Medscape is available in 5 Language Editions – Choose your Edition here.


Hepatitis A Treatment & Management

  • Author: Richard K Gilroy, MBBS, FRACP; Chief Editor: BS Anand, MD  more...
Updated: Jan 28, 2016

Approach Considerations

Treatment generally involves supportive care, with specific complications treated as appropriate. Liver transplantation, in selected cases, is an option if the patient has fulminant hepatic failure (FHF).

Patients at risk of developing acute hepatitis A virus (HAV) infection should undergo immunization for the virus. In addition, immunization of those at greater risk for morbidity from acute HAV infection is important.

A German study of immunization rates in patients with autoimmune liver disease identified that seroconversion rates in this population were lower; however, more importantly, the study identified that vaccination was not offered to a large proportion of this population.[18] It is not difficult to identify a low risk-benefit ratio in patients with chronic liver disease, and the author recommends vaccination for HAV in all who have no contraindication.

The advent of new antiviral agents, such as direct-acting antivirals (DAAs) and host-targeting agents (HTAs), has expanded the potential therapeutic options available against HAV.[19] Kanda et al noted that amantadine and interferon-lambda 1 (IL-29) inhibit HAV internal ribosomal entry site (IRES)-mediated translation and HAV replication, whereas Janus kinase (JAK) inhibitors inhibit La protein expression, HAV IRES activity, and HAV replication.[19]

See the following for more information:


Supportive Care

For acute cases of HAV infection, therapy is generally supportive, with no specific treatment of acute uncomplicated illness. Locating the primary source and preventing further outbreaks are paramount. Initial therapy often consists of bed rest. The patient should probably not work during the acute phase of the illness.

Nausea and vomiting are treated with antiemetics. Dehydration may be managed with hospital admission and intravenous (IV) fluids. In most instances, hospitalization is unnecessary. The majority of children have minimal symptoms; adults are more likely to require more intensive care, including hospitalization.

About 3-8% of cases of fulminant hepatic failure (FHF) are caused by HAV; however, only 1-2% of HAV infections in adults lead to FHF. Refer patients with FHF to facilities with expertise in liver transplantation.

Acetaminophen may be cautiously administered but is strictly limited to a maximum dose of 3-4 g/day in adults. Other treatments are directed by specific complications.


Liver Transplantation

Patients with fulminant hepatic failure (FHF) are considered for liver transplantation. Recurrent disease after liver transplantation has not been reported. Patient selection for liver transplantation may be difficult, in that 60% of patients recover from FHF without needing the transplant (much as with acetaminophen toxicity), and predicting who needs this life-saving procedure is difficult.

Late referral has ominous implications, with the accompanying comorbidities (eg, renal failure, coagulopathy, cerebral edema) and waiting times contributing to poor outcomes.

Liver transplantation for chronic relapsing HAV infection has occurred in the context of decompensation with good results; however, there is a report of clinical recurrence after liver transplantation.


Postexposure Prophylaxis

Passive immunization with Gammagard reduces infection when administered within 14 days of exposure (ie, postexposure prophylaxis). Recommendations for providing postexposure prophylaxis are developed on the basis of risk.

Postexposure prophylaxis is recommended for nonimmunized close contacts of those recently diagnosed with acute HAV infection. The appropriate public health authority should be notified after a diagnosis of HAV infection, and the process of contact tracing should be initiated. In the United States, as many as 10% of cases of acute HAV infection are seen in commercial food handlers. In any suspected food handler transmission, it is imperative that health department officials be notified immediately.

In many instances, preexposure prophylaxis has been somewhat replaced by immunization (see Immunization). For travelers, cost-benefit analysis suggests that vaccination is preferred over gamma globulin when an extended stay in the area of risk (ie, high endemicity) is longer than 3 months or when repeat travel to the area (ie, >2 visits outside a 3-mo period) is likely.



Vaccination is highly effective at preventing HAV disease. The efficacy of the hepatitis A vaccine ranges from 80% to 100% after 1-2 doses compared to placebo. Current dosing recommendations are available (see Medication).

Immunization is indicated for individuals traveling to areas of high endemicity who have less than 2 weeks before departure. Both the vaccination and intramuscular (IM) immunoglobulin should be administered to provide long-term immunity, particularly in persons who intend to travel to these areas repeatedly.

People with chronic liver disease of any cause should consider hepatitis A vaccination. Response rates in patients with advanced liver disease and in those on immunosuppressive therapies are likely to be lower. The potentially disastrous outcome of acute HAV infection in this group cannot be overemphasized.

Hepatitis A vaccination in some low-risk groups who are potential sources of larger outbreaks of infection (eg, food handlers) has been implemented by some employers, although cost-benefit analysis for the employer does not seem to support such measures.

Epidemiologic studies of current and historical information related to hepatitis A infection patterns and risk factors show strong associations between socioeconomic improvement, increased water and sanitation, and decreasing HAV infection rates.[20, 21]

Areas in which a transition of epidemic hepatitis A (childhood acquisition very high) to endemic hepatitis A is occurring will likely lead to an increase in adult-acquired infections and the morbidity associated with this in the absence of vaccination programs.

