Alcohol-associated hepatitis (AH) is the most severe form of alcohol-related liver disease. The natural course of alcohol-related liver disease is influenced by heavy alcohol consumption and abstinence periods. Differentiating between AH and decompensated cirrhosis (DC) could be extremely challenging in clinical practice due to clinical and bioclinical similarities. The severity of AH is made on bioclinical grounds, the severe form necessitating corticotherapy treatment. Liver biopsy is still the standard of care for establishing the diagnosis in atypical presentations. The pathogenesis of AH is an interplay between gene expression, cytokine dysregulation, the immune system and the gut microbiota. Non-invasive tests are increasingly and widely used for the purpose of early diagnosis and reliable prognostication. The non-invasive tests are emerging in concordance with disease pathogenesis. In this review, we describe the non-invasive tools that can distinguish AH from DC. We outline the available cut-offs and their performance in diagnosis and prognosis, as well as in assessing the treatment response to corticotherapy. Promising circulating biomarkers like keratin 18, microRNAs and sphingolipids will be in the review.

Background and Aims: Severe alcoholic hepatitis is characterized by an increased risk of infections. Polymorphisms in immune response-related genes may influence susceptibility to infections in alcoholic hepatitis. This study aimed to investigate the association between two clusters of differentiation 14’s (CD14) single nucleotide polymorphisms (SNPs), rs2569190 and rs5744455, and the occurrence of infections in severe alcoholic hepatitis, the response to corticotherapy and the mortality rates at one and three months. Methods: Patients with severe alcoholic hepatitis were genotyped for CD14 - rs2569190 and rs5744455 SNPs. Genotype and allele frequencies were compared between patients who presented infections and those who did not. Results: A total of 97 patients with biopsy proven sAH were included in the study, out of which 47 (48.4 %) had an associated infection. rs5744455 SNP was significantly associated with the presence of infection. Patients carrying the rs5744455T variant allele had a lower incidence of infections compared to those with the wild-type allele (32% vs 68%; p=0.002). In contrast, the rs2569190 SNP revealed no significant differences, either in the single genotype analysis (p=0.608) or under a dominant model (p=0.318). Community-acquired infections were primarily urinary tract infections (21.65%), followed by pulmonary infections (4.12%), with Escherichia coli responsible for 41.67% of cases. Healthcare-associated infections were more varied, including urinary tract (7.22%), respiratory (6.19%), digestive (7.21%), cutaneous (3.09%), and blood infections (5.15%). Klebsiella pneumoniae was the most prevalent strain, accounting for 16.67% of these infections. Conclusions: Our findings highlight a potential protective role of the CD14 rs5744455T variant allele against infections in sAH, suggesting that genetic variability may influence infection susceptibility in this population.