Plasma Multi-Omics Outlines the Association of Urobilinogen with Corticosteroid Nonresponse, Infl ammation and Intestinal Permeability in Severe Alcohol-related Hepatitis
Severe alcohol-related hepatitis (SAH) is a severe form of acute decompensation in alcoholic liver disease, marked by rapid onset of jaundice, malaise, anorexia, tender hepatomegaly and features of systemic infl ammatory response syndrome, with a 40% mortality rate at 90 days.
Corticosteroid therapy, the standard medical treatment, is effective in 60% of patients.
Lille’s score, an international assessment, employs bilirubin levels to evaluate corticosteroid response at day 7. However, metabolic by-products of bilirubin, including urobilinogen, remain unstudied in steroid nonresponse.
Urobilinogen, a metabolic by-product of bilirubin produced in the gut by bacteria, plays a role in a detrimental cycle, altering gut integrity, circulating into the bloodstream, activating neutrophils and modulating glucocorticoid response, inducing immune fl are.
Removal of bilirubin and its metabolic by-products, such as urobilinogen, from the bloodstream is crucial to controlling immune fl are in SAH patients.
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