PREVALENCE OF THE I/D ACE GENE POLYMORPHIC VARIANT IN PATIENTS WITH A COMORBID COURSE OF UTERINE LEIOMYOMA AND GENITAL ENDOMETRIOSIS

Authors

  • S. O. Vovk-Shulha I.HORBACHEVSKY TERNOPIL NATIONAL MEDICAL UNIVERSITY, Y. SEMENYUK RIVNE REGIONAL CLINICAL HOSPITAL
  • S. V. Khmil I.HORBACHEVSKY TERNOPIL NATIONAL MEDICAL UNIVERSITY

DOI:

https://doi.org/10.11603/mcch.2410-681X.2024.i1.14594

Keywords:

uterine leiomyoma, genital endometriosis, infertility, in vitro fertilization, ACE gene polymorphism, prevalence

Abstract

Introduction. Angiotensin-converting enzyme (ACE) gene polymorphism is associated not only with the risk of essential hypertension, but also with the risk of uterine leiomyoma (LM), because leiomyomatosis nodes are closely connected to the systemic vascular network through the vessels that feed them and participate in many chains of signal transmission, including angiotensin II, which is formed under the influence of angiotensin-converting enzyme (ACE).

The aim of the study – to investigate the prevalence of the I/D polymorphic variant of the ACE gene in patients with a comorbid course of intramural LM and genital endometriosis.

Research Methods. For 33 patients with a comorbid course of intramural LM and genital endometriosis and 30 patients with isolated intramural LM, a molecular genetic study of the I/D polymorphic variant of the ACE gene was applied according to the standard operating procedure developed in the interdepartmental educational and research laboratory of I. Horbachevsky Ternopil National Medical University.

Results and Discussion. The analysis of the frequency distribution of alleles for the I/D polymorphic variant of the ACE gene showed that in patients with comorbid intramural LM and genital endometriosis, as well as with isolated intramural LM, the distribution of I and D alleles is even, while in the control group carriers of the I allele predominate (in 2.3 times) in relation to carriers of the D allele, χ2=6.35; p=0.042. At the same time, the presence of the D allele increases the risk of intramural LM in patients with a comorbid course by 2.98 times and by 2.85 times if it is isolated. In contrast, the protective properties of allele I of the ACE gene were found both in patients with acomorbid course of intramural LM and genital endometriosis, and in patients with isolated intramural LM. When analyzing the dominant model of inheritance of the I/D polymorphic variant of the ACE gene in patients with a comorbid course of intramural LM and genital endometriosis, a significant lower frequency of registration of genotype II was established, which reduces the risk of leiomyoma (OR=0.16; 95% CI 0.04−0.63) compared to the control. At the same time, carriers of the D allele (genotype ID+DD) of this research group have a 6.4-fold increased risk of developing leiomyoma (OR=6.40; 95% CI 1.59−25.72). In patients with isolated LM, it was established that carriers of the D allele (genotype ID+DD) have a 3.76-fold increased risk of developing leiomyoma (OR=3.76; 95% CI 1.00−14.07).

Conclusions. Analyzing the odds ratio and its confidence interval for the alleles of the I/D polymorphic variant of the ACE gene, it was established that the presence of the D allele almost equally increases the risk of intramural LM both under the condition of its comorbid course with genital endometriosis and its isolated course (in 2.98 and 2.85 times, respectively). During the analysis of the dominant model of inheritance of the I/D polymorphic variant of the ACE gene, it was established that in the case of comorbid course of intramural LM and genital endometriosis, carriers of the D allele (genotype ID+DD) have a 6.4-fold increased risk of leiomyoma, and in the case of an isolated course – a 3.76-fold increased risk.

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Published

2024-04-29

How to Cite

Vovk-Shulha, S. O., & Khmil, S. V. (2024). PREVALENCE OF THE I/D ACE GENE POLYMORPHIC VARIANT IN PATIENTS WITH A COMORBID COURSE OF UTERINE LEIOMYOMA AND GENITAL ENDOMETRIOSIS. Medical and Clinical Chemistry, (1), 27–34. https://doi.org/10.11603/mcch.2410-681X.2024.i1.14594

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Section

ORIGINAL INVESTIGATIONS