[How to slow down parathyroid hormone (PTH) secretion without the risk of inducing an adynamic bone disease].

Medical treatment for secondary hyperparathyroidism (HPTH-II) consists in correcting: hypocalcemia by providing a supply of calcium salts, vitamin D or its derivatives; hyperphosphatemia by a suitable diet and by using gastrointestinal phosphate-binders; metabolic acidosis by providing sodium bicarbonate. Very recently, this treatment armamentarium was expanded by the advent of a new therapeutic agent called a calcimimetic (cinacalcet HCL). Cinacalcet increases the calcium sensitivity of the calcium receptor (CaR) of parathyroid cells and thereby induces a rapid and sustained decrease in PTH secretion. When treatment with medical inhibitors proves to be ineffective or involves risks due to an increase in the calcium-phosphorus ion product and the occurrence or worsening of cardiovascular calcifications, it is then necessary to resort to surgical reduction of PTH production by surgical parathyroidectomy (PTX). The very high efficacy of medical inhibitory treatment of HPTH-II logically poses the problem of excessive inhibition of the secretion of PTH and its corollary, the increased risk of adynamic osteopathy. The primary purpose of this article is to provide the reader with an updated review of these problems consisting, on the one hand, of inhibiting PTH secretion and, on the other, of maintaining a sufficient level of bone remodeling to prevent any possible repercussions on other organs.