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Review Article
Mechanisms of Disease
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Volume 360:268-279 January 15, 2009 Number 3
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Endometriosis
Serdar E. Bulun, M.D.

Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Endometriosis is an estrogen-dependent inflammatory disease that affects 5 to 10% of women of reproductive age in the United States.1 Its defining feature is the presence of endometrium-like tissue in sites outside the uterine cavity, primarily on the pelvic peritoneum and ovaries. The main clinical features are chronic pelvic pain, pain during intercourse, and infertility.1 Endometriosis can be the result of diverse anatomical or biochemical aberrations of uterine function. For example, endometriosis commonly develops in young women with vaginal obstruction of outflow, possibly because of large quantities of backwashed menstrual tissue that has become implanted on pelvic organs.2 In contrast, . . . [Full Text of this Article]

Cellular Origins

Molecular Mechanisms

Estrogen Formation in Endometriosis

            Origins of Estrogen in Endometriosis

            Estrogen Production and Inflammation

            Prostaglandin E2 and Biosynthesis of Estradiol

Prostaglandin Production in Endometriosis

Progesterone Resistance in Endometriosis

Epigenetic Changes in Endometriosis

Conclusions


Source Information

From the Division of Reproductive Biology Research, Department of Obstetrics and Gynecology, Feinberg School of Medicine, Northwestern University, Chicago.

Address reprint requests to Dr. Bulun at the Division of Reproductive Biology Research, Dept. of Obstetrics and Gynecology, Feinberg School of Medicine, Northwestern University, 303 E. Superior St., Rm. 4-123, Chicago, IL 60611, or at s-bulun@northwestern.edu.


Related Letters:

Endometriosis
Colette S., Donnez J., Bulun S. E.
Extract | Full Text | PDF  
N Engl J Med 2009; 360:1911-1912, Apr 30, 2009. Correspondence

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