Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2012 Mar;37(1):75-92.

Anomalies in the inflammatory response in endometriosis and possible consequences: a review

Affiliations
  • PMID: 22382616
Review

Anomalies in the inflammatory response in endometriosis and possible consequences: a review

K Khoufache et al. Minerva Endocrinol. 2012 Mar.

Abstract

Defined by the presence of endometrial-like cells outside the uterus, endometriosis is one of the most diagnosed gynecological disorders, affecting 5 to 10 % of reproductive age women, but the true incidence is unknown. Endometriosis is a major cause of pelvic pain, dysmenorrhea, dyspareunia, infertility and menstrual irregularities, but there is no clear correlation between the symptoms and the extent of the disease. Despite decades of intensive investigations, little is known about the pathogenesis of endometriosis. The disease is often associated with chronic pelvic inflammation. Abnormal levels of immune cells such macrophages, dendritic and natural killer cells were found in the peritoneal cavity of patients. However these cells seem to be unable to detect and eliminate ectopic endometrial cells. Several studies showed that peritoneal immune cells are dysfunctional and may rather contribute to endometriosis development. A review of relevant clinical and scientific studies was carried out. This review sheds light on cellular and immunological pro-inflammatory changes which were observed in patients with endometriosis, their impact on angiogenesis, apoptosis, extracellular matrix remodeling and hormonal production and consequences on fertility.

PubMed Disclaimer

Similar articles

Cited by

Publication types

MeSH terms

LinkOut - more resources