Risk factors related to significant hepatic inflammation in patients with acute drug-induced liver injury

急性药物性肝损伤患者出现显著肝脏炎症的相关危险因素

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Abstract

BACKGROUND AND AIMS: Currently, research on biopsy-proven acute drug-induced liver injury (DILI) remains limited. This study aimed to identify clinical characteristics and risk factors for significant hepatic inflammation in patients with acute DILI. METHODS: An ambispective cohort study was conducted on biopsy-proven acute DILI patients admitted to our hospital from 2012 to 2018. Using the Scheuer scoring system, patients were categorized into G0-2 or G3-4 groups and followed up for 12 months after first admission. Clinical characteristics and outcomes were retrieved from medical records. RESULTS: The median age of the 157 enrolled patients (65.6% female) was 40.4 (interquartile range (IQR), 31.9-49.1) years. The median latency and length of hospitalization were 30.0 (IQR, 5.0-60.0) and 18.0 (IQR, 12.0-26.0) days. The proportions of patients in the G0-2 and G3-4 groups were 54.8% and 45.2%, respectively. Logistic regression analysis revealed that females (odds ratio (OR): 2.623, 95% confidence interval (CI): 1.169-5.887, p = 0.019), higher body mass index (OR: 1.168, 95% CI: 1.029-1.325, p = 0.016), higher total bilirubin (OR: 1.004, 95% CI: 1.000-1.007, p = 0.047), and lower prothrombin activity (OR: 0.976, 95% CI: 0,957-0.995, p = 0.013) were associated with significant hepatic inflammation. The predominance of the hepatocellular injury pattern (60.5%) at admission transformed into a predominance of the cholestatic pattern (60.5%) at discharge. During follow-up, 23 patients (14.6%) developed chronic DILI, with nine patients (5.7%) progressing to cirrhosis. Moreover, 15 female patients (9.6%) developed autoimmunity (3cases in the G0-2 group vs 12 cases in the G3-4 group, p < 0.05). CONCLUSION: Acute DILI patients with high-risk factors were more likely to develop significant hepatic inflammation, and females with significant inflammation were at a higher risk of developing autoimmunity during follow-up.

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