hepatitis b case presentation ppt

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Hepatitis B Training Presentation for Health Workers

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NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

StatPearls [Internet].

Hepatitis b.

Nishant Tripathi ; Omar Y. Mousa .

Affiliations

Last Update: July 9, 2023 .

• Continuing Education Activity

Hepatitis B infection is a serious global healthcare problem. Often transmitted via body fluids like blood, semen, and vaginal secretions, the hepatitis B virus can cause liver injury. After infection with the hepatitis B virus, the majority of adults are able to clear the infection. Patients can present with acute symptomatic disease or have an asymptomatic disease that is identified during screening for the hepatitis B virus. This article focuses on identifying who is at risk of hepatitis B, and clinical evaluation and management of patients with hepatitis B by an interdisciplinary team. It also focuses on preventive measures.

• Describe the epidemiology of hepatitis B.
• Outline the common blood tests for the diagnosis of hepatitis B infection.
• Review the complications of hepatitis B infection.
• Explain the importance of collaboration and communication amongst the interdisciplinary teams to enhance the delivery of care for patients affected by hepatitis B.
• Introduction

Hepatitis B viral infection is a serious global healthcare problem. It is a potentially life-threatening liver infection caused by the hepatitis B virus (HBV). It is often transmitted via body fluids like blood, semen, and vaginal secretions. The majority (more than 95%) of immunocompetent adults infected with HBV can clear the infection spontaneously. Patients can present with acute symptomatic disease or have an asymptomatic infection that is identified during screening for HBV. The clinical manifestations of HBV infection vary in both acute and chronic diseases. During the acute infection, patients can have subclinical or anicteric hepatitis, icteric hepatitis, or less commonly fulminant hepatitis. In chronic infection, patients can have an asymptomatic carrier state, chronic hepatitis, cirrhosis, and hepatocellular carcinoma.

Initial symptoms are nonspecific and may include anorexia, nausea, vomiting, abdominal pain, and jaundice. In cases of severe liver damage, patients can develop jaundice, hepatic encephalopathy, ascites, gastrointestinal bleeding secondary to esophageal varices, coagulopathy, or infections. Diagnosis is based on serologic blood tests in patients with suspected signs and symptoms and associated risk factors for viral hepatitis. This will be discussed in more detail below.

Transmission of hepatitis B involves the transfer of the virus from infected people to non-immune people in various ways. Major modes of transmission for hepatitis B are as follows:

1. Horizontal transmission: It involves the transmission of hepatitis B through sexual contact or mucosal surface contact. Unprotected sex and injection drug use are major modes of transmission in low to intermediate prevalence areas. [1]  

2. Vertical transmission: Vertical transmission involves the maternal-to-newborn perinatal transmission of the virus. [2]  It is the predominant mode of transmission in high-prevalence areas. 

Sexual contact includes unprotected intercourse (vaginal, oral, or anal) and mucosal contact involves any contact involving an infected patient’s saliva, vaginal secretion, semen, and blood.

Prevalence areas are based on the percentage of the population with hepatitis B surface antigen (HBsAg) positivity with greater than or equal to 8% representing high prevalence areas, 2-7% representing low to intermediate prevalence areas, and less than 2% representing low prevalence areas. [3]

• Epidemiology

HBV infection has the potential for progression to a chronic state and thus presents as a global public health threat for its associated morbidity and mortality. While hepatitis B vaccines are available, limited access to healthcare and lack of proper health education contributes to the increasing global prevalence of hepatitis B. Lower incidence of hepatitis B in the United States compared to Asia and Africa is due to better access to healthcare and better use of vaccinations and other preventive measures. 

 U.S. Statistics 

• Around 60,000 new cases of HBV infection annually [4]
• 2 million or more people with chronic hepatitis B infection [4]
• Prevalence is higher in black, Hispanic, and Asian populations compared to whites [5]  
• Prevalence is lower in people less than 12 years of age born in the U.S. 
• Accounts for 5% to 10% of chronic end-stage liver disease, and 10% to 15% of cases of hepatocellular cancer
• Causes 5000 deaths annually 

Worldwide Statistics

• 350-400 million of the world population has chronic hepatitis B. [6]
• The following population is known to have a higher prevalence: Asian Pacific Islanders, Alaskan Eskimos, and Australian aborigines. [6]
• The following geographic regions have higher prevalence: the Indian sub-continent, sub-Saharan Africa, and central Asia.
• The prevalence of hepatitis B is reduced after the initiation of the hepatitis B vaccination program.
• 10 genotypes (A-J) of hepatitis B have been identified. [7]

High-risk groups for HBV infection include intravenous drug users, infants born to infected mothers, males who have sexual intercourse with other males, hemodialysis patients (and workers), healthcare workers, household contacts of known patients with chronic HBV. A majority of the global HBV disease burden is primarily through vertical transmission.

