Chronic Viral Hepatitis: Diagnosis and Therapeutics (Clinical Gastroenterology)

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Those who recover should acquire lifelong immunity. However, a subset of patients will be chronically infected and very few patients 0. In primary infection, HBsAg becomes detectable after 4 to 10 weeks of incubation period, followed by antibodies against the core antigen HBcAb in IgM form during early period [ 2 ]. Circulating HBeAg becomes detectable in most cases. When liver injury occurs in acute infection, alanine aminotransferase levels do not increase until after viral infection is well established, reflecting the time required to generate the T-cell-mediated immune response that triggers liver injury.

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Once this response has commenced, viral titer in blood and liver begins to drop. Age at the time of infection is a strong determinant of chronicity, the earlier the acquisition of infection, the higher probability of developing chronic infection. Levels of viremia in chronic infection are generally significantly lower than during primary infection.

In adult acquired disease, the early phase of infection often is accompanied by significant disease activity with elevated ALT levels versus those who acquired the infection perinatally usually have normal ALT levels. Many patients with perinatal infection enter the immunoactive phase and develop HBeAg positive chronic hepatitis with elevated ALT levels only after years of infection [ 13 ]. A key event in natural history of progression is HBeAg seroconversion to HBeAb with marked reduction of HBV replication followed by gradual histological improvement [ 14 ].

These individuals have a naturally occurring mutant form of HBV that does not produce HBeAg, due to a mutation in the precore or core promoter region. Most frequent precore mutation is a G-A change at nucleotide GA which creates a stop codon and results in loss of HBeAg synthesis; the most common core promoter mutation involves a 2 nucleotide substitution at nucleotide and [ 15 ]. HBeAg-negative carriers are a heterogeneous group and most of them have low viral DNA levels, relatively normal levels of alanine aminotransferase, and a fair prognosis.

HBeAg-negative chronic hepatitis B precore mutant emerges as the predominant species during the course of typical HBV infection with wild-type virus and is selected during the immune clearance phase HBeAg seroconversion [ 17 ]. The prognosis of the inactive carrier is generally good and well supported by long-term follow-up studies [ 20 , 21 , 22 ]. Recurrent episodes of reactivation or sustained reactivation can occur and contribute to progressive liver disease and decompensation.

Management of Hepatitis C: Evaluating Suitability for Drug Therapy

Frequently, HBV reactivation is usually asymptomatic, but it may mimic acute viral hepatitis. Apparently, women and older carriers have higher clearance of HBsAg. However, these flares in the immunosuppressed individuals rarely result in significant hepatic decompensation. However, cirrhosis and hepatoma are two major long-term complications of chronic HBV infection that significantly increases morbidity and mortality. In patients without cirrhosis, if untreated, the incidence of liver related death is low and ranges from 0 to 1.

In untreated individuals with predominantly HBeAg positive chronic hepatitis B, the incidence of cirrhosis ranges from 2 to 5. Also, older age and persistent viral replication are predictors for development of cirrhosis as well as mortality. Genotype C is associated with a higher risk of cirrhosis than genotype B based on studies in Asian patients [ 27 ]. The presence of any other independent hepatotoxic factors such as alcohol ingestion, HCV co-infection can contribute to progression to cirrhosis.

Once cirrhosis is established, individuals can decompensate over time.

[] Clinical studies and treatment of hepatitis C and B

The development of hepatocellular carcinoma HCC and liver failure are main cause of death from chronic hepatitis B. Various factors involving the host and the virus may contribute to the development of hepatocellular carcinoma Table 2. It is estimated that over , people die each year from the consequence of HBV infection [ 9 ].

Diagnosis of Management of Hepatitis C - Steven-Huy Han, MD - UCLA Primary Care Update 2015

HCC incidence is three to six times higher in males than in females, suggesting a tumorigenic effect of androgens [ 10 , 29 ]. Having a first degree relative with HCC, the presence of cirrhosis, and reversion activity are all thought to contribute to HCC development [ 10 , 29 , 30 , 31 ].

