Comparative clinical and moleculare-genetic features adenomyose and endometrioma

In: HEALTH OF WOMAN · 2016 · pp. 118–120 · doi:10.15574/hw.2016.110.118 · W3092226512
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This study examined clinical and genetic features of adenomyosis and endometrioma, finding a higher frequency of the GSTT1 null genotype in adenomyosis patients compared to controls.

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This study investigated the role of specific allele variants in genes CYP19, GSTT1, and GSTM1 within the pathogenesis of adenomyosis and ovarian endometriomas. The researchers compared genetic data from 100 women with genital endometriosis, divided into groups with adenomyosis or endometriomas, against a control group of 50 healthy women. They found no statistically significant differences in deletion frequencies for the GSTM1 gene between patients and controls, while the frequency of homozygotes for the null allele of GSTT1 was slightly higher in the adenomyosis group. The authors concluded that these results differed from previous literature, possibly because their cohort consisted exclusively of severe stage IV disease cases, suggesting more complex genomic disruptions in advanced stages. This paper is centrally about adenomyosis and endometrioma, focusing on comparative molecular-genetic features between these two forms of endometriosis.

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- Comparative clinical and moleculare-genetic features adenomyose and endometrioma Comparative clinical and moleculare-genetic features adenomyose and endometrioma HEALTH OF WOMAN. 2016.4(110):118–120; doi 10.15574/HW.2016.110.118 Comparative clinical and moleculare-genetic features adenomyose and endometrioma Prudnikov P. M. National Medical Academy of Postgraduate Education P. L. Shupyk, Kiev The objective: role definition allele variants of genes CYP19, GSTT1, GSTM1, р53 in патогенезе and a clinical current adenomyose and endometrioma ovariums. Patients and methods. 100 women with genital endometriosis and 50 women without the given disease are surveyed. The group 1 was made by 50 women with adenomyose, middle age has made them – 44.9±0.7 years, group 2 50 women with endometruioma ovariums have made, middle age 32.6±0.8 years. From them 10 patients with relapse endometrioma ovariums after the combined treatment. The diagnosis at all patients is verified intraoperative and by results of histologic research. The control group has been generated from 50 women at which inspection has been excluded genital endometriosis, without clinical displays of infringements ovariale-menstruale functions, at the age from 17 till 35 years. Results. The analysis of polymorphic variants of the gene glutathione-S-transferase M1 no statistically significant differences in frequencies deletions between the group of patients with adenomyosis and control group (52.0% and 42.0% respectively). Null genotype frequency in patients did not differ from the frequency of the population. The frequency of homozygotes for the null allele of the gene glutathione-S-transferase T1 was somewhat higher in the patients with adenomyosis compared to the control group (34.0% and 22.0% respectively). When analyzing the gene glutathione -S-transferase M1 in the group of patients with ovarian endometrioma also no statistically significant differences from the control group on the frequency of zero genotypes (54.0% and 42.0% respectively). Conclusion. Results of the spent researches testify that on one of genes GST is not revealed authentic distinctions between groups of sick and healthy women that differs with the literature data a little. Apparently, it is possible to explain it to that the analyzed group included patients with a heavy endometriosis of IV stage whereas in the previous researches carried out the endometriosis analysis as a whole, without a disease stage. Probably, at development of heavy forms of disease there can be any other more serious breakages in genome, as is a scientific direction of our further researches. Key words: adenomyose, endometrioma, clinic, genetics. REFERENCES 1. Adamjan LV. 2008. Endometrioses: the Management for doctors. М, Medicine:317. 2. Ajlamazjan EK. 2012. A genital endometriosis: new approaches to therapy: a management for doctors. SPb:25. 3. Kohanevich EV. 2008. Pressing questions гинекологии. К, ООО «Book-plus»:161. 4. Baskakov VP. 2012. Endometrioznaja illness. St.-Petersburg: Open Company «Publishing house N-L»:452. 5. Bezhenar VF, Povzun SA, Fridman DB. 2012. The analysis of efficiency of ways of reception bioptate for histologic verification adenomyose. Magazine of obstetrics and female deseases LIV;4:37-39 6. Sorokina AV, Totchiev GF, Toktar LR. 2010. Modern approaches to genetic diagnostics adenomyose. Bulletin RUDN. Obstetrics and ginecology 5:181-191. 7. Radzinsky VE, Sorokina AV, Zhilina NV. 2010. Immunological and genetic determinants adenomyose from a position of demonstrative medicine. Bulletin RUDN: Obstetrics and ginecology 6:138-145.

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