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Both covert hepatic encephalopathy (CHE) and overt hepatic encephalopathy (OHE) impair the ability to operate machinery. The legal responsibilities of US physicians who diagnose and treat patients with hepatic encephalopathy vary among states. It is imperative that physicians know the laws regarding reporting in their state. OHE represents a neuropsychiatric impairment that meets general reporting criteria. The medical advisory boards of the states have not identified OHE as a reportable condition. In the absence of validated diagnostic guidelines, physicians are not obligated to perform tests for CHE. There is a need for explicit guidance from professional associations regarding this issue., (Copyright © 2015 Elsevier Inc. All rights reserved.)

In the direct-acting antiviral (DAA) era of hepatitis C virus (HCV) therapy, health care providers must be knowledgeable about genotype and subtype of HCV infection and interpretation of quantitative HCV viral assays to monitor treatment responses. They may also choose to assess interleukin 28B genotypes or resistance-associated variants after ineffective DAA therapy. DAA therapies require understanding of performance characteristics of quantitative HCV RNA assays and the definitions of terms used to report results. Only quantitative HCV RNA assays with a limit of detection of 10 to 15 IU/mL are appropriate for managing patients on DAA therapy., (Copyright © 2013. Published by Elsevier Inc.)

Chronic hepatitis C (CHC) is a leading cause of chronic hepatitis, cirrhosis, liver failure, and hepatocellular carcinoma (HCC) worldwide. Currently, pegylated interferon (Peg-IFN) and ribavirin therapy achieve curative responses in 40% to 80% of patients, depending on genotype. Recognition of new therapeutic targets for HCV therapy has led to development of novel therapies. The purpose of this review is to summarize the status of novel therapeutics for CHC that promise to increase the safety and efficacy of therapy., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Hepatitis C virus-Human immunodeficiency virus (HCV-HIV) coinfections are identified in up to 30% of patients infected with HIV and in 8% of patients infected with HCV. Now that progression of HIV and deaths due to AIDS can be prevented by highly active antiretroviral therapy (HAART), it is clear that HCV coinfection is associated with accelerated progression to cirrhosis and increased liver-related morbidity and mortality. Antiviral therapy with pegylated interferon and ribavirin for HCV in HCV-HIV coinfected patients is less successful than in patients with HCV monoinfection, and HAART can cause drug-induced liver injury. Multiple barriers limit the number of HCV-HIV coinfected patients who receive antiviral therapy for HCV, and the role of orthotopic liver transplantation (OLT) in HIV monoinfected and HCV-HIV coinfected patients remains controversial. Clinical trials of HCV-specific protease or polymerase inhibitors combined with pegylated interferon and ribavirin are needed urgently in coinfected patients, both before and after OLT., (Copyright © 2011 Elsevier Inc. All rights reserved.)

The hepatitis B virus (HBV) is an enveloped, hepatotrophic, oncogenic hepadnavirus that is noncytopathic for hepatocytes. HBV infection results in a variety of outcomes that are determined by the quality, quantity, and kinetics of the host innate and adaptive immune responses. Whether HBV infection is cleared or persists as a progressive or nonprogressive liver disease is determined by both viral and host factors. Replicative intermediates can persist in the liver under immunologic control after resolution of acute or chronic hepatitis B, conferring a risk for reactivation following a course of immunosuppression or chemotherapy.

AMA are detected in the serum of 92% to 95% of patients with PBC using indirect immunofluorescent methods. AIC is the term used to describe the 5% to 8% of AMA-negative PBC patients who uniformly have ANA and SMA. Recent applications of more sensitive and specific tests to detect serum AMA have shown that most, if not all, patients with AIC actually do have AMA. Emerging evidence that AMA and mitochondrial autoantigens play important roles in the immunopathogenesis of NSDC also suggests that AIC and PBC are likely to be a single disease, exhibiting variation in the types of autoantibodies and in both the concentrations and immunoglobulin isotypes of AMA.

Refinements in the understanding of the mechanisms of immunocyte activation and the emergence of new immunosuppressive agents with highly selective actions has created opportunities for improving the treatment of autoimmune hepatitis. Drugs, such as budesonide and deflazacort, may inhibit immunocyte activation and limit corticosteroid-related side effects. Agents, such as cyclosporine and tacrolimus, can impair calcineurin activity and restrict the generation of transcription factors necessary for T cell responses. Intravenous immunoglobulin can bind anti-idiotype antibodies and reduce interleukin-2 secretion, and monoclonal antibodies directed against critical components of the T cell activation cascade can dampen the immune reaction. Drugs, such as mycophenolate mofetil, cyclophosphamide, methotrexate, and KF20444, can inhibit T cell proliferation, and other interventions promise to deplete activated T cells, impair effector mechanisms, and induce self-tolerance.

Currently available evidence is insufficient to classify PBC and AIC as separate diseases. The ultimate answer to the question of whether AIC, defined as AMA-negative PBC with ANA or SMA, is a disease distinct from AMA-positive PBC with or without ANA will require a detailed comparison of etiologic factors and pathogenetic mechanisms, once they are elucidated. It is intriguing to consider the suggestion of Heathcote that the term autoimmune cholangitis be adopted to describe PBC with or without detectable AMA. However, it is improbable that the venerable term PBC will be supplanted. Hepatologists will probably continue to use the terms AIC and AMA-negative PBC interchangeably, with little risk of being misunderstood.