Progesterone Receptor Gene Polymorphism Promoter Region +331G/A Increases Risk of Endometriosis

Syifa Alkaf, Aerul Chakra, Усман Саид, Irsan Saleh
In: Indonesian Journal of Obstetrics and Gynecology · 2016 · pp. 52–56 · doi:10.32771/inajog.v4i1.73 · W2944067760
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This case-control study found that the progesterone receptor gene polymorphism promoter region +331G/A genotype significantly increases the risk of endometriosis.

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This observational case-control study investigated the association between progesterone receptor gene promoter region +331G/A polymorphism and disease risk in women undergoing surgical procedures for endometriosis or adenomyosis. The researchers analyzed blood samples from patients at a hospital in Palembang, Indonesia, comparing genotype frequencies between affected cases and healthy controls using PCR-RFLP techniques. Results indicated that women carrying the heterozygous +331G/A genotype faced a significantly increased risk of developing endometriosis compared to those with the wild-type G/G genotype, with an odds ratio of 3.29. This paper is centrally about endometriosis — specifically examining genetic predispositions related to progesterone receptor polymorphisms in an Indonesian population.

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Abstract

Objective: To identify relationship between progesterone receptor gene polymorphism promoter region +331G/A with the risk of endometriosis. Method: An observational case-control study. Population are women with endometriosis and/or adenomyosis who have been performed laparotomy/laparoscopy at Obstetrics and Gynecology Department Dr. Mohammad Hoesin General Hospital Palembang, January-November 2013. Subjects fulfilled inclusion criteria, given informed consent and performed blood sampling continued by PCRRFLP. Results were divided into A/A genotype (homozygote mutant), G/A (heterozygote mutant), and G/G (homozygote wild type). Data were analyzed by SPSS 21.0 version. Result: PCR-RFLP results for+331G/A genotype were 26 (54.1%) in case group and 14 (26.4%) in control. +331A/A genotype was not found in both groups. There was significant increase risk of endometriosis in women carrying genotype +331G/A to those with genotype +331G/G with OR 3.29 (p
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Progesterone Receptor Gene Polymorphism Promoter Region +331G/A Increases Risk of Endometriosis DOI: https://doi.org/10.32771/inajog.v4i1.73Abstract Objective: To identify relationship between progesterone receptor gene polymorphism promoter region +331G/A with the risk of endometriosis. Method: An observational case-control study. Population are women with endometriosis and/or adenomyosis who have been performed laparotomy/laparoscopy at Obstetrics and Gynecology Department Dr. Mohammad Hoesin General Hospital Palembang, January-November 2013. Subjects fulfilled inclusion criteria, given informed consent and performed blood sampling continued by PCRRFLP. Results were divided into A/A genotype (homozygote mutant), G/A (heterozygote mutant), and G/G (homozygote wild type). Data were analyzed by SPSS 21.0 version. Result: PCR-RFLP results for+331G/A genotype were 26 (54.1%) in case group and 14 (26.4%) in control. +331A/A genotype was not found in both groups. There was significant increase risk of endometriosis in women carrying genotype +331G/A to those with genotype +331G/G with OR 3.29 (p<0.05). Conclusion: Polymorphism on progesterone receptor gene +331G/A increases risk of endometriosis in Malay population in Indonesia. Compared to previous studies, there is interesting finding that polymorphic alels were found more commonly in our study. [Indones J Obstet Gynecol 2016; 1: 52-56] Keywords: endometriosis, polimorphism, progesterone reseptor, +331G/ADownloads Download data is not yet available. Downloads Published 2016-01-14 Versions How to Cite Alkaf, S., Chakra, A., Said, U., & Saleh, I. (2016). Progesterone Receptor Gene Polymorphism Promoter Region +331G/A Increases Risk of Endometriosis. Indonesian Journal of Obstetrics and Gynecology, 4(1), 52–56. https://doi.org/10.32771/inajog.v4i1.73 Issue Section Case Report

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endometriosisadenomyosis

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Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

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