Linked Life Data

12582474

Source:http://linkedlifedata.com/resource/pubmed/id/12582474

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2003-2-12
pubmed:abstractText
The development of human benign prostatic hyperplasia and its related signs and symptoms clearly requires a combination of testicular androgens and aging. Although the role of androgens as a causative factor for human benign prostatic hyperplasia is debated, they undoubtedly play at least a permissive role. The principle prostatic androgen is dihydrotestosterone. Two isoenzymes of 5-alpha reductase have been discovered. Type 2 is dominant in the genital issue. Testosterone is reduced by the 5-a reductase to dihydrotestosterone. Benign prostatic hyperplasia is predominantly due to stromal hyperplasia of the gland and affects more than 70% of men of 70 years or older with or without obstruction. Recent studies identified transforming growth factor-b, fibroblast growth factor and insulin-like growth factor family members as key regulators of cell proliferation and extracellular matrix turnover with interrelated activities. Furthermore, estrogens, andenergic signaling and inflammatory processes have been shown to have an impact. Without a solid understanding of the physiology and pathophysiology of benign prostatic hyperplasia it can be difficult to interpret the results of clinical trials and symptoms.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1699-3993
pubmed:author
pubmed:copyrightInfo
(c) 2002 Prous Science. All rights reserved.
pubmed:issnType
Print
pubmed:volume
38
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
867-76
pubmed:dateRevised
2006-10-26
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
The pathophysiology of benign prostatic hyperplasia.
pubmed:affiliation
Department of Urology, University Hospital of Vienna, Vienna, Austria. bdjavan@hotmail.com
pubmed:publicationType
Journal Article, Review