Hypercalcemia. Pathophysiological aspects

Title:

Hypercalcemia. Pathophysiological aspects

Creator:

Ivana Žofková

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:5ccfd22b-b956-4280-a559-08e4c7da1c79
uuid:5ccfd22b-b956-4280-a559-08e4c7da1c79
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, hyperkalcémie, hypercalcemia, primary hyperparathyroidism, malignancies, granulomatous diseases, familiar hypocalciuric hypercalcemia, MEN1, MEN2, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

The metabolic pathways that contribute to maintain serum calcium concentration in narrow physiological range include the bone remodeling process, intestinal absorption and renal tubule resorption. Dysbalance in t hese regulations may lead to hyper - or hypocalcemia. Hypercalcemia is a potentionally life -threatening and relatively common clinical problem, which is mostly associated with hyperparathyroidism and/or malignant diseases (90 %). Scarce causes of hypercalce mia involve renal failure, kidney transplantation, endocrinopathies, granulomatous diseases, and the long -term treatment with some pharmaceuticals (vitamin D, retinoic acid, lithium). Genetic causes of hypercalcemia involve familial hypocalciuric hypercalc emia associated with an inactivation mutation in the calcium sensing receptor gene and/or a mutation in the CYP24A1 gene. Furthermore, hypercalcemia accompanying primary hyperparathyroidism, which develops as part of multiple endocrine neoplasia (MEN1 and MEN2), is also genetically determined. In this review mechanisms of hypercalcemia are discussed. The objective of this article is a review of hypercalcemia obtained from a Medline bibliographic search., I. Žofková., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2016 Volume:65 | Number:1

Harvested from:

CDK

Metadata only:

false