• Pathophysiology

Hepatitis B virus is transmitted via percutaneous inoculation or through mucosal exposure with infectious bodily fluids. Oral-fecal transmission is possible but considerably rare. The incubation period of HBV infection is typically between 30 and 180 days, and while recovery is common in immunocompetent patients, a small percentage can progress to a chronic state, serologically defined as the presence of HBsAg for greater than six months. HBsAg is transmitted via blood contact or body secretions, and the risk of acquiring hepatitis B is considerably higher in individuals with close contact with HBsAg-positive patients.

The pathogenesis of liver disease in HBV infection is mainly immune-mediated, and in some circumstances, HBV can cause direct cytotoxic injury to the liver. HBsAg and other nucleocapsid proteins that are present on cell membranes promote T cells-induced cellular lysis of HBV-infected cells. Cytotoxic T cell response to HBV-infected hepatocytes is relatively ineffective; a significant majority of HBV DNA is cleared from the hepatic system prior to maximal T cell infiltration, suggesting that the immune response is likely more robust in the early stages of infection. The immune response may not be the sole etiology behind hepatic injury in hepatitis B patients. Hepatitis B-associated injury is also seen in post-liver transplant patients with hepatitis B that are on immunosuppressant therapy. The histological pattern that follows from this infection is termed fibrosing cholestatic hepatitis and is thought to be associated with an overwhelming exposure to HBsAg. This lends credence to the idea that hepatitis B may possess pathogenicity regardless of the immune system’s response. [8]

• Histopathology

Acute Hepatitis B Infection: Histologic findings include "lobular disarray, ballooning degeneration, multiple apoptotic bodies, Kupffer cell activation, and lymphocyte-predominant lobular and portal inflammation. [9]

Chronic Hepatitis B Infection:  Lymphocyte-predominant portal inflammation with interface hepatitis and spotty lobular inflammation. [9]

• History and Physical

Patients infected with HBV could be asymptomatic initially and, depending on the particular genotype, might not be symptomatic throughout the infected state. In these particular cases, careful history taking is important to establish a diagnosis. However, when symptomatic from acute HBV infection, patients can present with serum sickness-like syndrome manifested as fever, skin rash, arthralgia, and arthritis. This syndrome usually subsides with the onset of jaundice. Patients may also have fatigue, abdominal pain, nausea, and anorexia.

History taking should emphasize the social history, including sexual practices (e.g., unprotected, same-sex, etc.), illicit drug use, profession (e.g., healthcare worker, sex worker), and living arrangements (i.e., within the same household as a patient with HBV infection). Patients in high-risk groups (i.e., healthcare workers, IV substance abuse patients, etc.) or those from highly endemic areas may warrant testing. Those with certain mental illnesses like bipolar disorder, schizophrenia, or manic disorder are at an increased risk for contracting HBV infection during manic states within which one may participate in risky sexual behaviors, including unprotected sex.

Physical examination should also assess for stigmata of chronic liver disease, including jaundice, ascites, hepatomegaly, splenomegaly, palmar erythema, Dupuytren contractures, spider nevi, gynecomastia, caput medusa, and hepatic encephalopathy which suggests portal hypertension and cirrhosis.

Extrahepatic manifestations include polyarteritis nodosa and glomerular disease (membranous nephropathy and, less often, membranoproliferative glomerulonephritis). Aplastic anemia has also been described.

Diagnosis of Hepatitis B is based on proper history taking, physical examination, laboratory works, and imaging. 

Initial symptoms are nonspecific and can include anorexia, nausea, vomiting, abdominal pain, dark urine, clay-colored stool, and jaundice. In cases of severe liver damage, advanced findings specific to liver damage are common and can include hepatic encephalopathy, confusion, coma, ascites, gastrointestinal bleeding, coagulopathy, or infections. In cases of chronic hepatitis B, patients can have a chronic inactive infection, or they can develop findings of acute hepatitis known as chronic active hepatitis. 

The diagnosis of hepatitis B relies on the appropriate history/physical and evaluation of serum or viral biomarkers. Viral serology of hepatitis B is usually detectable 1-12 weeks after initial infection with the primary viral marker being hepatitis B surface antigen (HBsAg). The presence of HBsAg rarely persists beyond 6 months after infection and typically precedes detectable quantities of the corresponding antibody to surface antigen (Anti-HBsAg). The period of time between the disappearance of HBsAg and the appearance of Anti-HBsAg is termed “the window period” or “serological gap.” During the window period, other viral serology could also be undetectable. HBsAg is the first virological marker to be detected thanks to its exposure on the viral surface and is indicative of an acute infection. Immune-mediated destruction of the nucleocapsid allows exposure of core antigen (HBcAg) or e antigen (HBeAg) with subsequent antibody development. Liver enzymes are typically elevated within the latter part of the replicative phase on infection thanks to active inflammatory processes, otherwise, liver transaminases could also be within their reference ranges. Hence, liver transaminases should not be a sole guide to diagnosing suspected hepatitis B infection.

