Review: New perspectives in the management of primary hyperparathyroidism

Abstract

Primary hyperparathyroidism (PHPT) is a biochemical syndrome caused by the inappropriate or unregulated overproduction of parathyroid hormone, leading to hypercalcaemia. It was previously considered a relatively rare disorder, with clinical manifestations dominated by renal and/or bone disease. However, in modern times the diagnosis is most frequently recognized coincidentally on biochemical testing in patients evaluated for unrelated complaints. Parathyroidectomy is the only curative treatment for PHPT, with improved outcomes in symptomatic patients following this procedure. However, surgical intervention in patients with no clear clinical features remains controversial. The National Institutes for Health (NIH) have developed consensus guidelines giving specific indications for when surgery is recommended in patients with asymptomatic PHPT. This article examines the impact of treatment on asymptomatic PHPT, focusing on bone disease, neurocognitive function, quality of life, cardiovascular disease and mortality. Medical treatment options, including bisphosphonates and cinacalcet, are also discussed.

Review: Endocrine and metabolic emergencies: hypercalcaemia

“…It is licensed in the US for THPT in the context of advanced CKD, parathyroid carcinoma and additionally PHPT deemed unsuitable for surgery in the UK. It reduces serum calcium levels significantly in most patients with PHPT, and in approximately two thirds of those with parathyroid carcinoma [Ayuk et al 2010;Marcocci et al 2009;Silverberg et al 2007]. The use of cinacalcet in the management of hypercalcaemic crisis has not yet, to the best of the authors' knowledge, been the subject of a RCT, but many case studies and reports demonstrate safety and effectiveness of its application in the context of refractory hyperparathyroid disease.…”

“…Myopathy is occasionally seen. Hypertension as a consequence of calciummediated vasoconstriction can occur in chronic disease [Ayuk et al 2010] but is less likely in the acute volume-contracted state. Bradyarrhythmias or heart block are frequently seen in severe hypercalcaemia, however, and relate to detrimental effects on the cardiac action potential as a consequence of increased extracellular calcium.…”

“…Cinacalcet, a calcimimetic which activates the CsR thereby reducing PTH secretion, is in current use [Ayuk et al 2010]. It is licensed in the US for THPT in the context of advanced CKD, parathyroid carcinoma and additionally PHPT deemed unsuitable for surgery in the UK.…”

“…A unique calcium receptor on the parathyroid cell membrane (extracellular calcium-sensing receptor [CsR]) responds rapidly to changes in plasma calcium levels [Ayuk et al 2010]. When the plasma calcium level is high, appropriate inhibition of PTH release should occur, whilst a decrease in plasma calcium prompts a rapid adaptive increase in PTH release.…”

Tumor Pardo Multifocal Como Manifestación Del Hiperparatiroidismo Primario Por Adenoma Paratiroideo Asociado a Carcinoma Papilar De Tiroides

“…Los principales efectos del hiperparatiroidismo se manifiestan a nivel del sistema renal y óseo 5 . Las manifestaciones esqueléticas son raras, sin embargo, es común la disminución de la densidad mineral de los huesos corticales 6 ; una rara complicación de presentación tardía es el Tumor Pardo que se caracteriza por un intenso proceso reactivo del tejido óseo secundario a la rápida acción osteoclástica de la hipercalcemia 7 , más raro aún es su asociación con un Carcinoma Papilar tiroideo que fue descrito en 1935 por Hellwig, quien notó la presencia de nódulos tiroideos en ratas que recibieron una dieta rica en calcio y pobre en yodo 8 ; más tarde, en 1954, Taylor reportó la capacidad bociógena del calcio en ratas y la posible relación de la hipercalcemia para el desarrollo de patología tiroidea maligna 9 .…”