Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2009-7-24
pubmed:abstractText
Primary hyperparathyroidism (PHPT) is one of the most frequent endocrinological disorders. In PHPT, there is abnormal regulation of parathyroid hormone (PTH) by calcium, which translates into inappropriately high PTH secretion for the level of calcemia. Most patients with PHPT have increased serum PTH levels, with increases in serum calcium, especially ionic calcium. The incidence of PHPT rises with age, the mean age at diagnosis being 55 years. This disorder affects mainly women with a female-to-male ratio of approximately 3:1. Most (80-85%) of cases are produced by chief cell parathyroid adenomas. The factors involved in the genesis of PHPT are largely unknown. Gene mutations affecting oncogenes (cyclin D1, RET) or tumor suppressor genes (MEN1, HRPT2) are found in a minority of cases. These mutations are especially important in familial forms of PHPT, such as multiple endocrine neoplasia syndrome (MEN1, MEN2A). No mutations affecting the calcium-sensing receptor (CaSR) or vitamin D receptor (VDR) gene have been found. In parathyroid adenomas and hyperplasias, there may be abnormal Wnt signalling, with mutations of the coreceptor LRP5 gene and beta-catenin accumulation. Expression of the Klotho protein, which intervenes in serum calcium regulation, is reduced. Low levels of 25(OH) vitamin D frequently coexist, although whether vitamin D deficiency plays a pathogenic role in PHPT is unknown.
pubmed:language
spa
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1579-2021
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
56 Suppl 1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2-7
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
[Concept, etiology and epidemiology of primary hyperparathyroidism].
pubmed:affiliation
Servicio de Endocrinología y Nutrición, Hospital Universitario 12 de Octubre, Madrid, España. gmdiazguerra@gmail.com
pubmed:publicationType
Journal Article, English Abstract