[COVID-19 as a trigger of autoimmune hepatitis. Case report].

Over the past two years, the entire medical community has taken up the fight against the new coronavirus infection. At the initial encounter with COVID-19, it seemed that this virus mainly affects the respiratory system. Still, with long-term observation, it turned out that the consequences of this disease can be much more severe and associated with lung damage and thromboembolic complications, and be a trigger for autoimmune diseases. According to the literature, after suffering COVID-19, some patients debuted systemic lupus erythematosus, hemolytic anemia, thrombocytopenia, developed GuillainBarr syndrome, vasculitis, and multiple sclerosis, and a case of autoimmune hepatitis (AIH) was described in foreign literature. AIH is a fairly rare disease, the prevalence of which in Europe is 1618 cases per 100 thousand inhabitants, affecting mainly women. It is known that chemicals and drugs (minocycline, diclofenac, methyldopa, infliximab, etanercept), viruses (HAV, HEV, EBV, HCV, CMV), environmental factors can serve as triggers of the autoimmune process in the liver. This article presents two clinical cases of AIH that developed after suffering a new coronavirus infection, which we consider as the initial provoking factor of autoimmune inflammation. Given the rarity of AIH, the description of new triggers is of clinical interest. It may be useful for doctors of different specialties since they faced drug-induced liver damage against the background of antiviral and immunobiological therapy. In the domestic literature, there have not yet been any publications devoted to the debut of AIH in adults after coronavirus infection.

[Atrial Fibrillation in Patients With Chronic Obstructive Pulmonary Disease Is Associated With Polymorphism of Interleukin 6 Gene].

UNLABELLED: It can be suggested that development of atrial fibrillation (AF) in patients with chronic obstructive pulmonary disease (COPD) is directly related to the system of inflammation. Genetic polymorphism of factors of this system can be one of components of mechanism of AF in COPD. Aim: to elucidate polymorphic markers of genes of factors of the system of inflammation associated with AF in patients with COPD. Material and methods. We examined 208 patients with COPD (52 with and 156 without AF). Examination included spirometry, echocardiography, and study of frequencies of polymorphic markers G(-238)A, G(-308)A of tumor necrosis factor (TNF) gene, C(-819)T of interleukin (IL) 10 gene, G(-174)C of IL-6 gene, rs2228145(AC) of IL-6R gene, and rs2069762(A/C) of IL-2 gene. RESULTS. Factors associated with AF were left atrial volume (odds ratio [OR] 1.021, 95% confidence interval [ClI] 1.004-1.043, p = 0,027), right atrial volume (OR 1.02, 95% CI 1.001-1.040, p=0.021), and carriage of C allele of polymorphic marker G(-174)C of IL-6 gene (OR 6.02, 95% Cl 1.87-19.38, p = 0.003). CONCLUSION: C allele of polymorphic marker G(-174)C of IL-6 gene can be considered to be independently associated with development of AF in patients with COPD.

[Genetic Features of Factors of Inflammation and Fibrosis Possible Common Pathway of Formation of Predisposition to Atrial Fibrillation and Chronic Obstructive Pulmonary Disease].

Atrial fibrillation (AF) and chronic obstructive pulmonary disease (COPD) have common pathogenetic mechanisms. It is obvious that hereditary predisposition also increases risk of both diseases. In this context consideration of genetic risk factors will enable in perspective distinguishing a group at highest risk among patients with COPD and become a basis for elaboration of novel approaches to treatment.

[Association of parameters of heart rate variability with severity of bronchial obstruction and presence of pulmonary hypertension in patients with chronic obstructive pulmonary disease].

With the aim of assessing parameters of heart rate variability (HRV) and heart rhythm turbulence (HRT) in patients with chronic obstructive pulmonary disease (COPD) in dependence on severity of the course of this disease and presence of pulmonary hypertension (PH) we examined 73 patients (28 with COPD and 45 healthy subjects). Invasive measurement of central hemodynamics was conducted. Compared with the control group in patients with COPD we revealed lowering of temporal as well as frequency HRV parameters. No significant changes of HRV parameters depended on severity of COPD course. However a tendency to maximal lowering of HRV parameters was noted in the group of patients with COPD with first sec forced expiratory volume <50%. Comparison of patients with and without PH with controls revealed tendency to maximal lowering of HRV parameters in the PH group. Thus measurement of HRV can be used for supplementary assessment of severity of the disease and detection of PH.