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INTRODUCTION:In the published studies of early liver transplantation (LT) for alcohol-associated hepatitis (AH), patients with a prior liver decompensation are excluded. The appropriateness of this criteria is unknown.Methods:Among 6 American Consortium of Early Liver Transplantation for Alcohol-Associated Hepatitis sites, we included consecutive early LT for clinically diagnosed AH between 2007 and 2020. Patients were stratified as first vs prior history of liver decompensation, with the latter defined as a diagnosis of ascites, hepatic encephalopathy, variceal bleeding, or jaundice, and evidence of alcohol use after this event. Adjusted Cox regression assessed the association of first (vs prior) decompensation with post-LT mortality and harmful (i.e., any binge and/or frequent) alcohol use.Results:A total of 241 LT recipients (210 first vs 31 prior decompensation) were included: median age 43 vs 38 years (P = 0.23), Model for End-Stage Liver Disease Sodium score of 39 vs 39 (P = 0.98), and follow-up after LT 2.3 vs 1.7 years (P = 0.08). Unadjusted 1- and 3-year survival among first vs prior decompensation was 93% (95% confidence interval [CI] 89%–96%) vs 86% (95% CI 66%–94%) and 85% (95% CI 79%–90%) vs 78% (95% CI 57%–89%). Prior (vs first) decompensation was associated with higher adjusted post-LT mortality (adjusted hazard ratio 2.72, 95% CI 1.61–4.59) and harmful alcohol use (adjusted hazard ratio 1.77, 95% CI 1.07–2.94).DISCUSSION:Prior liver decompensation was associated with higher risk of post-LT mortality and harmful alcohol use. These results are a preliminary safety signal and validate first decompensation as a criterion for consideration in early LT for AH patients. However, the high 3-year survival suggests a survival benefit for early LT and the need for larger studies to refine this criterion. These results suggest that prior liver decompensation is a risk factor, but not an absolute contraindication to early LT.

The global burden of viral hepatitis remains substantial despite advances in antiviral therapy and effective vaccines. There are five hepatitis viruses (hepatitis A, B, C, D, and E). Mortality related to hepatitis B virus and hepatitis C virus infections is among the top four global infectious diseases, together with human immunodeficiency virus infection, malaria, and tuberculosis. Of those deaths, approximately 47% are attributable to hepatitis B virus, 48% to hepatitis C virus and the remainder to hepatitis A virus and hepatitis E virus. Ending hepatitis epidemics as a major public health threat is feasible with the tools and approaches currently available. Effective vaccines are available for preventing viral hepatitis A, B and E infections. New oral, well-tolerated treatment regimens for chronic hepatitis C patients can achieve cure rates of over 90%. Effective treatment is also available for people with chronic hepatitis B virus infection; although for most people such treatment needs to be long-term, and recent advanced aim at a "functional cure" of hepatitis B. In this review article, we discuss the most recent advances of the diagnosis and treatment of viral hepatitis.

Background:Copper is a mineral that is absorbed in the stomach, duodenum, and jejunum. Gastric bypass surgery, gastrectomy, and short-bowel syndrome commonly lead to copper malabsorption. Copper deficiency primarily presents with hematological and neurological sequelae, including macrocytic anemia and myelopathy. Although hematological disturbances often correct with copper supplementation, neurological manifestations of copper deficiency may be irreversible. We present the case of copper deficiency secondary to malabsorption and management strategies to prevent irreversible neurological sequelae. Presentation: A 48-year-old female with a history of hypothyroidism, ischemic stroke, and Crohn's disease, complicated by subtotal colectomy and small-bowel resections, was admitted for fatigue and progressive neurological deficiencies. Her vital signs were stable, and physical examination was remarkable for weakness of both upper and lower extremities, ataxia, and upper extremities paresthesia. Computed tomography scan of the head without contrast was unremarkable. Magnetic resonance imaging enterography revealed a focal area of narrowing of the remaining small bowel. Copper level was low at 39 μg/dL. After 5 days of intravenous replacement using trace element within parenteral nutrition, her copper level corrected to 81 μg/dL. Her ataxia improved after intravenous copper supplementation and did not recur. Conclusions: Our patient presented with copper deficiency secondary to malabsoprtion. This case highlights the importance of copper testing in the bariatric surgery population and in patients with short-bowel syndrome. Given the irreversible nature of neurological symptoms when compared with the expense of nutrition supplements, routine copper testing should be considered in patients with malabsorptive states or altered anatomy, regardless of initial presentation.