**5. Etiologic factors of endometriosis**

Genetic, hormonal, immunological, and environmental and angiogenetic factors are implicated in the pathogenesis of endometriosis. Heritable factors are important and there is strong evidence that a large proportion of female relatives are affected by the disease by a severe form of the disease. The relative risk of endometriosis in a first-degree relative is 7.2 and there are high concordance rates for the presence of endometriosis in monozygotic but not dizygotic twins (Kennedy, 1997, Kennedy, 1999). The finding of endometriosis in reproductive years and the hormone dependent response of endometrium implicates hormonal factors in the pathogenesis of endometriosis. The ovarian function is considered an important factor. The concentrations of microenvironmental steroid hormone are high, measuring 1000-fold higher in the ovarian follicles than the plasma .The peritoneal fluid is derived mainly by peri-follicular and corpus luteum exudates and presents high steroid hormone levels. It is estimated that the concentration of peritoneal estradiol during follicular phase increases progressively and reaches after the ovulation levels 100-fold higher that the plasma concentrations while the progesterone peritoneal levels are low in the follicular and increase rapidly after ovulation. There is evidence that the peritoneal fluid in women with endometriosis contain multiple types of free floating cells such as macrophages, leucocytes, lymphocytes, eosinophils and mast cells in greater numbers than in healthy women (Arid, 1997). Macrophages secret a high number of growth factors such as epidermal and transforming growth factor, fibroblast growth factor, interleukins 1,6 and 8, tumor necrosis factor-a. These factors play a role in the growth and regulation of the endometriotic foci. There is also reported a reduced T-mediated cytotoxicity to autologous endometrial cells and a decreased lymphocyte stimulation response to autologous endometrial antigens in patients with endometriosis. This findings support the theory that certain cell-mediated immune mechanisms limiting the growth of endometriotic implants may be impaired. Cyclo-0xygenase-2, involved in the synthesis of prostaglandins E2 may also play a role in the development of endometriosis. In the peritoneal fluid of women with endometriosis, potent angiogenetic growth factors were observed produced from peritoneal fluid macrophages, which probably are important in the development of endometriosis (Haney, 1991).

actual extend of the disease and the various local biochemical factors and the local action of activated mast cells may be responsible for this symptom. In rare cases with ovarian endometriosis, acute abdomen because of rupture of ovarian cystic masses and ascites raise

Levels of CA-125 may be elevated in the serum and peritoneal fluid of women with endometriosis and the concentration of serum CA-125 usually correlate with the severity and the clinical course of the disease. The sensitivity of the serum test is low for the screening of general population, but sensitive in the monitoring the response to hormonal treatment of women with endometriosis. Antiendometrial antibodies are found in 83% of women with confirmed endometriosis and the titers low after hormonal treatment and a

Genetic, hormonal, immunological, and environmental and angiogenetic factors are implicated in the pathogenesis of endometriosis. Heritable factors are important and there is strong evidence that a large proportion of female relatives are affected by the disease by a severe form of the disease. The relative risk of endometriosis in a first-degree relative is 7.2 and there are high concordance rates for the presence of endometriosis in monozygotic but not dizygotic twins (Kennedy, 1997, Kennedy, 1999). The finding of endometriosis in reproductive years and the hormone dependent response of endometrium implicates hormonal factors in the pathogenesis of endometriosis. The ovarian function is considered an important factor. The concentrations of microenvironmental steroid hormone are high, measuring 1000-fold higher in the ovarian follicles than the plasma .The peritoneal fluid is derived mainly by peri-follicular and corpus luteum exudates and presents high steroid hormone levels. It is estimated that the concentration of peritoneal estradiol during follicular phase increases progressively and reaches after the ovulation levels 100-fold higher that the plasma concentrations while the progesterone peritoneal levels are low in the follicular and increase rapidly after ovulation. There is evidence that the peritoneal fluid in women with endometriosis contain multiple types of free floating cells such as macrophages, leucocytes, lymphocytes, eosinophils and mast cells in greater numbers than in healthy women (Arid, 1997). Macrophages secret a high number of growth factors such as epidermal and transforming growth factor, fibroblast growth factor, interleukins 1,6 and 8, tumor necrosis factor-a. These factors play a role in the growth and regulation of the endometriotic foci. There is also reported a reduced T-mediated cytotoxicity to autologous endometrial cells and a decreased lymphocyte stimulation response to autologous endometrial antigens in patients with endometriosis. This findings support the theory that certain cell-mediated immune mechanisms limiting the growth of endometriotic implants may be impaired. Cyclo-0xygenase-2, involved in the synthesis of prostaglandins E2 may also play a role in the development of endometriosis. In the peritoneal fluid of women with endometriosis, potent angiogenetic growth factors were observed produced from peritoneal fluid macrophages, which probably are important in the development of endometriosis (Haney,

the suspicion of malignancy (Henkel et al, 1999).

**4. Serum markers in endometriosis** 

**5. Etiologic factors of endometriosis** 

good response.

1991).
