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    O. M. Bilovol, I. I. Knyazkova, O. M. Kіrіenko, N. V. Kuzminova, D. O. Kirіenko, M. V. Bogun, A. O. Havryliuk

    SOLUBLE GENE-EXPRESSED STIMULATING GROWTH FACTOR RECEPTOR 2 AS A POSSIBLE SERUM MARKER OF DIASTOLIC DYSFUNCTION IN PATIENTS WITH HYPERTENSIVE DISEASE AND TYPE 2 DIABETES MELLITUS


    About the author: O. M. Bilovol, I. I. Knyazkova, O. M. Kіrіenko, N. V. Kuzminova, D. O. Kirіenko, M. V. Bogun, A. O. Havryliuk
    Heading CLINICAL MEDICINE
    Type of article Scentific article
    Annotation We examined 60 patients with stage II hypertension (HT), grade 2, mean age 54.7±3.8 years. The first group consisted of 30 patients with hypertension of the II stage, the second group included 30 patients with HT with comorbid moderate, subcompensated type 2 diabetes mellitus (DM). The control group consisted of 20 healthy individuals. All subjects underwent clinical and laboratory examination including the level of soluble growth-stimulating receptor expressed by gene 2 (sST2) in serum, echocardiography with an assessment of mitral Doppler blood flow. It was determined that the serum level of sST2 was significantly (p<0.05) higher in patients with comorbidity of HT and DM compared with HT without DM. Significant (p<0.05) positive correlations were found between sST2 level and regurgitation rate on tricuspid valve, E/e ', E/A ratio. The significant (p<0.05) negative relationships were found between sST2 and values of e's, e'l, e'avg. Therefore, an increased level of the sST2 biomarker is associated with the progression of left ventricular diastolic dysfunction in case of comorbidity of HT and type 2 DM. The results of the study suggest sST2 as one of the possible serum markers of diastolic left ventricular dysfunction in comorbid patients with HT and DM.
    Tags comorbidity of hypertension and type 2 diabetes mellitus, diastolic dysfunction, soluble growth-stimulating receptor expressed by gene 2
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    Publication of the article «World of Medicine and Biology» №1(79), 2022 year, 025-028 pages, index UDK 616.12-008.318.4: 616.12-008.331.1
    DOI 10.26724/2079-8334-2022-1-79-25-28