Obesity, non-alcoholic fatty liver disease, COVID-19: dangerous liaisons

Abstract

The pandemic of COVID-19 is changing the usual clinical practice. Most of the drugs used for the etiotropic and pathogenetic therapy of COVID-19 do not have a sufficient evidence base, approaches to therapy of liver, gastrointestinal tract and other body systems damage in the structure of COVID-19 and post COVID-19 syndrome are under development. Coronavirus infection is more severe in obese patients with associated diseases; the liver plays an important role in this process. Retrospective analysis of the medical histories of patients with a new coronavirus infection hospitalized in the clinic of North-Western State Medical University named after I.I. Mechnikov identified that 34.7% of patients were overweight, 51.3% obese, 77% abdominal obesity (alanine aminotransferase (ALAT) was on average 76.2 ± 58.8 U/L, aspartate aminotransferase (ACAT) 60.7 ± 48.6 U/L). At the time of hospitalization, increased transaminases was detected in 71% of patients and correlated with markers of the severe course of COVID-19 (the level of C-reactive protein, ferritin, % of blood oxygen saturation). In patients with severe new coronavirus infection, receiving therapy with JAK-kinase inhibitors and/or biological drugs, often was a significant increase of ALAT and ASAT up to 5–10 upper limits of the norm. In the process of histological examination of the liver tissue of patients who died of extremely severe course of infection, characteristic fatty degeneration of hepatocytes was revealed. Therapy with a multicomponent drug containing inosine, meglumine, methionine, nicotinamide and succinic acid contributed to a dynamic decrease of transaminases and an improvement in the course of the new coronavirus infection.

Keywords

• obesity
• abdominal obesity
• covid-19
• sars-cov-2
• hepatitis
• drug-induced hepatitis
• non-alcoholic fatty liver disease