[VEGF concentration in peritoneal fluid of patients with endometriosis]

E. Barcz, Ewa Barcz, Paweł Kamiński, P Kamiński, Kamiński P, L Marianowski, Marianowski L
Ginekologia polska · 2001 · vol. 72(5) , pp. 442–8 · PMID:11526791 · W2415610625
Other OA: closed CC0 ⤵ 8 in-corpus citations
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This study evaluated VEGF concentrations in peritoneal fluid from endometriosis patients and found no correlation with endometriosis severity, failing to support a role for VEGF in pathogenesis.

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Abstract

The theory of Sampson that endometrial cells and fragments desquamated during the menstrual period are transported through fallopian tubes into the peritoneal cavity where they implant, proliferate and develop into endometriotic lesions is generally accepted. There is increasing evidence that immunological mechanisms play a role in the pathogenesis and pathophysiology of endometriosis. Excessive endometrial angiogenesis is proposed as an important mechanism in the pathogenesis of endometriosis. Evidence is reviewed for the hypothesis that the endometrium of women with endometriosis has an increased capacity to proliferate, implant and grow in the peritoneal cavity. From the known angiogenic factors, vascular endothelial growth factor (VEGF) has emerged as a pivotally important regulator of normal angiogenesis and pathological neovascularization. In present study we evaluated the concentrations of VEGF in peritoneal fluid of patients with endometriosis and showed no correlation between AFS score and VEGF concentration in peritoneal and in ovarian endometriosis. Above results do not confirm former observations indicating the role of VEGF in endometriosis pathogenesis.

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Condition tags

endometriosis

MeSH descriptors

Ascitic Fluid Endometriosis Endothelial Growth Factors Lymphokines Pelvic Inflammatory Disease Adult Adult Ascitic Fluid Ascitic Fluid Endometriosis Endometriosis Endometriosis Endothelial Growth Factors Endothelial Growth Factors Female Female Humans Humans Laparoscopy Laparoscopy

Citation neighborhood (2-hop)

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

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