Fagan O, Armstrong P, Merwe KVD, Crosnoi D, Steele C, Sopena-Falco J, Parihar V. Viral hepatitis: A brief introduction, review of management, advances and challenges. World J Meta-Anal 2021; 9(2): 139-152 [DOI: 10.13105/wjma.v9.i2.139]
Corresponding Author of This Article
Vikrant Parihar, MBBS, MD, MRCP, Consultant Physician-Scientist, Department of Gastroenterology, Letterkenny University Hospital, Kilmacrennan Road, Letterkenny F92 AE81, Ireland. vikpar37@yahoo.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Minireviews
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This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Viral suppressive therapy (see criteria for commencement of treatment below)
Eradication therapy DAA (gold standard)
PEG-IFN (sparse data)
Supportive
Table 2 Diagnosing hepatitis A-E
Hepatitis
Serological testing
Molecular testing (via PCR), quantitative
A
Anti-HAV IgM (acute); Anti-HAV IgG (previous infection, vaccination); Note incubation period of 28 d[92]
HAV RNA
B
Anti-HBc (contact with HBV infection); HBsAg (current infection) appears 1-3 wk post exposure, duration > 24 wk denotes chronicity; Anti-HBS (vaccination, cleared HBV infection); HBeAg (high replication phase (> 10000 IU/mL); Anti-HBe (low replication phase (< 10000 IU/mL); Note incubation 90 d (ranges 45-160 d); Window period 1: first about 8 d of infection; Window period 2: clearance of HBsAg during this period Anti-HBc IgM is detectable[93]
Table 3 European Association for the Study of the Liver 2017 clinical practice guidelines on the management of hepatitis B virus infection[12]
Clinical practice guidelines
All patients with HBeAg-positive or -negative chronic hepatitis B, defined by HBV DNA (2000 IU/mL, ALT) upper limit of normal (ULN) and/or at least moderate liver necroinflammation or fibrosis, should be treated (Evidence level I, grade of recommendation 1)
Patients with compensated or decompensated cirrhosis need treatment, with any detectable HBV DNA level and regardless of ALT levels (Evidence level I, grade of recommendation 1)
Patients with HBV DNA (20000 IU/mL, and ALT) 2 × ULN should start treatment regardless of fibrosis degree (Evidence level II-2, grade of recommendation 1)
Patients with HBeAg-positive chronic HBV infection, defined by persistently normal ALT and high HBV DNA levels, may be treated if they are older than 30 years regardless of the severity of liver histological lesions (Evidence level III, grade of recommendation 2)
Patients with HBeAg-positive or HBeAg-negative chronic HBV infection and family history of HCC or cirrhosis and extra-hepatic manifestations can be treated even if typical treatment indications are not fulfilled (Evidence level III, grade of recommendation 2)
Table 4 Comparing pegylated-interferon therapy to nucelos(t)ide analogues therapy
PEG-IFN
NA
Route of administration
Subcutaneous
Oral
Length of treatment
48 wk
Long-term in chronic HBV (stopping may be considered in some cases[13]); 8-16 wk in HCV