Pathomorphological features of liver injury in patients with coronavirus disease, type 2 diabetes mellitus, and their comorbidity
DOI:
https://doi.org/10.26641/1997-9665.2025.2.29-36Keywords:
COVID-19, type 2 diabetes mellitus, liver, steatosis, fibrosis, thrombosis, inflammatory infiltration, pathological anatomy, comorbidityAbstract
Background. COVID-19, caused by the SARS-CoV-2 virus, is characterized by systemic organ involvement, with the liver being one of the primary targets. Comorbidity with type 2 diabetes mellitus (T2DM) significantly aggravates the clinical course and worsens the prognosis. Objective. To determine the pathomorphological features of liver injury in patients with COVID-19, T2DM, and their combination; to identify characteristic morphological changes; and to assess the impact of comorbidity on the morphological phenotype of hepatic alterations. Methods. A pathomorphological study was conducted on liver tissue samples from 120 deceased patients (40 in each group): Group I – COVID-19 + T2DM; Group II – COVID-19 without T2DM; Group III – T2DM without COVID-19. Standard methods of tissue fixation and staining were employed, as well as grading systems for steatosis (Brunt & Kleine) and fibrosis (METAVIR), followed by statistical analysis. Results and Conclusion. In patients with comorbid COVID-19 and T2DM, a toxico-metabolic morphological phenotype was identified, characterized by a combination of severe macrovesicular and microvesicular steatosis, centrilobular necrosis, advanced fibrosis (up to stage F4), pronounced congestion, a moderate incidence of thrombosis, and inflammatory infiltration observed in 50% of cases. This phenotype reflects a synergistic damaging effect of viral and metabolic factors on hepatocytes, the stromal-vascular component, and the hepatic immune microenvironment. In patients with COVID-19 without diabetes, a vascular-thrombotic injury phenotype was observed, characterized by a high frequency of microvascular thrombosis (62.5%), moderate necrosis, mild steatosis, minimal fibrosis, and inflammatory infiltration observed in 35% of cases. This pattern likely reflects acute endothelial dysfunction and coagulation imbalance, accompanied by moderate immune involvement. In patients with T2DM without COVID-19, a metabolically adaptive phenotype prevailed, characterized by mild to moderate steatosis, occasional foci of fibrosis, absence of necrosis, minimal microcirculatory disturbances, and less pronounced inflammatory infiltration (22.5%), indicating a chronic course. The comorbidity of COVID-19 and T2DM gives rise to a distinct morphological phenotype of liver injury that differs significantly from the changes observed in the isolated forms of each disease. These findings support the need for a personalized approach to clinico-morphological assessment and therapeutic strategy.
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