Endometriosis is the presence of endometrial tissue, which is the normal lining of the uterus, in locations outside the uterus. Several studies have looked into several factors involved in endometriosis to better understand and disease and proper management can be developed. Suzumori, Sugiura-Ogasawara, Katano and Suzumori found that levels of placental growth factor released into the peritoneal fluid where significantly higher in women with endometriosis than in women without endometriosis (2003).
Samples were obtained from patients during laparoscopic surgery or laparotomy for cystectomy, adnexectomy or total abdominal hysterectomy. Surrey and Hornstein assessed the long term drug effect of GnRH agonists given singly or in combination with “add-back” regimens in patients with endometriosis (2002). The sample population included patients with symptomatic endometriosis who were randomized in a double-masked, placebo-controlled clinical trial. The results showed that the addition of GnRH agonists improved pain relief and preserved bone mineral density.
These were based on quantitative scoring of physical findings and symptomatology and bone mineral density measurements using dual energy x-ray absorptiometry. Stefansson, Geirson, Steinthorsdottir, Jonson, Manolescu and Kong investigated the genetic factors which may be contribute to the risk of developing endometriosis based on observation that endometriosis are prevalent in nuclear families (2002). The sample population were women who were diagnosed with pelvic endometriosis through laparoscopy or during laparotomy in gynecology departments in Iceland.
The investigators believed that the correlation of endometriosis and family clustering can be evaluated because of the large population-based genealogical database available in Iceland. Through several measures of kinship and familiarity, the study showed that women were significantly more related than matched control groups. Narvekar, Cameron, Critchley, Lin, Cheng and Baird examined the extent of endometrial proliferation and the content and distribution of steroid receptor in women treated with low dose mifepristone (2004).
Reference
Gupta, S. , Agarwal, A. , Sekhon, L. Krajcir, N. , Cocuzza, M. & Falcone, T. (2006). Serum and peritoneal abnormalities in endometriosis: potential use as diagnostic markers. Minerva Ginecol. 58, 527-551. Narvekar, N. , Cameron, S. , Critchley, H. O. D. , Lin, S. , Cheng, L. & Baird, D. T. (2004). Low- Dose Mifepristone Inhibits Endometrial Proliferation and Up-Regulates Androgen Receptor. The Journal of Clinical Endocrinology & Metabolism. 89(5),2491–2497. Stefansson, H. , Geirson, R. T. , Steinthorsdottir, V. , Jonson, H. , Manolescu, A.& Kong, A. (2002).
Genetic factors contribute to the risk of developing endometriosis. Human Reproduction. 17(3), 555-559. Surrey, E. S & Hornstein, M. D. (2002). Prolonged GnRH Agonist and Add-Back Therapy for Symptomatic Endometriosis: Long-term Follow-up. Obstetrics & Gynecology. 99, 709– 719. Suzumori, N. , Sugiura-Ogasawara, M. , Katano, K. & Suzumori, K. (2003). Women with endometriosis have increased levels of placental growth factor in the peritoneal fluiuid compared with women with cystadenoma. Human Reproduction. 18(12), 2595-2598.