Chronic hepatitis B (CHB) is one of the important public health problems worldwide. Major advances have been made in the treatment of CHB during the past several years. This article systemically reviews advances in the application of HBV DNA quantitation and three approved drugs for HBV treatment, and presents an updated and practical clinical approach to managing CHB. Highly sensitive PCR-based quantitation of HBV DNA makes it possible to precisely determine pre-treatment HBV load and monitor HBV DNA response during treatment. HBV DNA level, HBeAg status, degree of hepatic histological activity and fibrosis, and serum transaminases are the most important parameters in determining indication, regimen, and duration of HBV treatment. Although interferon alfa-2b, lamivudine, and adefovir are all approved as initial HBV treatment, understanding the advantages and advantages of each agent is important in choosing the best treatment for each individual patient with CHB.

There are two discrete forms of steatosis that may be found in patients infected with hepatitis C virus (HCV). Metabolic steatosis can coexist with HCV, regardless of genotype, in patients with risk factors such as obesity, hyperlipidemia, and insulin resistance. The second form of hepatic steatosis in HCV patients is a result of the direct cytopathic effect of genotype 3 viral infections. There have been proposed mechanisms for this process but it remains elusive. Both categories of steatosis tend to hasten the progression of liver fibrosis and therefore prompt recognition and management should be initiated in patients with HCV and steatosis. The authors review the current understanding of the relationship between hepatitis C infection and hepatic steatosis and discuss future research directions.

Chronic hepatitis B continues to be a global problem, with an estimated 240 million cases according to the World Health Organization. Chronic infection with the hepatitis B virus (HBV) is associated with cirrhosis, hepatic decompensation, and hepatocellular carcinoma. There are currently several US Food and Drug Administration-approved medications for treating chronic hepatitis B, with Lamivudine (LAM) being the first oral agent made available. The major problem with LAM is significantly decreased effectiveness over time due to the development of anti-HBV resistance that can lead to virologic and biochemical breakthrough as well as hepatitis B flare, progression of liver disease, and decompensation of pre-existing cirrhosis. Despite its high anti-HBV resistant rate, LAM remains widely used in underdeveloped countries due to its wide availability and low cost compared to other antiviral medications, including those that are more effective. Therefore, it is still clinically important to learn how to prevent and treat LAM resistant strains of HBV. Several regimens with the other available antiviral agents have been studied, including switching to monotherapy with either Adefovir, Entecavir, or Tenofovir, adding Adefovir to LAM, and switching to a combination of Adefovir and Entecavir. This review article will examine molecular mechanisms and diagnosis of LAM anti-HBV resistance, risks for and approaches to reduce LAM anti-HBV resistance, and currently available rescue therapy regimens for LAM resistance.

Hepatitis C virus (HCV) infection is a major public health problem and a leading cause of chronic liver disease. Chronic HCV infection often follows a progressive course over years and can result in cirrhosis, hepatocellular carcinoma, and need for liver transplantation. In the United States alone, the estimated prevalence of HCV infection is up to 5.1 million persons. The optimal approach to detecting HCV infection is to screen persons for possible history of risks of exposure to virus and to test those selected individuals with risk factors. Both host and viral factors may be important contributors to the natural history of HCV. Currently, effective pharmacologic therapy are available to induce sustained virologic response (SVR) or virologic "cure," which results in improved morbidity and mortality. Patient education before treatment is essential and should include a full discussion of potential side effects. It is important to work collaboratively and closely with patients to ensure early recognition of adverse events and to effectively manage them in order to ensure treatment compliance. This paper provides a thorough overview on screening for the diagnosis, clinical management, and treatment indications and contraindications for chronic hepatitis C.

