Parathyroid
tumors are almost invariably associated with
parathormone (PTH) hypersecretion resulting in primary (PHPT) or secondary (SHPT)
hyperparathyroidism. PHPT is the third most common endocrine disorder with a prevalence of 1-2% in post-menopausal women; SHPT is a major complication of
chronic kidney failure, the prevalence of which is increasing. The calciumsensing receptor (CASR) is the key molecule regulating PTH synthesis and release from the parathyroid cells in response to changes in extracellular
calcium concentrations. A potent calcimimetic,
cinacalcet, has been developed in the last ten years and made available for medical treatment of both PHPT and SHPT.
Cinacalcet has been demonstrated to be effective in inhibiting PTH secretion, though the drug fails to normalize PTH release, both in PHPT and SHPT patients with different degrees of disease severity, including patients with
parathyroid carcinomas and with MEN1-related parathyroid
tumors. Here we reviewed the molecular aspects of CASR target
therapy and the effect of the CASR gene single nucleotide polymorphisms. Clinical data concerning the efficacy and safety of
cinacalcet in controlling
hyperparathyroidism are reported, focusing on the treatment of the different types of parathyroid
tumors. Finally, limits of this target
therapy are analyzed, pointing out the lack of efficacy in improving kidney and bone morbidities in PHPT and
cardiovascular diseases in SHPT. Though
cinacalcet is a target therapeutic option for parathyroid
tumors, further approaches are warranted to fully control these metabolic disorders and the underlying
tumors.