Chronically infected subjects have a times increased risk of hepatocellular carcinoma compare with non-carriers [ 20 ]. Hence, it is advocated that all HBV infected patients, regardless of cirrhosis status, should get screening for HCC every 6 months with alpha-fetoprotein AFP and liver sonogram. Currently, there is no consensus as to when such screening should commence, but it is reasonable to start screening immediately once these patients seek medical attention.

It has been encouraging to witness the recent discoveries in HBV infection with insights into the existence of genotype subgroups, mutant variants, knowledge regarding host, viral and environmental factors on the disease course, as well as advances in new treatment modalities. However, despite the much progress in understanding the natural history of HBV infection, we still have a long way to go before we can conquer hepatitis B infection. For instance, more studies are needed to clarify whether there is an association between genotype, mutant variants and the development of hepatocellular carcinoma.

In the HBeAg-positive subgroup, there still lacks a consensus on how to manage these patients when they present with signs of mild liver disease activity with alanine aminotransferase less than 2 fold increase; future studies with longer follow-up may help us gain knowledge about the HBV behavior in these individuals. There is much more to be understood about mutations and their impacts on the clinical course and long-term outcome of hepatitis B infection. For instance, it has been suggested that mutations can arise from vaccine-induced antibodies and this renders the immune response generated by the vaccination ineffective.

Therefore, mutations may play a key role in the difficulties of managing hepatitis B infection. Hence, further research and understanding in this sector may bring exciting new information and better understanding of the natural history of HBV and supplement our existing armamentarium to combat this persistent worldwide prevalent disease. Zhang has no disclosable financial arrangements or interest with any corporations.

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Viral Hepatitis

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Ann Intern Med. Natural history of HBV infection: a 9 years follow-up of the Dionysos cohort. Chronic viral hepatitis affect hundreds of millions of people worldwide, and each year millions more people become infected. In Chronic Viral Hepatitis, Second Edition, a panel of distinguished clinicians and clinical investigators build upon the first edition by comprehensively reviewing all the relevant new information regarding resistance, side effects, and therapies for chronic viral hepatitis. The text covers recent advances in the understanding of pathogenesis of viral hepatitis while discussing promising agents in development for its treatment.

The authors devote special attention to reactivation of hepatitis B with chemotherapy and immunosuppression, herbal and non-traditional therapies, chronic viral hepatitis in the pediatric population, and immunology and immunotherapy of HCV and provide relative costs for all diagnostic and therapeutic options. Authoritative and up-to-date, Chronic Viral Hepatitis, Second Edition offers today's gastroenterologists, internists, hepatologists, and infectious disease specialists a practical guide to the recognition, diagnosis and treatment of chronic viral hepatitis from a multidisciplinary approach.

The book does a remarkable job of presenting knowledge about chronic hepatitis of viral etiology to a general internal medicine audience. The purpose is to provide the reader with a comprehensive overview of the field of chronic viral hepatitis, with a focus on epidemiology, natural history, the problem of co-infections, and treatment.

Diagnosis and Therapeutics

The objectives are worthy of publication and do not duplicate recent book publications. The authors fully meet the objectives. The book is comprehensive yet not cumbersome and introduces the reader to a wide range of disciplines. Internists and gastroenterologists will reap great rewards from reading this book, but several chapters of the book also reach out to a larger audience. The editing is good, and the text is lucid, succinct, and comprehensive. There is even an interesting chapter on alternative medicine and treatment of chronic hepatitis.

This comprehensive approach to patient's health is generally typical of the book and is one of the features that make it stand out. Koff and Wu set out to construct a contemporary comprehensive overview of the field of chronic viral hepatitis. They gathered together 16 well-researched, well-written chapters by 14 preeminent senior hepatologists, and 16 associates.

References are abundant, and emphasis on higher quality published research is employed throughout.