Chronic Hepatitis C virus (HCV) infection carries a significant clinical burden in the United States, affecting more than 4.6 million Americans. Untreated chronic HCV infection can result in cirrhosis, portal hypertension, and hepatocellular carcinoma. Previous interferon based treatment carried low rates of success and significant adverse effects. The advent of new generation oral antiviral therapy has led to major improvements in efficacy and tolerability but has also resulted in an explosion of data with increased treatment choice complexity. Treatment guidelines are constantly evolving due to emerging regimens and real world treatment data. There also still remain subpopulations for whom current treatments are lacking or unclearly defined. Thus, the race for development of HCV treatment regimens still continues. This review of the current literature will discuss the current recommended treatment strategies and briefly overview next generation agents.

Direct acting antiviral treatment (DAA) has been the standard of care for hepatitis C virus (HCV) infection, but its long-term benefits in alanine aminotransferase (ALT) and aspartate aminotransferase (AST) improvement and hepatic fibrosis assessed by aspartate aminotransferase-to-platelet ratio index (APRI) and Fibrosis-4 index (FIB-4) scores remain unknown. The purpose of the present study was to assess DAA's long-term benefits, including frequencies of posttreatment week 96 ALT/AST < 30 (males)/19 (females) (<30/19), improvement of APRI and FIB-4 scores, and the associated factors. This was a single-center, retrospective study on 157 patients with HCV with DAA-mediated sustained virological response (SVR) 12. At posttreatment week (post-Rx wk) 96, 75.4% had ALT < 30/19; 62.7%, AST < 30/19; and 60.1%, both ALT/AST < 30/19. ALT/AST < 30/19 at post-Rx wk 96 was associated with ALT/AST < 30/19 at post-Rx wk 12 (p = 0.026), independently of Child-Turcotte-Pugh < 6 (p = 0.862), platelets ≤ 120 × 10⁹ /L (p = 0.343). Improvement rates of APRI < 0.5 and FIB-4 < 1.45 from baseline to post-Rx wk 96 were from 30.9% to 80.5%, and from 23% to 37.8%, respectively. Both APRI and FIB-4 improvement was associated with both ALT/AST < 30 (males)/19 (females) at post-Rx wk 12 (p = 0.012 and 0.011, respectively). Conclusion: The present study showed that DAA-mediated SVR12 in patients with HCV resulted in (1) high and durable rates of ALT (75.4%), AST (62.7%), and both ALT/AST (60.1%) < 30/19, and (2) high rates of APRI < 0.5 (80.5%) and FIB-4 < 1.45 (37.8%) at post-Rx wk 96, demonstrated clinical value of ALT/AST < 30/19 and excellent long-term outcomes of DAA-mediated SVR12 in these patients.

Background and Aims: Hepatitis C virus (HCV) infection results in hepatocytic injury with elevation of both alanine aminotransferase (ALT) and aspartate aminotransferase (AST). It remains to be determined if direct-acting antiviral treatment can terminate hepatocytic injury following virologic response. To this end, we evaluated the pattern and predicting factors of ALT and AST normalization during and after direct-acting antiviral treatment with sustained virologic response at 12 weeks (SVR12). Methods: Single-center retrospective study on 115 HCV-infected patients who achieved SVR12 was performed. Results: At treatment week 2, 100% and 45.9% showed decline in HCV RNA to <700 IU/mL and undetectable levels, respectively, and this was associated with 85.5%, 83.9% and 77.4% ALT normalization, AST normalization and ALT and AST normalization. At end of treatment, 85.6% of patients with baseline elevation of both ALT and AST had normalization of both ALT and AST. At posttreatment weeks 12 and 24, 90.8% and 94.8% had normalization of both ALT and AST. HCV clearance also resulted in further decline of both ALT and AST in those with baseline <40 IU. Univariate analysis showed baseline Child-Pugh score of <6, model for end-stage liver disease score of <10, HCV genotype 1, and HCV RNA of <500 IU/mL at treatment week 2 were associated with sustained normalization of both ALT and AST at posttreatment week 12. On multivariate analysis, baseline model for end-stage liver disease score of <10 was significantly associated with normalization of both ALT and AST at posttreatment week 12, independent of baseline Child-Pugh score <6, HCV genotype 1, and HCV RNA of <500 IU/mL at treatment week 2. Conclusions: During direct-acting antiviral therapy, 85.5% and 83.9% had normalization of both ALT and AST as early as in week 2, providing biochemical evidence of hepatocytic injury resolution. Sustained normalization of both ALT and AST was seen in 90.8% at posttreatment weeks 12, and was independently associated with baseline model for end-stage liver disease score of <10.

