinical trials involving SHPT patients, the calcimimetic cinacalcet has been shown to decrease PTH, calcium, phosphorus and Ca × P. Significant improvements were seen regardless of initial disease severity, and benefits were maintained over the course of long-term therapy (up to 4 years), indicating effective disease stabilization. In conclusion, preclinical and clinical data provide both theoretical and empirical support for the use of calcimimetics in moderate and advanced SHPT to effectively stabilize disease.

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Available abstract

Standard therapy for secondary hyperparathyroidism (SHPT) includes dietary calcium supplementation, active vitamin D, and phosphate binders; however, these are often insufficient to allow patients to achieve their serum parathyroid hormone (PTH), calcium and calcium-phosphorus product (Ca × P) targets. Recent preclinical studies have demonstrated that treatment with type II calcimimetics that increase the sensitivity of the calcium-sensing receptor (CaR) to calcium can reverse the alterations in CaR and vitamin D receptor expression and parathyroid cell proliferation that are associated with SHPT. These data suggest that calcimimetic treatment could stabilize disease progression and improve maintenance of treatment goals. In clinical trials involving SHPT patients, the calcimimetic cinacalcet has been shown to decrease PTH, calcium, phosphorus and Ca × P. Significant improvements were seen regardless of initial disease severity, and benefits were maintained over the course of long-term therapy (up to 4 years), indicating effective disease stabilization. In conclusion, preclinical and clinical data provide both theoretical and empirical support for the use of calcimimetics in moderate and advanced SHPT to effectively stabilize disease.

Key concepts: Calcimimetic, Secondary hyperparathyroidism, Cinacalcet, Medicine, Vitamin D and neurology, Hyperparathyroidism, Parathyroid hormone, Calcitriol receptor

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