2008, Number 09
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Ginecol Obstet Mex 2008; 76 (09)
Endometriosis: physiopathology and investigation lines (part two)
Ayala YR, Mota GM
Language: Spanish
References: 33
Page: 549-557
PDF size: 277.66 Kb.
ABSTRACT
Sampson’s menstrual reflux theory (1927) is widely accepted as an explanation of endometriosis physiopathology, it proposes five basic necessary processes to its development: adhesion, invasion, recruitment, angiogenesis and proliferation. Several factors and physiologic processes are necessary for the survival and growth of endometrial tissue. Clinical manifestations of these disease are: dysmenorrhoea, dyspareunia, and peritoneal adhesions, that with other findings reveal an inflammatory process that requires cytokines, macrophages, NK cells, lymphocytes and prostaglandins whose qualitative functions may be compromised or may contribute to the peripheral generation of estrogens. Angiogenesis benefits the development of these endometrial tissue foci and probably stimulates several vascular growth factors, and sexual steroids. Endocrine factors are capital for this entity, as is demonstrated by the presence of estrogen receptors in macrophages, fibroblasts and endometrium among others, as well as the clinical symptoms control trough the blockage of the hypothalamus-pituitaryovary axis. Studies on the genetic and antioxidant factors have revealed key points that may be helpful in determining a proper diagnosis and treatment for endometriosis.
REFERENCES
Seli E, Berkkanoglu M, Arici A. Pathogenesis of endometriosis. Obstet Gynecol Clin N Am 2003;30:41-61.
Matarese G, De Placido G, Nikas Y, Alviggi C. Pathogenesis of endometriosis: natural immunity dysfunction or autoimmune disease? Trends Mol Med 2003;9:223-8.
Koninckx PR, Kennedy SH, Barlow DH. Endometriotic disease: the role of peritoneal fluid. Hum Reprod Update 1998;4:741-51.
Lebovic DI, Mueller MD, Taylor RN. Immunobiology of endometriosis. Fertil Steril 2001;75:1-10.
Kim JG, Keshava C, Murphy AA, Pitas RE, Parthasarathy S. Fresh mouse peritoneal macrophages have low scavenger receptor activity. J Lipid Res 1997;38:2207-15.
Surrey ES, Halme J. Effect of peritoneal fluid from endometriosis patients on endometrial estromal cell proliferation in vitro. Obstet Gynecol 1990;76:792-7.
Capellino S, Montagna P, Villaggio B, Sulli A, et al. Role of estrogens in inflammatory response: expression of estrogen receptors in peritoneal fluid macrophages from endometriosis. Ann N Y Acad Sci 2006;1069:263-7.
Dmowski WP, Steele RW, Baker GF. Deficient cellular immunity in endometriosis. Am J Obstet Gynecol 1981;141:377-83.
Prefumo F, Semino C, Melioli G, Venturini PL. A defective expression of ICAM-1 (CD-54) on secretory endometrial cells is associated with endometriosis. Immunol Lett 2002;80:49-53.
Arici A, Matalliotakis I, Goumenou A, Koumantakis G, et al. Altered expression of interleukin-18 in the peritoneal fluid of women with endometriosis. Fertil Steril 2003;80:889-94.
Karck U, Reister F, Schafer W, Zahradnik HP, Bredwoldt M. PGE2 and PGF2 alpha release by human peritoneal macrophages in endometriosis. Prostaglandins 1996;51:49-60.
Ota H, Igarashi S, Sasaki M, Tanaka T. Distribution of cyclooxigenase-2 in eutopic and ectopic endometrium in endometriosis and adenomyosis. Hum Reprod 2001;16:561-6.
Jabbour HN, Sales KJ, Smith OP, Battersby S, Boddy SC. Prostaglandin receptors are mediators of vascular function in the endometrial pathologies. Mol Cell Endocrinol 2006;252:191-200.
Ma W, Tan J, Matsumoto H, Robert B, et al. Adult tissue angiogenesis: evidence for negative regulation by estrogen in the uterus. Mol Endocrinol 2001;15:1983-92.
