Tratamiento odontológico en pacientes con patología hormonal paratiroid / Dental treatment in patients with hormonal pathology paratiroidea

Las glándulas paratiroides son glándulas endocrinas que se encuentran situadas en la parte anterior del cuello, rodeando a la tráquea y a la laringe. Secretan hormonas que van a desempeñar funciones esenciales para el desarrollo del organismo. La alteración en la secreción de dichas hormonas va a producir patologías de cierta importancia que deberán tenerse en cuenta a la hora de realizar los tratamientos odontológicos. Antes de realizar cualquier actuación terapéutica en odontología, se debe valorar el control de las diferentes patologías y, en el caso de que estén bien controladas, se tendrán en cuenta una serie de consideraciones para evitar complicaciones derivadas de las mismas (AU)

The parathyroid glands are endocrine glands that are located in the anterior part of the neck, surrounding the trachea and the larynx. They secrete hormones that are going to have essential functions for the development of the organism. The alteration in the secretion of hormones to produce pathologies of a certain importance that can be taken into account when performing dental treatments. Before carrying out any action, in dentistry, the control of the different pathologies must be assessed and, if they are well controlled, a series of considerations must be taken into account to avoid derivatives of them (AU)

Deleción en el gen STX16 asociada a pseudohipoparatiroidismo / STX16 deletion associated to pseudohypoparathyroidism

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Calcimimetic NPS R-568 prevents parathyroid hyperplasia in rats with severe secondary hyperparathyroidism.

UNLABELLED: Calcimimetic NPS R-568 prevents parathyroid hyperplasia in rats with severe secondary hyperparathyroidism. BACKGROUND: Secondary hyperparathyroidism (secondary HPT) in chronic renal insufficiency (CRI) is characterized by multiglandular hyperplasia. METHODS: In this study, we investigated the effects of the calcimimetic NPS R-568 on the parathyroid gland in rats with CRI induced by ligation of the renal arteries and severe secondary HPT induced by dietary phosphorus loading. Six days after surgery, high-phosphorus diet feeding was started, and NPS R-568 was administered to the rats for 56 days either by daily gavage (30 or 100 micromol/kg) or by continuous subcutaneous infusion (20 micromol/kg. day). RESULTS: After 54 days, serum PTH levels in vehicle-treated CRI rats were 1019 vs. 104 pg/mL in sham-operated controls. Infusion of NPS R-568 maintained serum PTH at levels comparable with those of sham-operated controls, whereas daily gavage also prevented much of the increase in CRI controls and decreased PTH levels intermittently in a dose-dependent fashion. Parathyroid gland enlargement was caused predominantly by hyperplasia. Total cell number per kg body wt was 3.5-fold higher in vehicle-treated CRI rats than in sham-operated controls. Both infusion and high-dose gavage of NPS R-568 completely prevented the increase in parathyroid cell number. CONCLUSION: These results demonstrate that the calcimimetic compound NPS R-568 can prevent both the increase in serum PTH levels and parathyroid hyperplasia in rats with CRI and severe secondary HPT. Moreover, these changes occurred despite decreases in serum 1, 25(OH)2D3 and increases in serum phosphate, suggesting a dominant role for the calcium receptor in regulating parathyroid cell proliferation.