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  1. Fadieienko GD, Chereliuk NI, Galchinskaya VY
    Wiad Lek, 2021;74(3 cz 1):523-528.
    PMID: 33813462
    OBJECTIVE: The aim: To analyze the status of Gut microbiota (GM) at the level of the main phylotypes in patients with NAFLD, depending on the body mass index (BMI) and gender in comparison with a group of practically healthy individuals.

    PATIENTS AND METHODS: Materials and methods: The study involved 120 patients with NAFLD, who were divided into two groups depending on BMI and the control group containing 20 practically healthy individuals.

    RESULTS: Results: In patients with NAFLD with comorbid obesity, a statistically significant increase in the relative amount of Firmicutes (52.12 [42.38; 67.39]%) and Firmicutes/Bacteroidetes ratio (3.75 [1.7; 9.5]) against the background of a significant decrease in the amount of Bacteroidetes (13.41 [7.45; 26.07]%); in NAFLD patients with overweight, the relative amount of Firmicutes was 49.39 [37.47; 62.73]%, Firmicutes / Bacteroidetes ratio was 1.98 [1.15; 5.92], and the relative amount of Bacteroidetes was 23.69 [12.11; 36.16]%. In the control group, the distribution of the basic GM phylotypes was significantly different; the relative amount of Bacteroidetes was almost the same as of Firmicutes - 34.65 [24.58; 43.53]% and 29.97 [22.52; 41.75]% respectively, and the Firmicutes/Bacteroidetes ratio was 0.64 [0.52; 1.47].

    CONCLUSION: Conclusions: The most statistically significant changes in the composition of IM occur due to the increase in the relative amount of Firmicutes and the ratio of Firmicutes/ Bacteroidetes against the background of a decrease in the relative amount of Bacteroidetes. These changes were directly proportional to the increase in BMI, but had no gender features.

  2. Pyvovar SM, Rudyk IS, Kopytsya MP, Lozyk TV, Galchinskaya VY, Bondar TM
    Pol Merkur Lekarski, 2019 Nov 29;47(281):170-176.
    PMID: 31812970
    The course of heart failure (HF) and its progression is associated with comorbidities, genetic factors and a dynamics of a number of biomarkers. The low triiodothyronine syndrome (LT3S) is observed in some patients with HF. Extremely little data are available in the literature regarding the effect of β-adrenoreceptors (β-AR) genes polymorphisms on the development of LT3S and many contradictory results about their association with HF course. This encourages new research in this area.

    AIM: The aim of study was to evaluate the relationship of β-adrenergic receptors gene polymorphisms with low triiodothyronine syndrome in patients with a heart failure.

    MATERIALS AND METHODS: 354 patients with HF on a background of postinfarction cardiosclerosis were included to the study. At 89 (25.1%) patients LT3S was diagnosed. The course of HF was studied for 2 years. Mean levels of thyroid stimulating hormone (TSH), free T3f and T4f were evaluated. Genotyping of 4 single nucleotide polymorphisms (Gly389Arg of β1-AR gene, Ser49Gly of β1-AR gene, Gln27Glu of β2- AR gene and Ser275 of GNβ3 gene) was performed by polymerase chain reaction. Genetic and epidemiological analysis was performed using the SNPStats program.

    RESULTS: The risk of LT3S in patients with HF increases with homozygous G/G variant of Gln27Glu polymorphism of the β2-AR gene (OR=2.21, p=0.037), described as a recessive model of inheritance. There was a tendency to increase the risk of LT3S development in the presence of the genotype C/T of the Ser275 polymorphism of the GNb3 gene (OR=1.75, p=0.054), described as an over-dominant model. The genotype C/G of the Gln27Glu polymorphism of the β2-AR gene was associated with a decreased risk of LT3S development (OR=0.54, p=0.037), described as over-dominant model. Patients with HF carriers the A allele (A/GA/A) of the Ser49Gly polymorphism of the β1-AR gene have a lower risk of repeated hospitalization due to HF decompensation (OR=0.50, p=0.032), described as a dominant model. There was a tendency to increase the risk of re-hospitalization in the G-allele (C/GG/ G) variant of the Gln27Glu polymorphism of the β2-AR gene (OR=1.68, p=0.057), described as a dominant heredity model. At patients with HF in combination with LT3S the risk of re-hospitalization increases at C/G variant of the Gln27Glu polymorphism of β2-AR gene (OR=1.25, p=0.025), described as an over-dominant model.

    CONCLUSIONS: The results suggest that congenital genetic alterations in β-adrenergic pathways may be associated with the development of LT3S in patients with HF and the features of the HF course.

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