The presence of antibodies to HBsAg indicates immunized status while the presence of antibodies to HBeAg refers to a possible chronic infection state. Seroconversion refers to the transition between an acute, immune-active phase to an inactive carrier state and is marked by the spontaneous development of antibodies to HBeAg. Earlier seroconversion has been related to more favorable outcomes while later seroconversion, in conjunction with recurrent bouts of reactivation and remission, is more liable to complications like liver cirrhosis, thus resulting in poorer outcomes. [10] The persistence of serum HBsAg for a duration of 6 months or greater delineates acute hepatitis B infection from chronic hepatitis B infection. Following groups of people should be screened for hepatitis B: [3]

• Persons born in high or intermediate endemic areas (HBsAg prevalence of greater than or equal to 2%). African countries, countries from North, Southeast, and East Asia. All countries from Australia and South Pacific (except for Australia and New Zealand). All countries from the Middle East (except for Israel and Cyprus). All countries from Eastern Europe (except for Hungary), Western Europe (Spain, Malta, and the indigenous population of Greenland), North America (Alaskan natives and indigenous populations of Northern Canada), Mexico, Guatemala, and Honduras. South America (Ecuador, Guyana, Suriname, Venezuela, and Amazonian areas). Caribbean (Antigua, Barbuda, Dominica, Grenada, Haiti, Jamaica, Saint Kitts and Nevis, Saint Lucia, and Turks and Caicos Islands).
• The unvaccinated U.S. citizens whose parents were born in high prevalence areas.
• History of illicit intravenous drug use.
• Men who have sex with men.
• Persons on immunosuppressive therapy.
• Persons with elevated ALT or AST of unknown origin.
• Blood, plasma, organ, tissues, or semen donors.
• Persons with end-stage renal disease.
• All pregnant women and infants born to HBsAg-positive mothers.
• Persons with chronic liver disease and HIV.
• Close contacts of HBsAg-positive persons, such as household, sexual, or needle-sharing.
• Persons with more than one sexual partner in the last six months.
• Persons requesting evaluation or treatment for sexually transmitted infections.
• Health care workers or public safety workers who are at risk for occupational exposure to blood or blood-contaminated body fluids.
• Residents and staff at facilities for developmentally disabled persons.
• Travelers to countries with an intermediate or high prevalence of Hepatitis B virus infection.
• Correctional facilities inmates.
• 19-59-year-old persons with diabetes who have not been vaccinated for Hepatitis B.
• Persons who are the source of blood or body fluid exposures that might require post-exposure prophylaxis.

Interpretation of Serologic Markers

Following serologic markers are often tested: Hepatitis B surface antigen (HBsAg), antibody to Hepatitis B surface antigen (anti-HBs), Hepatitis B core Ab (Anti-HBc) IgM, Hepatitis B core Ab (Anti-HBc) IgG, Hepatitis B e antigen (HBeAg), and Hepatitis B e antibody (anti-HBe). [10]

HBsAg: Acute infection (less than 6 months) or chronic infection (more than 6 months).

Anti-HBs: Recovery from acute infection or immunity from vaccination.

HBeAg: Mostly associated with high viral load.

Anti-HBe: Low replicative phase.

Anti-HBc IgM: Acute infection, an only marker present in the window period, can be present during exacerbation of chronic infection.

Anti-HBc IgG: Exposure to infection, chronic infection (if present along with HBsAg), recovery from acute infection (if present with anti-HBs), if isolated presence, may represent occult infection.

Other markers are: Hepatitis B viral DNA is for detection of viral load. Hepatitis B genotype provides input about disease progression and response to interferons. [11]

• Treatment / Management

Preventive measures constitute a major component of the management of hepatitis B. As of 2019, hepatitis B vaccines available in the United States are categorized into either single-antigen hepatitis B vaccines or combination vaccines.

Acute hepatitis B infection is self cleared in 95% of healthy adults. Management is supportive in a majority of patients. Patients with severe acute disease (2 of the 3: bilirubin more than 10 mg/dl, INR more than 1.6 and hepatic encephalopathy) and protracted acute severe disease (total bilirubin more than 3 mg/dl or direct bilirubin more than 1.5 mg/dl, INR more than 1.5, hepatic encephalopathy, or ascites) need antiviral treatment.

