2007, Número 08
<< Anterior Siguiente >>
Ginecol Obstet Mex 2007; 75 (08)
Endometriosis: fisiopatología y líneas de investigación (primera parte)
Ayala YR, Mota GM
Idioma: Español
Referencias bibliográficas: 36
Paginas: 477-483
Archivo PDF: 203.09 Kb.
RESUMEN
En la actualidad, la endometriosis sigue siendo una enfermedad cuyo diagnóstico, después de la sospecha clínica, sólo puede confirmarse con la visualización directa de las lesiones endometriósicas. Esto ha dificultado la disponibilidad de estadísticas de incidencia y prevalencia que verdaderamente cuantifiquen el alcance de este padecimiento. Las líneas actuales de investigación, basadas principalmente en la teoría de la menstruación retrógrada, han ido estableciendo los múltiples factores bioquímicos, inmunológicos y moleculares implicados en la fisiopatología de la endometriosis. La evolución de la endometriosis se divide en cinco procesos básicos: adhesión, invasión, reclutamiento, angiogénesis y proliferación. En este artículo se revisan los primeros dos debido a la importancia que guardan desde el punto de vista diagnóstico y terapéutico. Como parte de la adhesión se han investigado las características estructurales del epitelio peritoneal, la participación de integrinas, moléculas de adhesión intercelular (ICAM), cadherinas y el ácido hialurónico.
REFERENCIAS (EN ESTE ARTÍCULO)
Ahued Ahued JR, Fernandez del Castillo S C, Bailón Uriza R. Ginecologia y obstetricia aplicadas. 2ª ed. México: Editiorial El Manual Moderno, 2003;p:1005.
Velebil P, Wingo PA, Xia Z, Wilcox LS, Peterson HB. Rate of hospitalization for gynecologic disorders among reproductive-age women in the United States. Obstet Gynecol 1995;86(5):764-9.
Ezkenazi B, Warner ML. Epidemiology of endometriosis. Obstet Gynecol Clin North Am 1997;24(2):235-58.
Sampson JA. Peritoneal endometriosis due to menstrual dissemination of endometrial tissue into the peritoneal cavity. Am J Obstet Gynecol 1927;54:174-7.
Watkins RE. Uterine retrodisplacements, retrograde menstruation and endometriosis. West J Surg Obstet Gynecol 1938;46:480-94.
Keettel WC, Stein RJ. The viability of the cast-off menstrual endometrium. Am J Obstet Gynecol 1951;61:440-2.
Nawroth F, Rahimi G, Nawroth C, Foth D, et al. Is there an association between septate uterus and endometriosis? Hum Reprod 2006;21:542-4.
Ugur M, Turan C, Mungan T, Kuscu E, et al. Endometriosis in association with mullerian anomalies. Gynecol Obstet Invest 1995;40:261-4.
Jenkins S, Olive DL, Haney AF. Endometriosis: pathogenic implications of the anatomic distribution. Obstet Gynecol 1986;67:335-8.
Seli E, Berkkanoglu M, Arici A. Patogenesis of endometriosis. Obstet Gynecol Clin N Am 2003;30:41-61.
Van der Linden PJ, de Goeij AF, Dunselman GA, Erkens HW, Evers JL. Endometrial cell adhesión in an in vitro model using intact amniotic membranas. Fertil Steril 1996;65:76-80.
Witz CA, Montoya Rodriguez IA, Schenken RS. Whole explants of peritoneum and endometrium: a novel model of the early endometriosis lesion. Fertil Steril 1999;71:56-60.
Gaetje R, Rody A, Kissler S, Kaufmann M, Ahr A. Integrin expression in eutopic and ectopic endometrium. Zentralbl Gynakol 2006;128:135-7.
Rzymski P, Wozniak J, Opala T. Production of soluble intracelular adhesion molecule-1 (sICAM-1) in human endometrial cell culture. Wiad Lek 2003;56:430-3.
Wu MH, Yang BC, Lee YC, Wu PL, Hsu CC. The differential expression of intercellular adhesion molecule-1 (ICAM-1) and regulation by interferon-gamma during the pathogenesis of endometriosis. Am J Reprod Immunol 2004;51:373-80.
Van der Linden PJ, de Goeij AF, Dunselman GA, van der Linden EP, et al. Expression of integrins and E-cadherin in cells from menstrual effluent, endometriumm, peritoneal fluid, peritoneum, and endometriosis. Fertil Steril 1994;61:85-90.
