ABSTRACT
Tuberculosis remains a major global health concern, especially in the context of emerging drug-resistant strains and the high prevalence of HIV/AIDS. Understanding the pathomorphologic changes associated with DRTB and its coinfection with HIV/AIDS is crucial for designing effective diagnostic, preventive, and therapeutic interventions. The objectives of this study were to assess the pathomorphologic changes, investigate lung function and blood circulation, and explore risk factors and clinical predictors associated with cor pulmonale in patients with DRTB and DRTB/HIV/AIDS co-infections. The study included 72 patients, with 28 having isolated DRTB and 44 having DRTB/HIV/AIDS co-infections. Microscopic examination of lung tissue samples from isolated DRTB patients revealed fibrous and productive changes with inflammatory infiltration. Histological examination of the myocardium in these patients showed hypertrophy and diffuse cardiosclerosis. Patients with DRTB/HIV/AIDS co-infections exhibited extensive destructive changes in lung tissue, along with dystrophy of cardiomyocytes and focal lymphohistiocytic infiltration in the myocardium. The frequency of cor pulmonale formation was significantly higher in the co-infection group (22.7%) compared to the isolated DRTB group (10.7%). Histological samples suggested that co-infection with HIV/AIDS exacerbates myocardial damage caused by DRTB. This research demonstrates the distinct pathomorphologic changes observed in the lung tissue and myocardium of patients with isolated DRTB and DRTB/HIV/AIDS co-infections. The study findings support the association between co-infection and increased risk of cor pulmonale development. Understanding the mechanisms underlying these differences will help identify potential therapeutic targets to mitigate myocardial damage in patients with DRTB and its co-infection.
ABSTRACT
OBJECTIVE: The aim: To investigate the features of coagulation homeostasis in patients with liver cirrhosis (LC) in COVID-19 infection. PATIENTS AND METHODS: Materials and methods: At the clinical base of the Department of Propaedeutics of Internal Medicine, 32 patients with LC infected with COVID-19 were examined - 1 Group of patients. The study also included 30 patients with LC who were not infected with COVID-19 (2 Group of patients). RESULTS: Results: The analysis of the obtained data indicates disorders of the hemostasis system in patients with LC without the COVID-19 infection (Group 2), as well as in patients with LC at the time of being infected with COVID-19. The violation of the protein synthesis function of the liver is manifested through a decrease in the level of fibrinogen in blood serum (up to 2.0±0.5 gr/l in patients of Group 1 at the time of admission for inpatient care) and up to 21.9±0.5 gr/l in patients of group ÐÐ - Ñ<0.05. This was accompanied by an acceleration of prothrombin time, thrombin time and activated partial thromboplastic time in patients with LC, as well as an increase in the level of antithrombin III. The level of D-dimer was reduced both in patients of group II and in patients of group I at the time of being infected with COVID-19. CONCLUSION: Conclusions: Changes in coagulation homeostasis characteristic of hypocoagulation syndrome have been established in patients with LC. COVID-19 infection in patients with LC leads to hypercoagulation, especially in patients with complicated stage of LC (ascites, encephalopathy, hepatorenal syndrome).