Management of chronic hepatitis B should include identification of HIV, hepatitis C, and hepatitis D coinfection, hepatitis B virus replication status, and severity of the disease. [10]  The severity of the disease is based on clinical assessment, blood counts, liver enzymes, and liver histology. [10]  While non-invasive tests are useful (blood test, imaging to measure liver stiffness) for chronic hepatitis B with normal alanine transferase, for patients with elevated or fluctuating alanine transferase, liver biopsy is necessary to identify if they need antiviral treatment. [10]

FDA-approved medications for chronic hepatitis B include interferons (peginterferon alfa-2a, interferon alfa-2b), nucleoside analogs (entecavir, lamivudine, telbivudine), and nucleotide analogs (adefovir, tenofovir). Entecavir and tenofovir are preferred for acute HBV infection if treatment is warranted, due to their relatively higher barrier to resistance. Entecavir combination drugs have been developed. However, a 2018 meta-analysis based on 24 studies involved with entecavir polytherapy vs entecavir monotherapy determined that entecavir combination drugs were no more effective than entecavir monotherapy. [12]  Vertical transmission of hepatitis B remains a significant cause of the global HBV burden. In a 2015 prospective, multicenter trial, administration of tenofovir in HBsAg-positive and/or HBeAg-positive mothers demonstrated a benefit in reducing ALT levels in mothers and decreasing infant HBsAg levels at 6 months postpartum. [13]  Major drawbacks for this study, however, include a relatively small sample size (n=118) and the lack of a placebo-based control group.  Oral nucleos(t)ide therapy has been shown to suppress viral replication and thus decrease the viral burden. Lamivudine was the first effective agent to successfully used to suppress viral counts but was associated with high drug resistance. [14]  A 2014 clinical trial comparing entecavir vs lamivudine in chronic B hepatitis reported better virological response in the entecavir group compared to the lamivudine group. [15]  The 2013 GAHB trial was a placebo-controlled, double-blind study that compared lamivudine with a placebo. HBsAg clearance was achieved in a majority of patients with lamivudine therapy but the overall strength of the study was weakened by low recruitment numbers (n = 35). [16] For patients in the immune-tolerant phase of hepatitis B infection, a stage marked by normal liver transaminases and HBV DNA, antiviral medications were not recommended. A randomized controlled study showed suboptimal control of viral burden, likely secondary to high circulating levels of HBV DNA. [17]  Regarding monotherapy versus combined therapy, there have been several limited studies addressing this issue. In the 2018 POTENT study, there was no demonstrated difference between monotherapy versus sequential therapy although there was insufficient data for statistical significance for HBsAg seroconversion. [18]

The counseling of patients on the prevention of transmission is extremely valuable. Lifestyle modifications include reducing intake of agents with potential for liver damage such as alcohol, hepatotoxic medications, herbal medications, and herbal supplements. 

The goals of antiviral therapy are: [10]

• Suppression of hepatitis B virus replication
• Reduction of liver inflammation
• Prevention of progression to liver cirrhosis and hepatocellular carcinoma

Appropriate treatment response is indicated by the following findings: [10]

• Blood tests: normalization of ALT
• Undetectable hepatitis B viral DNA
• Loss of HBsAg and HBeAg with seroconversion to anti-HBs and anti-HBe
• Reduced inflammation on liver biopsy with no worsening of fibrosis

Surgical intervention for hepatitis B is only indicated for fulminant liver disease requiring transplantation.

• Differential Diagnosis

The differential diagnosis for hepatitis B infection is broad due to the presence of non-specific symptoms such as fatigue, abdominal pain, nausea, and vomiting. Other etiologies of hepatitis (i.e., hepatitis A, hepatitis C, hepatitis E, alcoholic hepatitis, and autoimmune hepatitis) should be considered in conjunction with appropriate history taking and pertinent laboratory investigation.

Iron overload (hemochromatosis) can be associated with abdominal tenderness and abnormal liver transaminase levels. Pertinent findings that favor a diagnosis of hemochromatosis compared to hepatitis B include diffuse skin discoloration (bronze diabetes) and impaired glucose tolerance.

Wilson disease is a disease of excessive copper accumulation. It is associated with psychiatric disturbances due to copper accumulation in the basal ganglia. Kayser-Fleischer rings are pathognomonic for Wilson disease but are not completely sensitive (requires an expert ophthalmologist to confirm this finding). Laboratory evaluation that favors a diagnosis of Wilson disease includes low serum ceruloplasmin levels and elevated urinary copper, and if abnormal, requires further evaluation by a hepatologist.

• Alcoholic hepatitis
• Autoimmune hepatitis
• Drug-induced liver injury
• Hemochromatosis
• Hepatitis A
• Hepatitis C
• Hepatitis D
• Hepatitis E
• Hepatocellular carcinoma
• Human immunodeficiency virus
• Wilson disease

Acute HBV infection can be treated symptomatically and in immunocompetent patients, can spontaneously resolve. Those that progress to the chronic state, however, are at increased risk for the development of hepatocellular carcinoma, cirrhosis, or fulminant liver failure. The likelihood of risk is dependent on the particular genotype, and the method of transmission as vertical transmission has a higher risk of long-term complications compared to horizontal transmission cases.

