Obstetrics & Gynecology Track the topics, authors and articles important to you
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Obstetrics & Gynecology 2006;108:162-168
© 2006 by The American College of Obstetricians and Gynecologists
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bedaiwy, M. A.
Right arrow Articles by Casper, R. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bedaiwy, M. A.
Right arrow Articles by Casper, R. F.
Related Collections
Right arrow General gynecology

ORIGINAL RESEARCH

Genetic Polymorphism in the Fibrinolytic System and Endometriosis

Mohamed A. Bedaiwy, MD1,2, Tommaso Falcone, MD2, Edward J. Mascha, PhD3 and Robert F. Casper, MD1

From the 1Division of Reproductive Sciences, Department of Obstetrics and Gynecology, University of Toronto, and the Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada; and 2Department of Obstetrics and Gynecology and 3Department of Quantitative Health Sciences, Cleveland Clinic Foundation, Cleveland, Ohio.

OBJECTIVE: Although most women experience retrograde menses during their reproductive life, endometriosis develops only in a small percentage. We hypothesized that persistence of a fibrin matrix in peritoneal pockets, as a result of hypofibrinolysis, could allow menstrually deposited endometrial fragments to initiate endometriosis. Fibrinolysis is modulated by several factors, and polymorphisms in the plasminogen activator inhibitor-1 (PAI-1) gene are considered to be one of the important determinants. The objective of this study was to evaluate PAI-1 genotypes in a group of women with or without endometriosis.

METHODS: In 118 women (75 with laparoscopically confirmed endometriosis and 43 controls), genomic DNA was extracted from blood and the PAI-1 promoter genotype was determined by polymerase chain reaction amplification of DNA using specific primers for the 4G or 5G allele followed by gel electrophoresis. A portion of the polymerase chain reaction product was purified and sequenced to confirm the gel electrophoresis results.

RESULTS: Endometriosis was more likely in patients with 4G/5G (odds ratio 38; 95% confidence interval [CI] 6–229) or 4G/4G (odds ratio 441; 95% CI 53–3,694) compared with 5G/5G PAI-1 genotype. Fifty-two of 75 women with endometriosis (69 %, 95% CI 58–79%) had the 4G/4G genotype compared with only 5 of 43 (12%; 95% CI 4–25%) controls. In contrast, the 5G/5G genotype associated with normal fibrinolysis was found in 2 of 75 (3%; 95% CI 0–9%) women with endometriosis compared with 24 of 43 (56%; 95% CI 40–71%) controls.

CONCLUSION: Hypofibrinolysis, associated with the 4G allele of the PAI-1 gene, was found significantly more often in women with endometriosis compared with controls. Persistence of fibrin matrix could support the initiation of endometriotic lesions in the peritoneal cavity, explaining why some women with retrograde menstruation develop endometriosis while others do not.

LEVEL OF EVIDENCE: II-2






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2006 by the American College of Obstetricians and Gynecologists.