View clinical trials related to Endometriosis.
Filter by:The purpose of this study is to demonstrate safety and efficacy of SH T00660AA for the treatment of endometriosis
The purpose of this study is to investigate differences in protein expression profiles of blood and peritoneal fluid samples obtained from patients who do, and those who do not, have endometriosis seen during laparoscopic surgery. These profiles may include both known and novel markers for diagnosing endometriosis.
This study was designed as a proof-of-concept trial to evaluate safety, tolerability, and the efficacy of 1800 mg (ZK 811752 600 mg given orally three times daily) over 12 weeks for the treatment of endometriosis associated pelvic pain (EAPP) in comparison to placebo.
Adenomyosis refers to the presence of endometrial glands and stroma that is haphazardly deep within the myometrium. However, the etiology and pathologic mechanism responsible for adenomyosis are not yet very well known. Our previous results revealed that the expression of killer inhibitory receptors on natural killer cells was decreased in eutopic endometrium in women with adenomyosis. It implies that the formation of adenomyosis might be due to abnormal endometrial tissues, but not the aberrant local immunological dysfunction in myometrium. Our further investigation revealed that in vitro coculture of macrophages and endometrial stromal cells (ESCs) increase the expression of IL-6 mRNA in ESC, which might further enhance the proliferation of ESC and subsequently result in the formation of ectopic endometrial implants in adenomyosis. Abnormal cell proliferation has been generally found in the tumorigenesis, including the formation of endometriosis. Adenomyosis is considered to have a similar pathophysiology with endometriosis, and it must be interesting to examine whether there is abnormal cell proliferation in the eutopic endometrium of adenomyosis. Lipopolysaccharide (LPS) was found to promote proliferation of ESCs via induction of TNF-a and IL-8 expression, whereas IFN-g significantly inhibited ESCs proliferation. Therefore, whether abnormal cell proliferation occurs under the effects of LPS and IFN-g in the eutopic endometrium of adenomyosis needs further clarification. Adenomyosis preferentially affects women between the ages of 35 and 50 years, and the symptoms subside gradually after menopause. It is well known that there is a close conjunction between estrogen and adenomyosis. Estradiol (E2) was demonstrated to induce endometrial cell proliferation, whereas medroxyprogesterone (MPA) inhibited endometrial cell proliferation via antagonizing estrogenic effects. Experiments to investigate these steroid effects on ESC proliferation in vitro in the eutopic endometrium of adenomyosis are of clinical relevance. In this study, we try to collect endometrial tissues from women with and without adenomyosis, and then purify ESCs from endometrium. ESCs are cultured for 2 days with the supplement of LPS, IFN-gamma, Estradiol, MPA and Estradiol+MPA. Quantification of cell proliferation was done with Cell Proliferation Assay Kit and immunocytochemical detection of Ki-67, in an attempt to examine the cell proliferation of ESCs in women with adenomyosis.
Our previous results revealed that the expression of killer inhibitory receptors (KIRs) on NK cells was decreased in eutopic endometrium in women with adenomyosis. It implies that the formation of adenomyosis might be due to abnormal endometrial tissues, but not the aberrant local immunological dysfunction in myometrium. In addition, in vitro coculture of macrophages and endometrial stromal cells (ESC) increase the expression of IL-6 mRNA in ESC, which might further enhance the proliferation of ESC and subsequently result in the formation of ectopic endometrial implants in adenomyosis. Besides, another possible mechanism is the abnormal apoptosis of ESC in adenomyosis. In endometriosis, apoptotic endometrial cells were found to be decreased, which possibly accounts for the formation of endometriosis. However, there have not been reports investigating the apoptosis of ESC in adenomyosis. In this study, we try to investigate apoptotic ESC with flow cytometry in women with and without adenomyosis. Annexin V, bcl-2, and caspase-3 were measured to represent the degree of apoptosis in ESC.
The objective of this study is to determine the safety and effectiveness of three doses of asoprisnil, compared to placebo, in the treatment of women with endometriosis.
The objective of this study is to determine the safety and efficacy of 3 asoprisnil doses (0.5 mg, 1.5 mg, and 5.0 mg) for 12 weeks in women with endometriosis.
The objective of this study is to determine the long-term safety of asoprisnil 5 mg for 12 months in women with endometriosis from study M01-398.
Long term treatment of progestin has been demonstrated to have an inhibitory effect on endometrial angiogenesis and the proliferation of endometrial stromal cells. As a result, progestin is now widely employed in the treatment of endometrial cancer, endometrial hyperplasia, and dysfunction uterine bleeding. In the treatment of adenomyosis, however, the beneficial effect of progestin was limited. It might imply that the behavior of endometrial cells in women with adenomyosis is different from that in women without adenomyosis. Our previous study revealed that the expression of killer inhibitory receptors (KIRs) on NK cells was decreased in eutopic endometrium in women with adenomyosis. It may be a compensatory effect in which the NK cytotoxicity is activated in order to wipe out the abnormal endometrial cells that might go out of the eutopic site of endometrium. It implies that the formation of adenomyosis might be due to “abnormal” endometrial tissues, but not the aberrant local immunological dysfunction in myometrium. This finding is compatible with previous reports in which eutopic endometrium obtained from women with endometriosis or adenomyosis was found to behave differently from endometrium in unaffected women. In this study, we try to collect endometrial tissues from women with and without adenomyosis, and then purify the endometrial stromal cells from endometrium. The endometrial stromal cells are cultured for 8 days with the supplement of medroxyprogesterone (MPA) or danazol. Quantification of IL-6 and IL-8 mRNA in endometrial cells, and the concentrations of IL-6 and IL-8 in cultured media will be done with real time RT-PCR and ELISA respectively. The expression of different cytokines of endometrial cells in response to progestin might be further elucidated after our experiment.
The purpose of this study is to compare the effect of rosiglitazone versus placebo on soluble proinflammatory markers in peritoneal fluid of women with endometriosis.