Abstract
BACKGROUND: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a common form of chronic liver disease, found in more than a quarter of the world's population. People with MASLD are at a high risk of acquiring severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. The risk of a mild cold turning into severe pneumonia is also high. The aim of our study was to evaluate the effect of MASLD as a risk factor for the severity of coronavirus disease-associated pneumonia (COVID-AP). METHODS: Our prospective, Russian cohort study included 100 adults (≥18 years old), of any sex, with COVID-AP. The SARS-CoV-2 infection was confirmed on nucleic acid amplification or using the SARS-CoV-2 antigen tests. Any possible secondary causes of liver steatosis were excluded, and alcohol consumption was assessed. The presence of significant hepatic steatosis (more than 30%) was estimated from computed tomography (CT) results. RESULTS: Based on the presence of significant steatosis, in combination with other metabolic factors, two groups were formed: 25 patients with MASLD and 74 patients without significant steatosis, serving as controls. One patient was excluded from the MASLD group due to alcohol abuse. The two groups were comparable by sex (P=0.58) and age (P=0.96). Body mass index (BMI) (P<0.001), waist circumference (P<0.001), and obesity rate (P=0.001) were significantly higher in the MASLD group. Presence of hypertension (HTN) (P=0.52) and type 2 diabetes mellitus (T2DM) (P=0.06) were comparable in the two groups. Based on the initial higher volume of lung damage upon admission (P=0.04), an increase in lung damage during standard glucocorticosteroid therapy and an anticoagulant drug (P=0.01), the higher levels level of C-reactive protein (P=0.01), and the need for biological therapy, pneumonia in the MASLD group was more severe compared with the control group. The relationship between the biological therapy and metabolic factors variables had an odds ratio (OR) of 11.4; P<0.001 for hepatic steatosis and of 2.3; P=0.046 for obesity. No association with T2DM (P=0.61) and HTN was found (P=0.76). To eliminate the possible interaction between obesity and hepatic steatosis, the Mantel-Hensel test was used. The adjusted OR for steatosis was 10.2; P=0.001 and for obesity the OR was 1.39; P=0.49. The need for antibiotic therapy was associated with the significant presence of steatosis (OR =3.1; P=0.02) and T2DM (OR =6.8; P=0.008), adjusted OR for steatosis was 2.6; P=0.057. The duration of hospitalisation between the two groups was comparable (P=0.07). Mortality was significantly increased in the MASLD group (P=0.02). CONCLUSIONS: Liver steatosis, regardless of other metabolic risk factors, increased the need for biological therapy, whereas the need for antibiotic therapy was a consequence of T2DM. Our study showed a more severe course of COVID-AP in people with MASLD and higher mortality.