Endometrial antibodies in serum and peritoneal fluid of infertile patients with and without endometriosis

Badawy, Shawky Z.A.; Cuenca, Violeta; Freliech, Heidi; Stefanu, C

doi:10.1016/s0015-0282(16)53534-1

Cited by 84 publications

(53 citation statements)

References 5 publications

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“…Our study concurred that the PF of women with endometriosis contains higher levels of components C3 and C4 (17)(18)(19). Because C3 plays an important role in the classic, alternative, and lectin pathways of the complement cascade and thus in inflammation, the higher secretion of this component may be relevant to the pathophysiology of endometriosis (20).…”

Section: Discussionsupporting

confidence: 90%

Levels of complement components iC3b, C3c, C4, and SC5b-9 in peritoneal fluid and serum of infertile women with endometriosis

Kabut

Kondera-Anasz

Sikora

et al. 2007

Fertility and Sterility

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Section: Discussionsupporting

confidence: 90%

Levels of complement components iC3b, C3c, C4, and SC5b-9 in peritoneal fluid and serum of infertile women with endometriosis

Kabut

Kondera-Anasz

Sikora

et al. 2007

Fertility and Sterility

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“…We, and others, however, have recently demonstrated markedly high levels of aromatase P450 mRNA and activity in pelvic endometriotic implants (Noble et al 1996, 1997, Kitawaki et al 1997. Moreover, prostaglandin (PG)E 2 , which is produced in very high levels in endometriotic tissues, was found to be the most potent inducer of aromatase activity in endometriosisderived stromal cells (Badawy et al 1984, De Leon et al 1988, Karck et al 1996, Noble et al 1996, 1997. The production of PGE 2 in eutopic endometrial stromal cells, in turn, was demonstrated to be greatly stimulated by cytokines and estradiol-17β via enhancement of cyclooxygenase-2 (COX-2) expression (Ishihara et al1995, Kennard et al 1995, Huang et al 1996.…”

Section: Introductionmentioning

confidence: 89%

Estrogen production in endometriosis and use of aromatase inhibitors to treat endometriosis.

Bulun

Zeitoun

Takayama

et al. 1999

Endocrine-Related Cancer

113

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Estrogen is the most important known factor that stimulates the growth of endometriosis. Estrogen delivery to endometriotic implants was classically viewed to be only via the circulating blood in an endocrine fashion. We recently uncovered an autocrine positive feedback mechanism, which favored the continuous production of estrogen and prostaglandin (PG)E 2 in the endometriotic stromal cells. The enzyme, aromatase, is aberrantly expressed in endometriotic stromal cells and catalyzes the conversion of C 19 steroids to estrogens, which then stimulate cyclooxygenase-2 to increase the levels of PGE 2 . PGE 2 , in turn, is a potent inducer of aromatase activity in endometriotic stromal cells. Aromatase is not expressed in the eutopic endometrium. Aromatase expression in endometriosis and its inhibition in eutopic endometrium are controlled by the competitive binding of a stimulatory transcription factor, steroidogenic factor-1, and an inhibitory factor, chicken ovalbumin upstream promotertranscription factor to a regulatory element in the aromatase P450 gene promoter. In addition, we find that endometriotic tissue is deficient in 17β-hydroxysteroid dehydrogenase type 2, which is normally expressed in eutopic endometrial glandular cells and inactivates estradiol-17β to estrone. This deficiency is another aberration that favors higher levels of estradiol-17β in endometriotic tissues in comparison with the eutopic endometrium. The clinical relevance of local aromatase expression in endometriosis was exemplified by the successful treatment of an unusually aggressive form of recur- Endocrine-Related Cancer (1999) 6 293-301 rent endometriosis in a postmenopausal woman using an aromatase inhibitor.

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“…Approximately 30-50% of peritoneal fluid cells are lymphocytes (Oosterlynck et al, 1992) and their total number is higher in women with endometriosis (Badawy et al, 1984).…”

Section: Lymphocytesmentioning

confidence: 99%

Peritoneal environment, cytokines and angiogenesis in the pathophysiology of endometriosis

Gazvani¹,

Templeton²

2002

Reproduction

331

195

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Endometriosis, defined by the presence of viable endometrial tissue outside the uterine cavity, is a common condition affecting 2-3% of women of reproductive age. Today, a composite theory of retrograde menstruation with implantation of endometrial fragments in conjunction with peritoneal factors to stimulate cell growth is the most widely accepted explanation. There is substantial evidence that immunological factors and angiogenesis play a decisive role in the pathogenesis of endometriosis. In women with endometriosis, there appears to be an alteration in the function of peritoneal macrophages, natural killer cells and lymphocytes. Furthermore, growth factors and inflammatory mediators in the peritoneal fluid, produced mainly by peritoneal macrophages, are altered in endometriosis, indicating a role for these immune cells and mediators in the pathogenesis of this disease.

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Endometrial antibodies in serum and peritoneal fluid of infertile patients with and without endometriosis

Cited by 84 publications

References 5 publications

Levels of complement components iC3b, C3c, C4, and SC5b-9 in peritoneal fluid and serum of infertile women with endometriosis

Levels of complement components iC3b, C3c, C4, and SC5b-9 in peritoneal fluid and serum of infertile women with endometriosis

Estrogen production in endometriosis and use of aromatase inhibitors to treat endometriosis.

Peritoneal environment, cytokines and angiogenesis in the pathophysiology of endometriosis

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