Nikitenko LL, MacKenzie IZ, Rees MC, Bicknell R. Adrenomedullin is an autocrine regulator of endothelial growth in human endometrium. Mol Hum Reprod 2000;6:811-9.
Risau W. Mechanisms of angiogenesis. Nature 1997;386:671-4.
Hornung D, Lebovic DI, Shifren JL, Vigne JL, Taylor RN. Vectorial secretion of vascular endothelial growth factor by polarized human endometrial epithelial cells. Fertil Steril 1998;69:909-15.
Girling JE, Rogers PA. Recent advances in endometrial angiogenesis research. Angiogenesis 2005;8:89-99.
Capellino S, Montagna P, Villaggio B, Sulli A, et al. Role of estrogens in inflammatory response: expression of estrogen receptors in peritoneal fluid macrophages from endometriosis. Ann NY Acad Sci 2006;1069:263-7.
Noble LS, Takayama K, Zeitoun KM, Putman JM, et al. Prostaglandin E2 stimulates aromatase expression in endometriosis-derived stromal cells. J Clin Endocrinol Metab 1997;82:600-6.
Zeitoun KM, Bulun SE. Aromatase: a key molecule in the pathophysiology of endometriosis and a therapeutic target. Fertil Steril 1999;72:961-9.
Zeitoun K, Takayama K, Sasano H, Suzuki T, et al. Deficient 17beta-hydroxysteroid dehydrogenase type 2 expression in endometriosis: failure to metabolize 17beta-estradiol. J Clin Endocrinol Metab 1998;83:4474-80.
Crosignani P, Olive D, Bergqvist A, Luciano A. Advances in the management of endometriosis: an update for clinicians. Hum Reprod Update 2006;12:179-89.
Mote PA, Balliene RL, McGowan EM, Clarke CL. Colocalization of progesterone receptors A and B by dual immunofluorescent histochemistry in human endometrium during the menstrual cycle. J Clin Endocrinol Metab 1999;84:2963-71.
Bruner-Tran KL, Zhang Z, Eisenberg E, Winneker RC, Osteen KG. Down regulation of endometrial matrix metalloproteinase-3 and -7 expression in vitro and therapeutic regression of experimental endometriosis in vivo by a novel progesterone receptor agonist, tanaproget. J Clin Endocrinol Metab 2006;91:1555-60.
Morimoto C, Osuga Y, Yano T, Takemura Y, et al. GnRH II as a possible cytostatic regulator in the development of endometriosis. Hum Reprod 2005;3212-8.
Arvantis DA, Koumantakis GE, Goumenou AG, Matalliotakis IM, et al. CYP1A1, CYP19, GSTM1 polymorphisms increase the risk of endometriosis. Fertil Steril 2003;79:702-9.
Goumenou AG, Matalliotakis IM, Tzardi M, Fragouli IG, et al. p16, retinoblastoma (pRb), and cyclin D1 protein expression in human endometriotic and adenomyotic lesions. Fertil Steril 2006;85:1204-7.
Zervou S, Karteris E, Goumenou AG, Vatish M, et al. The Glu298→Asp polymorphism of the endothelial nitric oxide synthetase gene is associated with endometriosis. Fertil Steril 2003;80:1524-5.
Agarwal A, Gupta S, Sharma RK. Role of oxidative stress in female reproduction. 2005;14:28.
Leyendecker G, Kunz G, Wildt L, Beil D, Deininger H. Uterine hyperperistalsis and dysperistalsis as dysfunctions of the mechanism of rapid sperm transport in patients with endometriosis and infertility. Hum Reprod 1996;11:1542-51.
Szczepanska M, Kozlik J, Skrzypczak J, Mikolajczyk M. Oxidative stress may be a piece in the endometriosis puzzle. Fertil Steril 2003;79:1288-93.
Hernández CA, Bujalil LB, De la Jara J, Mier J, Bouchán P. Endometriosis y consumo deficiente de moléculas antioxidantes relacionado con estrés oxidante periférico y peritoneal. Ginecol Obstet Mex 2006;74:20-28.