Hepatitis C virus (HCV) infection is a major worldwide public health concern. It is a common cause of chronic liver disease and hepatocellular carcinoma. HCV antibody and HCV RNA testing are available diagnostic studies that offer high degree of accuracy. Current standard therapy includes a combination of pegylated interferon and ribavirin. Response rate is approximately 40% for genotype 1 and 80% for genotypes 2 and 3, respectively. Successful treatment can stop the progression of chronic liver disease, reduce the need for liver transplantation, and possibly decrease the risk for Hepatocellular carcinoma (HCC). Evaluating for potential treatment candidacy is an important initial step in the management of chronic HCV infection as not all individuals may need or qualify for the treatment. Understanding the natural history, the different diagnostic modalities, the current therapeutic options and, the treatment response and adverse effect profiles can help the practitioners better manage chronic HCV infection.

Chronic Hepatitis C virus (HCV) infection carries a significant clinical burden in the United States, affecting more than 4.6 million Americans. Untreated chronic HCV infection can result in cirrhosis, portal hypertension, and hepatocellular carcinoma. Previous interferon based treatment carried low rates of success and significant adverse effects. The advent of new generation oral antiviral therapy has led to major improvements in efficacy and tolerability but has also resulted in an explosion of data with increased treatment choice complexity. Treatment guidelines are constantly evolving due to emerging regimens and real world treatment data. There also still remain subpopulations for whom current treatments are lacking or unclearly defined. Thus, the race for development of HCV treatment regimens still continues. This review of the current literature will discuss the current recommended treatment strategies and briefly overview next generation agents.

Background and Aims: Hepatitis C virus (HCV) infection results in hepatocytic injury with elevation of both alanine aminotransferase (ALT) and aspartate aminotransferase (AST). It remains to be determined if direct-acting antiviral treatment can terminate hepatocytic injury following virologic response. To this end, we evaluated the pattern and predicting factors of ALT and AST normalization during and after direct-acting antiviral treatment with sustained virologic response at 12 weeks (SVR12). Methods: Single-center retrospective study on 115 HCV-infected patients who achieved SVR12 was performed. Results: At treatment week 2, 100% and 45.9% showed decline in HCV RNA to <700 IU/mL and undetectable levels, respectively, and this was associated with 85.5%, 83.9% and 77.4% ALT normalization, AST normalization and ALT and AST normalization. At end of treatment, 85.6% of patients with baseline elevation of both ALT and AST had normalization of both ALT and AST. At posttreatment weeks 12 and 24, 90.8% and 94.8% had normalization of both ALT and AST. HCV clearance also resulted in further decline of both ALT and AST in those with baseline <40 IU. Univariate analysis showed baseline Child-Pugh score of <6, model for end-stage liver disease score of <10, HCV genotype 1, and HCV RNA of <500 IU/mL at treatment week 2 were associated with sustained normalization of both ALT and AST at posttreatment week 12. On multivariate analysis, baseline model for end-stage liver disease score of <10 was significantly associated with normalization of both ALT and AST at posttreatment week 12, independent of baseline Child-Pugh score <6, HCV genotype 1, and HCV RNA of <500 IU/mL at treatment week 2. Conclusions: During direct-acting antiviral therapy, 85.5% and 83.9% had normalization of both ALT and AST as early as in week 2, providing biochemical evidence of hepatocytic injury resolution. Sustained normalization of both ALT and AST was seen in 90.8% at posttreatment weeks 12, and was independently associated with baseline model for end-stage liver disease score of <10.