• Complications

Unlike hepatitis A and hepatitis E, in which there is no chronic state, HBV infection has the potential for the development of a chronic state. Chronic hepatitis B predisposes a patient to the development of portal hypertension, cirrhosis, and its complications or hepatocellular carcinoma (HCC). As such, patients with HBV infection should be monitored closely, and a referral to a specialist is highly recommended.Fulminant liver failure from HBV infection requires an emergent liver transplant evaluation at a liver transplant center.

• Consultations

Hepatitis B management ideally involves interprofessional collaboration. Primary care, gastroenterology, hepatology, infectious disease, liver transplant, and palliative care services are among the different services involved.

• Deterrence and Patient Education

Patient education remains one of the most important components in preventative measures regarding HBV infection.

Education should be provided to expecting parents (particularly those from highly endemic regions) about the importance of vaccination and to clarify erroneous beliefs about vaccinations.Patient education should also include counseling about the avoidance of risky behaviors that predispose an individual to be infected, including promiscuous sexual activity or intravenous drug abuse. They should also be advised not to share items such as shaving razors, toothbrushes, or hair combs due to possible transmission via mucosal contact or through microtrauma to protective barriers.

• Pearls and Other Issues

Hepatitis D (a member of the delta virus family) has been long associated with HBV infections and cannot exert pathological influence without the presence of HBV infection. Two forms of infection exist; coinfection (acquired at the same time) and superinfection (hepatitis D infection in a patient with chronic hepatitis B infection). Superinfection tends to be more severe than coinfection. Due to the preexisting hepatitis B infection, anti-HBcAg IgM is undetectable in superinfection states but can be noted in coinfection.

• Enhancing Healthcare Team Outcomes

As hepatitis B infection is highly transmissible via accidental needlesticks, healthcare providers involved in taking care of a patient with HBV should exercise caution and practice proper preventative measures such as vaccination. Patient education should also include counseling about HBV transmission. The interprofessional team's role is crucial in ensuring the best patient outcomes.

The vaccination rate is low in many developing countries, and the majority of patients are undiagnosed. Educational programs and improved awareness among the general public and healthcare providers are necessary to improve the identification of the patients, reduce transmission of the disease, and reduce the complications of hepatitis B infection.

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Disclosure: Nishant Tripathi declares no relevant financial relationships with ineligible companies.

Disclosure: Omar Mousa declares no relevant financial relationships with ineligible companies.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

• Cite this Page Tripathi N, Mousa OY. Hepatitis B. [Updated 2023 Jul 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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• Acute hepatitis B virus infection and severe non-immune haemolytic anaemia: a rare relationship
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• http://orcid.org/0000-0003-3985-0718 Inês Furtado 1 ,
• Diana Valadares 2 ,
• Filipe Gaio Nery 2
• 1 Internal Medicine Department , Centro Hospitalar do Porto , Porto , Portugal
• 2 Department of Intensive Care , Centro Hospitalar do Porto , Porto , Portugal
• Correspondence to Dr Inês Furtado, inessilvafurtado{at}gmail.com

The clinical presentation of acute hepatitis B virus (HBV) infection is usually related to the onset of liver failure and damage. Anaemia may occur, but it is only rarely attributed to haemolysis. The authors report about the case of a 41-year-old woman with the diagnosis of acute HBV infection and coagulopathy (without encephalopathy) who developed non-immune haemolytic anaemia. Total recovery of the analytical liver profile, coagulopathy and anaemia was achieved through treatment targeting HBV.This case shows that, although rare, non-immune haemolytic anaemia may occur in association with acute HBV infection and that HBV suppression seems to lead to progressive anaemia resolution.

• infectious diseases
• hepatitis and other gi infections
• hepatitis b
• haematology (incl blood transfusion)

https://doi.org/10.1136/bcr-2017-221763

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Contributors FGN and DV contributed to the conception or design of the work. IF was responsible for data collection, analysis and interpretation. IF drafted the initial version of the article which was critically revised by FGN and DV. FGN, DV and IF approved the final version of the article to be published.

Competing interests None declared.

