Dissemin is shutting down on January 1st, 2025

Published in

Oxford University Press (OUP), The Journal of Clinical Endocrinology & Metabolism, p. jc.2015-3909

DOI: 10.1210/jc.2015-3909

Links

Tools

Export citation

Search in Google Scholar

Presentation of Hypoparathyroidism: Etiologies and Clinical Features

This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

Full text: Download

Green circle
Preprint: archiving allowed
Green circle
Postprint: archiving allowed
Red circle
Published version: archiving forbidden
Data provided by SHERPA/RoMEO

Abstract

Context: Understanding the etiology, diagnosis, and symptoms of hypoparathyroidism may help to improve quality of life and long-term disease outcomes. This paper summarizes the results of the findings and recommendations of the Working Group on Presentation of Hypoparathyroidism. Evidence Acquisition: Expertsconvenedin Florence, Italy, inMay2015andevaluated the literatureand recent data on the presentation and long-term outcomes of patients with hypoparathyroidism. Evidence Synthesis: The most frequent etiology is surgical removal or loss of viability of parathyroid glands. Despite precautions and expertise, about 20-30% of patients develop transient and 1-7% developpermanentpostsurgicalhypoparathyroidismafter totalthyroidectomy.Autoimmunedestruction is the main reason for nonsurgical hypoparathyroidism. Severe magnesium deficiency is an uncommon but correctable cause of hypoparathyroidism. Several genetic etiologies can result in the loss of parathyroid function or action causing isolated hypoparathyroidism or a complex syndrome with other symptoms apart from those of hypoparathyroidism or pseudohypoparathyroidism. Neuromuscular signs or symptoms due to hypocalcemia are the main characteristics of the disease. Hyperphosphatemia can contribute to major long-term complications such as ectopic calcifications in the kidney, brain, eye, or vasculature. Bone turnover is decreased, and bone mass is increased. Reduced quality of life and higher risk of renal stones, renal calcifications, and renal failure are seen. The risk of seizures and silent or symptomatic calcifications of basal ganglia is also increased. Conclusions: Increased awareness of the etiologyandpresentation of the diseaseandnewresearch efforts addressing specific questions formulated during the meeting should improve the diagnosis, care, and long-term outcome for patients.