An excellent illustration of why this is likely is that the most prevalent risk factor for HAV acquisition in the United States is international travel.[22] This study also lends further support to the importance of vaccination for international travelers. Hepatitis A is the most frequent vaccine-preventable disease in travelers, and it has the highest mortality and morbidity rates for any vaccine-preventable infection in travelers.[23, 24, 25]

The global burden of acute cases of hepatitis A is changing and certainly is decreasing in Western societies.[20] In the United States, vaccination programs targeting children during urban outbreaks have demonstrated significant benefits.[26, 27] Immunization programs applied to high-risk groups show morbidity and cost benefits. Approximately 20% of individuals with acute HAV infection may require hospitalization.

A 2012 Cochrane review of 9 studies including 732,380 participants reaffirmed the benefit of pre-exposure vaccination. Data from the review show that both the inactivated and live attenuated vaccines were effective for pre-exposure prophylaxis and that either vaccine provided approximately a 10-fold reduction in acute infections when compared to placebo. An interesting subgroup analysis of quality studies showed that if infections were to occur they occurred in the first year. In addition, pre-exposure prophylaxis was cost-effective and shared comparable risk of non-serious local and systemic adverse events in those receiving the inactive vaccine compared to those receiving the placebo. However, there were insufficient data on the safety of the live attenuated vaccine to render conclusions on safety and efficacy over time.[28]

Global immunization appears to be prohibitively expensive. The hepatitis A vaccine is not yet licensed for use in persons younger than 2 years.


Diet and Activity

Encourage patients to have an adequate diet. Patients should avoid alcohol and medications that may accumulate in liver disease. Otherwise, no specific dietary restrictions are necessary.

Bed rest during the acute illness may be important, although data to support this practice are lacking. Restricting transmission is important, especially in the early phases of the illness. Returning to work should probably be delayed for 10 days after the onset of jaundice.



Control at the source, with treatment of contacts to prevent further cases of disease is the primary goal. Long-term secondary goals include immunization, which increases herd immunity and reduces the likelihood of further outbreaks in high-risk communities. Education about transmission and prevention of transmission (eg, hand washing, safe food sources) is also important.

Contributor Information and Disclosures

Richard K Gilroy, MBBS, FRACP Associate Professor, Medical Director of Liver Transplantation and Hepatology, Department of Internal Medicine, Kansas University Medical Center

Disclosure: Received salary from gilead, NPS pharmaceuticals, salix pharmaceuticals, AbbVie for speaking and teaching.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Additional Contributors

George Y Wu, MD, PhD Professor, Department of Medicine, Director, Hepatology Section, Herman Lopata Chair in Hepatitis Research, University of Connecticut School of Medicine

George Y Wu, MD, PhD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, American Medical Association, American Society for Clinical Investigation, Association of American Physicians

Disclosure: Received consulting fee from Springer for consulting; Received consulting fee from Gilead for review panel membership; Received honoraria from Vertex for speaking and teaching; Received honoraria from Bristol-Myers Squibb for speaking and teaching; Received royalty from Springer for review panel membership; Received honoraria from Merck for speaking and teaching.


Sandeep Mukherjee, MB, BCh, MPH, FRCPC Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center

Sandeep Mukherjee, MB, BCh, MPH, FRCPC is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Merck Honoraria Speaking and teaching; Ikaria Pharmaceuticals Honoraria Board membership

  1. Longatti A. The dual role of exosomes in hepatitis A and C virus transmission and viral immune activation. Viruses. 2015 Dec 17. 7(12):6707-15. [Medline].

  2. Liu W, Zhai J, Liu J, Xie Y. Identification of recombination between subgenotypes IA and IB of hepatitis A virus. Virus Genes. 2010 Apr. 40(2):222-4. [Medline].

  3. Kaplan G, Totsuka A, Thompson P, et al. Identification of a surface glycoprotein on African green monkey kidney cells as a receptor for hepatitis A virus. EMBO J. 1996 Aug 15. 15(16):4282-96. [Medline].

  4. Wheeler C, Vogt TM, Armstrong GL, et al. An outbreak of hepatitis A associated with green onions. N Engl J Med. 2005 Sep 1. 353(9):890-7. [Medline].

  5. Wasley A, Grytdal S, Gallagher K, Centers for Disease Control and Prevention (CDC). Surveillance for acute viral hepatitis--United States, 2006. MMWR Surveill Summ. 2008 Mar 21. 57(2):1-24. [Medline].

  6. Ansaldi F, Bruzzone B, Rota MC, et al. Hepatitis A incidence and hospital-based seroprevalence in Italy: a nation-wide study. Eur J Epidemiol. 2008. 23(1):45-53. [Medline].

  7. Dominguez A, Bruguera M, Plans P, et al. Declining hepatitis A seroprevalence in adults in Catalonia (Spain): a population-based study. BMC Infect Dis. 2007. 7:73. [Medline].

  8. Aggarwal R, Goel A. Hepatitis A: epidemiology in resource-poor countries. Curr Opin Infect Dis. 2015 Oct. 28(5):488-96. [Medline].

