Drug-induced liver injury (DILI) remains one of the most challenging adverse drug reactions in clinical practice, particularly in its idiosyncratic form, which is not dose-dependent and is largely driven by host-specific immune and genetic factors. Recent genomic studies have revealed strong associations between certain human leukocyte antigen (HLA) alleles and susceptibility to DILI, supporting an immunogenetic mechanism in which drug or metabolite–protein adducts act as neoantigens, triggering aberrant T-cell activation and hepatocellular injury. This review summarizes current evidence on the contribution of HLA polymorphisms to the pathogenesis of idiosyncratic DILI, highlighting allele-specific risk patterns, such as HLA-B*57:01 associated with flucloxacillin, HLA-DRB1*15:01–DQB1*06:02 in amoxicillin–clavulanate, and HLA-B*35:02 in minocycline-induced liver injury. Furthermore, ethnic variability and allele-haplotype interactions are discussed as potential modulators of susceptibility and clinical phenotype. By integrating genetic and immunological insights, the identification of HLA signatures offers promising tools for precision medicine, enabling earlier identification of at-risk individuals and improved prevention of severe hepatotoxic reactions.

Background/Objectives: Objective end-product assessment of microsurgical anastomoses is intensive and partly subjective. Vision-capable large language models (LLMs) may enable standardized image-based scoring, but their agreement with expert assessment remains uncertain. Methods: We studied 200 end-to-end femoral artery anastomoses, performed on chicken legs by novice, intermediate, and experienced microsurgeons. Images were scored independently by two blinded expert panels; disagreements were adjudicated by a third senior reviewer to establish expert consensus. Two LLMs, ChatGPT 5.2 Thinking Extended and Gemini 3.1 Pro, were evaluated using the exact same prompt and rubric. Each image was analyzed three times per model. Final scores were aggregated by median for numeric items and majority vote for categorical items. The primary endpoint was exact-match agreement with expert consensus. Agreement within ±1 was also assessed for numeric items. Agreement was measured using simple percentage agreement, Light’s kappa, and Krippendorff’s alpha; Bland–Altman analysis was used for numeric count items. Results: LLM 1 achieved a higher overall exact-match agreement than LLM 2 (0.659 vs. 0.539). Both models performed better on categorical than numeric items (0.713 vs. 0.610 and 0.651 vs. 0.445, respectively). LLM 1 showed the greatest advantages for gaps, knots, oblique stitches, and wide bites. Krippendorff’s alpha was positive for most endpoints with LLM 1, whereas LLM 2 showed negative values throughout. Allowing a ±1 tolerance for numeric items greatly improved agreement, suggesting only minor counting discrepancies, from 0.610 to 0.900 for LLM 1 and from 0.445 to 0.826 for LLM 2. Conclusions: Under a constrained scoring workflow, LLMs partially approximated intraluminal microsurgical end-product scoring. LLM 1 outperformed LLM 2, but agreement remained insufficient to replace the expert assessment entirely. These models can be assistive tools within a human-in-the-loop framework.

Autoimmune liver diseases (AILD), including autoimmune hepatitis (AIH) and autoimmune sclerosing cholangitis (ASC), are rare but important causes of chronic liver disease in children. Although HLA-DRB1 alleles have been associated with disease susceptibility, their role in modulating the clinical phenotype and long-term outcome of pediatric AILDs remains incompletely understood. We aimed to characterize the distribution of HLA-DRB1 alleles and genotype combinations and describe the accompanying clinical features in a pediatric AILD cohort. Thirty children diagnosed with AIH-1 (n = 14), AIH-2 (n = 6), or ASC (n = 10) underwent HLA-DRB1 genotyping. Clinical presentation, fibrosis stage, treatment response, and associated autoimmune diseases were retrospectively analyzed. The most frequent alleles copies were HLA-DRB1*03 (n = 15), predominantly identified in AIH, and HLA-DRB1*13 (n = 14), identified in both AIH and ASC. Genotype combinations involving these alleles were observed across a broad spectrum of clinical presentations, fibrosis stages, treatment responses, and extrahepatic autoimmune manifestations. In this small cohort, HLA-DRB1*14-containing genotypes were observed in several patients with severe disease features, including advanced fibrosis, cirrhosis, treatment-refractory disease, and ulcerative colitis. Patients carrying HLA-DRB1*11, HLA-DRB1*15, or HLA-DRB1*16 had favorable hepatic outcomes despite severe initial presentation or associated extrahepatic autoimmune manifestations; however, the number of carriers was small. Clinical features varied among patients carrying different genotype combinations; however, the independent contribution of the accompanying allele could not be assessed. Our findings illustrate marked clinical heterogeneity among children carrying different HLA-DRB1 alleles and genotype combinations. In this exploratory cohort, selected HLA-DRB1 combinations co-occurred with distinct clinical patterns. HLA profiling may have a role in future risk stratification and individualized follow-up of children with AILD, but these observations are hypothesis-generating, they do not support genotype-based clinical management and require validation in larger, multicenter cohorts.

Autoimmune hepatitis (AIH) is a progressive inflammatory liver disease characterized by hypergammaglobulinemia, circulating antibodies, and distinctive histological features, with a higher prevalence in females. Immune responses targeting hepatic antigens are considered the main mechanism behind AIH. Many cytokines are involved in the inflammatory response typical of this disease. Interleukin 17 (IL-17) is a powerful pro-inflammatory protein that serves as a key link between the innate and adaptive immune systems. It plays an important role in regulating the inflammatory response in various tissues, including the liver. Several studies have shown that increased IL-17 levels are associated with the severity and progression of AIH. This review explores IL-17’s role in the AIH inflammatory pathway and summarizes existing evidence linking it to liver damage. We also highlight the potential of future therapies targeting this cytokine.