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Viral Hepatitis Clinical Presentation

• Author: Naga Swetha Samji, MD; Chief Editor: BS Anand, MD  more...
• Sections Viral Hepatitis
• Pathophysiology
• Epidemiology
• Patient Education
• Physical Examination
• Approach Considerations
• Hepatitis A
• Hepatitis B
• Hepatitis C
• Hepatitis D and E
• Histologic Findings
• Acute Hepatitis A
• Acute Hepatitis B
• Chronic Hepatitis B
• Acute Hepatitis C
• Chronic Hepatitis C
• Treatment of Hepatitis D and E
• Medication Summary
• Interferons
• Corticosteroids
• Vaccines, Viral, Prevention
• Immune Globulins
• Questions & Answers
• Media Gallery

The clinical presentation of infectious hepatitis varies with the individual, as well as with the specific causative virus. Some patients may be entirely asymptomatic or only mildly symptomatic at presentation. Others may present with rapid onset of fulminant hepatic failure (FHF). The classic presentation of infectious hepatitis involves four phases, as follows:

Phase 1 (viral replication phase): Patients are asymptomatic; laboratory studies demonstrate serologic and enzyme markers of hepatitis

Phase 2 (prodromal phase): Patients experience anorexia, nausea, vomiting, alterations in taste, arthralgias, malaise, fatigue, urticaria, and pruritus, and some develop an aversion to cigarette smoke; when seen by a healthcare provider during this phase, patients are often diagnosed as having gastroenteritis or a viral syndrome

Phase 3 (icteric phase): Patients may note dark urine, followed by pale-colored stools; in addition to the predominant gastrointestinal (GI) symptoms and malaise, patients become icteric and may develop right upper quadrant pain with hepatomegaly

Phase 4 (convalescent phase): Symptoms and icterus resolve, liver enzymes return to normal

The incubation period of hepatitis A virus (HAV) is 2-7 weeks (average, 28 days). Clinical symptoms then develop, often with a presentation similar to that of gastroenteritis or a viral respiratory infection. The most common signs and symptoms include fatigue, nausea, vomiting, fever, hepatomegaly, jaundice, dark urine, anorexia, and rash.

HAV infection usually occurs as a mild self-limited disease and confers lifelong immunity to the virus. Chronic HAV infection does not occur. [ 9 ]

The incubation period for hepatitis B virus (HBV) is 30-180 days (average, approximately 75 days). Patients then enter the prodromal or preicteric phase, characterized by the gradual onset of anorexia, malaise, and fatigue. During this phase, as the liver becomes inflamed, the liver enzymes start to elevate, and the patient may experience right upper quadrant pain. About 15% of patients develop an illness resembling serum sickness. These patients may experience fever, arthritis, arthralgias, or an urticarial rash.

As the disease progresses to the icteric phase, the liver becomes tender, and jaundice develops. Patients may note that their urine darkens and their stools lighten in color. Other symptoms in this stage include nausea, vomiting, and pruritus.

From this point on, the clinical course may be highly variable. Whereas some patients experience fairly rapid improvements in their symptoms, others go on to experience prolonged disease with slow resolution. Still others may have symptoms that periodically improve, only to worsen later (relapsing hepatitis). Finally, there is an unfortunate subset of patients in whom the disease rapidly progresses to FHF; this may occur over days to weeks.

The incubation period for hepatitis C virus (HCV) is 15-150 days, with symptoms developing anywhere from 5-12 weeks after exposure. During acute HCV infection, symptoms may appear similar to those of HBV infection. In up to 80% of cases, however, the patients are asymptomatic and do not develop icterus. [ 1 , 18 ]

Hepatitis D

The incubation period of hepatitis D virus (HDV) is approximately 35 days. Patients simultaneously infected with HBV and HDV often have an acute, self-limited infection. [ 48 , 55 ] Fewer than 5% of these patients develop chronic HDV infection.

Chronic HBV carriers who become superinfected with HDV tend to have a more severe acute hepatitis; 80% of these patients go on to develop chronic HDV infection. Chronic infection with HBV and HDV may lead to fulminant acute hepatitis and severe chronic active hepatitis with progression to cirrhosis. [ 48 , 55 ] Over the long term, as many as 70-80% of these patients have evidence of chronic liver disease with cirrhosis, compared with only 15-30% of patients with chronic HBV alone.

Hepatitis E

The incubation period of hepatitis E virus (HEV) is 2-9 weeks (average, 45 days). HEV usually causes an acute self-limited disease similar to HAV infection. Fulminant disease does occur in about 10% of cases. In women who are pregnant, HEV infection has a case-fatality rate of 15-20%. [ 34 ] No reports exist of chronic infection with HEV. [ 34 ]

Physical findings in patients with hepatitis vary with the type of hepatitis and the time of presentation.

Patients often present with low-grade fever. Those experiencing significant vomiting and anorexia may show signs of dehydration, such as tachycardia, dry mucous membranes, loss of skin turgor, and delayed capillary refill.

Patients in the icteric phase may have icterus of the sclerae or mucous membranes, or discoloration of the tympanic membranes. The skin may be jaundiced and may reveal macular, papular, or urticarial rashes.

In viral hepatitis, the liver may be tender and diffusely enlarged with a firm, sharp, smooth edge. If the patient has a nodular liver or a mass is palpated, clinicians should suspect an abscess or tumor.

