Overview

This trial is active, not recruiting.

Condition endometriosis
Sponsor National Taiwan University Hospital
Start date September 2005
End date March 2006
Trial size 45 participants
Trial identifier NCT00173212, 9461700522, NTUH.95-000357

Summary

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.

United States No locations recruiting
Other Countries No locations recruiting

Study Design

Observational model defined population
Time perspective cross-sectional

Eligibility Criteria

Female participants from 35 years up to 50 years old.

Inclusion Criteria: - women with adenomyosis - at early- to mid-secretory phases Exclusion Criteria: - postmenopausal - malignancy

Additional Information

Principal investigator Jehn-Hsiahn Yang, M.D.
Description Eutopic endometrium was obtained and separated into single endometrial stromal cell (ESC) in women with adenomyosis (study group) and without adenomyosis (control group). 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.
Trial information was received from ClinicalTrials.gov and was last updated in September 2005.
Information provided to ClinicalTrials.gov by National Taiwan University Hospital.