  9. Kanyenda TJ, Abdullahi LH, Hussey GD, Kagina BM. Epidemiology of hepatitis A virus in Africa among persons aged 1-10 years: a systematic review protocol. Syst Rev. 2015 Sep 26. 4:129. [Medline].

  10. Chobe LP, Arankalle VA. Investigation of a hepatitis A outbreak from Shimla Himachal Pradesh. Indian J Med Res. 2009 Aug. 130(2):179-84. [Medline].

  11. Cao J, Wang Y, Song H, et al. Hepatitis A outbreaks in China during 2006: application of molecular epidemiology. Hepatol Int. 2009 Jun. 3(2):356-63. [Medline]. [Full Text].

  12. Kamath SR, Sathiyasekaran M, Raja TE, Sudha L. Profile of viral hepatitis A in Chennai. Indian Pediatr. 2009 Jul. 46(7):642-3. [Medline].

  13. Fischer GE, Thompson N, Chaves SS, et al. The epidemiology of hepatitis A virus infections in four Pacific Island nations, 1995-2008. Trans R Soc Trop Med Hyg. 2009 Sep. 103(9):906-10. [Medline].

  14. Amin J, Gilbert GL, Escott RG, et al. Hepatitis A epidemiology in Australia: national seroprevalence and notifications. Med J Aust. 2001 Apr 2. 174(7):338-41. [Medline].

  15. Cooksley WG. What did we learn from the Shanghai hepatitis A epidemic?. J Viral Hepat. 2000 May. 7 Suppl 1:1-3. [Medline].

  16. Mofenson LM, Brady MT, Danner SP, et al. Guidelines for the prevention and treatment of opportunistic infections among HIV-exposed and HIV-infected children: recommendations from CDC, the National Institutes of Health, the HIV Medicine Association of the Infectious Diseases Society of America, the Pediatric Infectious Diseases Society, and the American Academy of Pediatrics. MMWR Recomm Rep. 2009 Sep 4. 58:1-166. [Medline]. [Full Text].

  17. Kodani M, Mixson-Hayden T, Drobeniuc J, Kamili S. Rapid and sensitive approach to simultaneous detection of genomes of hepatitis A, B, C, D and E viruses. J Clin Virol. 2014 Oct. 61(2):260-4. [Medline].

  18. Worns MA, Teufel A, Kanzler S, et al. Incidence of HAV and HBV infections and vaccination rates in patients with autoimmune liver diseases. Am J Gastroenterol. 2008 Jan. 103(1):138-46. [Medline].

  19. Kanda T, Nakamoto S, Wu S, et al. Direct-acting antivirals and host-targeting agents against the hepatitis A virus. J Clin Transl Hepatol. 2015 Sep 28. 3(3):205-10. [Medline].

  20. Jacobsen K, Wierman S. Hepatitis A virus seroprevalence by age and world region. 1990-2005. Vaccine. 2010. 28(41):6653-6657.

  21. Jacobsen KH, Koopman JS. Declining hepatitis A seroprevalence: a global review and analysis. Epidemiol Infect. 2004 Dec. 132(6):1005-22. [Medline]. [Full Text].

  22. Klevens RM, Miller JT, Iqbal K, et al. The evolving epidemiology of hepatitis a in the United States: incidence and molecular epidemiology from population-based surveillance, 2005-2007. Arch Intern Med. 2010 Nov 8. 170(20):1811-8. [Medline].

  23. Costas L, Vilella A, Trilla A, et al. Vaccination strategies against hepatitis A in travelers older than 40 years: an economic evaluation. J Travel Med. 2009 Sep-Oct. 16(5):344-8. [Medline].

  24. Marano C, Freedman DO. Global health surveillance and travelers' health. Curr Opin Infect Dis. 2009 Oct. 22(5):423-9. [Medline].

  25. Askling HH, Rombo L, Andersson Y, Martin S, Ekdahl K. Hepatitis A risk in travelers. J Travel Med. 2009 Jul-Aug. 16(4):233-8. [Medline].

  26. Centers for Disease Control and Prevention (CDC). National, state, and local area vaccination coverage among children aged 19-35 months - United States, 2008. MMWR Morb Mortal Wkly Rep. 2009 Aug 28. 58(33):921-6. [Medline].

  27. Centers for Disease Control and Prevention (CDC). Hepatitis a vaccination coverage among children aged 24-35 months - United States, 2006 and 2007. MMWR Morb Mortal Wkly Rep. 2009 Jul 3. 58(25):689-94. [Medline].

  28. Irving GJ, Holden J, Yang R, Pope D. Hepatitis A immunisation in persons not previously exposed to hepatitis A. Cochrane Database Syst Rev. 2012 Jul 11. 7:CD009051. [Medline].

  29. Petrignani M, Verhoef L, Vennema H, et al. Underdiagnosis of foodborne hepatitis A, The Netherlands, 2008-2010(1.). Emerg Infect Dis. 2014 Apr. 20 (4):596-602. [Medline].

Hepatitis A virus as viewed through electron microscopy.
Hepatitis A. Time course of infection.
Hepatitis A.
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.