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• Viral Hepatitis. Hepatitis A virus as viewed through electron microscopy.
• Viral Hepatitis. Liver biopsy specimen showing ground-glass appearance of hepatocytes in a patient with hepatitis B.
• Viral Hepatitis. Liver biopsy with hematoxylin stain showing stage 4 fibrosis (ie, cirrhosis) in a patient with hepatitis B.
• Viral Hepatitis. Liver biopsy with trichrome stain showing stage 3 fibrosis in a patient with hepatitis B.
• Viral Hepatitis. Hepatic carcinoma, primary. Large multifocal hepatocellular carcinoma in an 80-year-old man without cirrhosis.
• Viral Hepatitis. Triple-phase computed tomography scan depicting liver cancer, revealing classic findings of enhancement during the arterial phase and delayed hypointensity during the portal venous phase.
• Table 1. Diagnostic Tests for Hepatitis B
• Table 2. Histologic Grading for Hepatitis C–Induced Liver Disease

Contributor Information and Disclosures

Naga Swetha Samji, MD Physician, Bellin Clinic, Bellin Health Systems Naga Swetha Samji, MD is a member of the following medical societies: American College of Gastroenterology , American College of Physicians , Wisconsin Medical Society Disclosure: Nothing to disclose.

Adrienne M Buggs, MD, FACEP, FAAEM Medical Policy Advisor, Office of Merchant Mariner Credentialing, United States Coast Guard Adrienne M Buggs, MD, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine , American College of Emergency Physicians , American College of Occupational and Environmental Medicine Disclosure: Nothing to disclose.

Praveen K Roy, MD, MSc Clinical Assistant Professor of Medicine, University of New Mexico School of Medicine Praveen K Roy, MD, MSc is a member of the following medical societies: Alaska State Medical Association , American Gastroenterological Association Disclosure: Nothing to disclose.

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.

Eugene Hardin, FAAEM, FACEP Former Chair and Associate Professor, Department of Emergency Medicine, Charles Drew University of Medicine and Science; Former Chair, Department of Emergency Medicine, Martin Luther King Jr/Drew Medical Center

Disclosure: Nothing to disclose.

Douglas M Heuman, MD, FACP, FACG, AGAF Chief of GI, Hepatology, and Nutrition at North Shore University Hospital/Long Island Jewish Medical Center; Professor, Department of Medicine, Hofstra North Shore-LIJ School of Medicine

Douglas M Heuman, MD, FACP, FACG, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases , American College of Physicians , and American Gastroenterological Association

Disclosure: Novartis Grant/research funds Other; Bayer Grant/research funds Other; Otsuka Grant/research funds None; Bristol Myers Squibb Grant/research funds Other; Scynexis None None; Salix Grant/research funds Other; MannKind Other

Julian Katz, MD Clinical Professor of Medicine, Drexel University College of Medicine

Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology , American College of Physicians , American Gastroenterological Association , American Geriatrics Society , American Medical Association , American Society for Gastrointestinal Endoscopy , American Society of Law, Medicine & Ethics , American Trauma Society , Association of American Medical Colleges , and Physicians for Social Responsibility

Joseph K Lim, MD Associate Professor of Medicine, Director, Yale Viral Hepatitis Program, Section of Digestive Diseases, Yale University School of Medicine

Joseph K Lim, MD is a member of the following medical societies: American Association for the Study of Liver Diseases , American College of Gastroenterology , American College of Physicians , American Gastroenterological Association , and American Society for Gastrointestinal Endoscopy

Robert M McNamara, MD, FAAEM Chair and Professor, Department of Emergency Medicine, Temple University School of Medicine

Robert M McNamara, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine , American Medical Association , Pennsylvania Medical Society , and Society for Academic Emergency Medicine

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

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

Disclosure: Medscape Salary Employment

Rajeev Vasudeva, MD, FACG Clinical Professor of Medicine, Consultants in Gastroenterology, University of South Carolina School of Medicine

Rajeev Vasudeva, MD, FACG is a member of the following medical societies: American College of Gastroenterology , American Gastroenterological Association , American Society for Gastrointestinal Endoscopy , Columbia Medical Society, South Carolina Gastroenterology Association, and South Carolina Medical Association

Disclosure: Pricara Honoraria Speaking and teaching; UCB Consulting fee Consulting

David C Wolf, MD, FACP, FACG, AGAF Medical Director of Liver Transplantation, Westchester Medical Center; Professor of Clinical Medicine, Division of Gastroenterology and Hepatobiliary Diseases, Department of Medicine, New York Medical College

David C Wolf, MD, FACP, FACG, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases , American College of Gastroenterology , American College of Physicians , and American Gastroenterological Association

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• Hepatitis in Pregnancy
• Treatment Recommendations for HIV-Infected Patients With Co-infections
• Pediatric Vaccines: Global Brands and Country Availability
• Pediatric Hepatitis B
• Polyarteritis Nodosa
• Viral Hepatitis
• Fast Five Quiz: Hepatitis B Epidemiology and Prevention
• Simplifying Hepatitis B
• US FDA Declines Expanded Use Of Dynavax's Hepatitis B Vaccine on Insufficient Data
• Don't Forget Adult Hepatitis Vaccinations