Poncelet C, Leblanc M, Walker-Combrouze F, Soriano D, et al. Expression of cadherins and CD44 isoforms in human endometrium and peritoneal endometriosis. Acta Obstet Gynecol Scand 2002;81:195-203.
Chen GT, Tai CT, Yeh LS, Yang TC, Tsai HD. Identification of the cadherin subtypes present in the human peritoneum and endometriotic lesions: potential role for P-cadherin in the development of endometriosis. Mol Reprod Dev 2002;62:289-94.
Deschaud H, Witz CA, Montoya Rodriguez IA, Degraffenreid LA, Schenken RS. Mesothelial cell-associated hyaluronic acid promotes adhesion of endometrial cells to mesothelium. Fertil Steril 2001;76:1012-8.
Zhang RJ, Wild RA, Ojago JM. Effect of tumor necrosis factor- alpha on adhesion of human endometrial stromal cells to peritoneal mesothelial cells: an in vitro system. Fertil Steril 1993;59:1196-201.
Gross J, Lapiere CM. Collagenolitic activity in amphibian tissues: a tissue culture assay. Proc Natl Acad Sci USA 1962; 48:1014-22.
Woessner JF. Matrix metalloproteinases in normal menstruation. Hum Reprod 1996; 11:124-33.
Salomonsen LA, Woolley DE. Menstruation induction by matrix metalloproteinases and inflammatory cells. J Reprod Immunology 1999; 44:1-27.
Hampton AL, Salamonsen LA. Expression of messenger ribonucleic acid encoding matrix metalloproteinases and their tissue inhibitors is related to menstruation. J Endocrinol 1994; 141:R1-3.
Kokorine I, Nisolle M, Donnez J, Eeckhout Y, et al. Expression of intestinal collagenase (matrix metalloproteinase-1) is related to the activity of human endometriotic lesions. Fertil Steril 1998;68:246-51.
Ueda M, Yamashita Y, Takehara M, Terai Y, et al. Survivin gene expression in endometriosis. J Clin Endocrinol Metab 2002;87:3452-9.
Bruner KL, Matrisian LM, Rodgers WH, Gorstein F, Osteen KG. Suppression of matrix metalloproteinases inhibits establishment of ectopic lesions by human endometrium in nude mice. J Clin Invest 1997;99:2851-7.
Hickey M, Crewe J, Mahoney LA, Doherty DA, et al. Mechanisms of irregular bleeding with hormone therapy: the role of matrix metalloproteinases and their tissue inhibitors. J Clin Endocrinol Metab 2006;91:3189-98.
Bruner KL, Eisenberg E, Gorstein F, Osteen KG. Progesterone and transforming growth factor-beta coordinately regulate suppression of endometrial matrix metalloproteinases in a model of experimental endometriosis. Steroids 1999;64:648-53.
Bruner KL, Rodgers WH, Gold LI, Korc M, et al. Transforming growth factor beta mediates the progesterone suppression of an epithelial metalloproteinase by adjacent stroma in the human endometrium. Proc Natl Acad Sci USA 1995;92(16):7362-6.
Keller NR, Sierra-Rivera E, Eisenberg E, Osteen KG. Progesterone exposure prevents matrix metaloproteinase-3 (MMP-3) stimulation by interleukin-1alpha in human endometrial stromal cells. J Clin Endocrinol Metab 2000;85:1611-9.
Kondera-Anasz Z, Sikora J, Mielczarek-Palacz A, Jonca M. Concentrations of interleukin (IL)-1alpha, IL-1 soluble receptor type II (IL-1sRII) and IL-1 receptor antagonist (IL-1 Ra) in the peritoneal fluid and serum of infertile women with endometriosis. Eur J Obstet Gynecol Reprod Biol 2005;123(2):198-203.
Braundmeier AG, Nowak RA. Cytokine regulate matrix metalloproteinases in human uterine endometrial fibroblast cells through a mechanism that does not involve increases in extracelular matrix metalloproteinase inducer. Am J Reprod Immunol 2006;56:201-14.
Braundmeier AG, Fazleabas AT, Lessey BA, Guo H, et al. Extracellular matrix metalloproteinase inducer regulates metalloproteinases in human uterine endometrium. J Clin Endocrinol Metab 2006;91:2358-65.
Ferrari MM, Biondi ML, Rossi G, Grijuela B, et al. Analysis of two polymorphisms in the promoter region of matrix metalloproteinase 1 and 3 genes in women with endometriosis. Acta Obstet Gynecol Scand 2006;85:212-17.