The history of parathyroid hormone (PTH) replacement therapy for hypoparathyroidism begins in 1929. In 2015, the Food and Drug Administration approved recombinant human PTH(1-84) [rhPTH(1-84)] as a treatment for hypoparathyroidism. Long-term studies of rhPTH(1-84), up to 6 years, have demonstrated continued efficacy of this replacement agent. Approaches to optimize PTH treatment in hypoparathyroidism include subcutaneous pump delivery systems, long-lived carrier molecules, and long-acting PTH analogues that show promise to prolong efficacy. Calcilytic compounds have been explored as a treatment for autosomal dominant hypocalcemia. Calcilytics are negative modulators of the calcium-sensing receptor and may present a therapeutic opportunity to increase endogenous PTH synthesis and secretion.

New Directions in Treatment of Hypoparathyroidism

Tabacco, Gaia;
2018-01-01

Abstract

The history of parathyroid hormone (PTH) replacement therapy for hypoparathyroidism begins in 1929. In 2015, the Food and Drug Administration approved recombinant human PTH(1-84) [rhPTH(1-84)] as a treatment for hypoparathyroidism. Long-term studies of rhPTH(1-84), up to 6 years, have demonstrated continued efficacy of this replacement agent. Approaches to optimize PTH treatment in hypoparathyroidism include subcutaneous pump delivery systems, long-lived carrier molecules, and long-acting PTH analogues that show promise to prolong efficacy. Calcilytic compounds have been explored as a treatment for autosomal dominant hypocalcemia. Calcilytics are negative modulators of the calcium-sensing receptor and may present a therapeutic opportunity to increase endogenous PTH synthesis and secretion.
2018
Bone mineral density; Bone turnover markers; Hypoparathyroidism; PTH (1–34); Treatment; Urinary calcium excretion; rhPTH (1–84)
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.12610/74230
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