The Estrogen Receptor Concentration and Col3A1 Gene Immunoexpression in Uterosacral Ligament is Correlated with Postmenopausal Uterine Prolapse

  • Erick C. Asmara Department of Obstetrics and Gynecology Faculty of Medicine University of Padjadjaran/ Dr. Hasan Sadikin Hospital Bandung

Abstract

Objective: To analyze correlation between concentration of estrogen receptor and imunoexpression of Col3A1 gene on uterosacral ligament of postmenopausal uterine prolapse patient.

Methods: This is a cross-sectional analytic observational study involving 32 subjects who met inclusion criteria. Samples are taken consecutively in Dr. Hasan Sadikin Hospital in January 1st - December 31st 2012. Statistical analysis was performed with non-parametric Mann-Whitney test and Spearman’s rho non-parametric correlation test.

Result: There is no significant difference of estrogen receptor concentration between postmenopausal women with and without uterine prolapse (p = 0.377), while there is no significant difference of Col3A1 gene immunoexpression between postmenopausal women
with and without uterine prolapse (p = 0.119) either. There is a significant positive correlation between the estrogen receptor concentration and Col3A1 gene immunoexpression in uterosacral ligament of postmenopausal uterine prolapse patients (p = 0.002, r= 0.711).

Conclusion: There is a positive correlation between the estrogen receptor concentration and Col3A1 gene immunoexpression in uterosacral ligament of postmenopausal uterine prolapse patients.

[Indones J Obstet Gynecol 2013; 37-2: 103-6]

Keywords: Col3A1 gene, estrogen receptor, menopause, uterine prolapse, uterosacral ligamen
Published
2016-12-16
How to Cite
ASMARA, Erick C.. The Estrogen Receptor Concentration and Col3A1 Gene Immunoexpression in Uterosacral Ligament is Correlated with Postmenopausal Uterine Prolapse. Indonesian Journal of Obstetrics and Gynecology (INAJOG), [S.l.], dec. 2016. ISSN 2338-7335. Available at: <http://inajog.com/ojs/index.php/journal/article/view/346>. Date accessed: 16 dec. 2017.
Section
Other