• Drug Interaction Checker
• Pill Identifier
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• 2002964662-overviewDiseases & Conditions Diseases & Conditions Pediatric Hepatitis B

• 2001/viewarticle/993770 Hepatitis B Vaccination Rates Lag in Patients With Psoriasis

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Hepatitis B

• Hepatitis B is a viral infection that attacks the liver and can cause both acute and chronic disease.
• The virus is most commonly transmitted from mother to child during birth and delivery, in early childhood, as well as through contact with blood or other body fluids during sex with an infected partner, unsafe injections or exposures to sharp instruments.
• WHO estimates that 254 million people were living with chronic hepatitis B infection in 2022, with 1.2 million new infections each year.
• In 2022, hepatitis B resulted in an estimated 1.1 million deaths, mostly from cirrhosis and hepatocellular carcinoma (primary liver cancer).
• Hepatitis B can be prevented by vaccines that are safe, available and effective.

Hepatitis B is an infection of the liver caused by the hepatitis B virus. The infection can be acute (short and severe) or chronic (long term).

Hepatitis B can cause a chronic infection and puts people at high risk of death from cirrhosis and liver cancer.

It can spread through contact with infected body fluids like blood, saliva, vaginal fluids and semen. It can also be passed from a mother to her baby.

Hepatitis B can be prevented with a safe and effective vaccine. The vaccine is usually given soon after birth with boosters a few weeks later. It offers nearly 100% protection against the virus.

Hepatitis B is a major global health problem. The burden of infection is highest in the WHO Western Pacific Region and the WHO African Region, where 97 million and 65 million people, respectively, are chronically infected. Sixty-one million people are infected in the WHO South-East Asia Region, 15 million in the WHO Eastern Mediterranean Region, 11 million in the WHO in the WHO European Region and 5 million in the WHO Region of the Americas.

Transmission

In highly endemic areas, hepatitis B is most commonly spread from mother to child at birth (perinatal transmission) or through horizontal transmission (exposure to infected blood), especially from an infected child to an uninfected child during the first 5 years of life. The development of chronic infection is common in infants infected from their mothers or before the age of 5 years.

Hepatitis B is also spread by needlestick injury, tattooing, piercing and exposure to infected blood and body fluids, such as saliva and menstrual, vaginal and seminal fluids. Transmission of the virus may also occur through the reuse of contaminated needles and syringes or sharp objects either in health care settings, in the community or among persons who inject drugs. Sexual transmission is more prevalent in unvaccinated persons with multiple sexual partners.

Hepatitis B infection acquired in adulthood leads to chronic hepatitis in less than 5% of cases, whereas infection in infancy and early childhood leads to chronic hepatitis in about 95% of cases. This is the basis for strengthening and prioritizing infant and childhood vaccination.

The hepatitis B virus can survive outside the body for at least 7 days. During this time, the virus can still cause infection if it enters the body of a person who is not protected by the vaccine. The incubation period of the hepatitis B virus ranges from 30 to 180 days. The virus may be detected within 30 to 60 days after infection and can persist and develop into chronic hepatitis B, especially when transmitted in infancy or childhood.

Most people do not experience any symptoms when newly infected.

Some people have acute illness with symptoms that last several weeks:

• yellowing of the skin and eyes (jaundice)
• feeling very tired
• pain in the abdomen.

When severe, acute hepatitis can lead to liver failure, which can lead to death.

Although most people will recover from acute illness, some people with chronic hepatitis B will develop progressive liver disease and complications like cirrhosis and hepatocellular carcinoma (liver cancer). These diseases can be fatal.

HBV-HIV coinfection

About 1% of persons living with HBV infection (2.7 million people) are also infected with HIV. Conversely, the global prevalence of HBV infection in HIV-infected persons is 7.4%. Since 2015, WHO has recommended treatment for everyone diagnosed with HIV infection, regardless of the stage of disease. Tenofovir, which is included in the treatment combinations recommended as first-line therapy for HIV infection, is also active against HBV.

It is not possible on clinical grounds to differentiate hepatitis B from hepatitis caused by other viral agents; hence laboratory confirmation of the diagnosis is essential. Several blood tests are available to diagnose and monitor people with hepatitis B. Some laboratory tests can be used to distinguish acute and chronic infections, whilst other can assess and monitor the severity of liver disease. Physical examination, ultrasound, fibroscan can also be performed to assess degree of liver fibrosis and scarring and monitor progression of liver disease. WHO recommends that all blood donations be tested for hepatitis B to ensure blood safety and avoid accidental transmission.

As of 2022, 13% of all people estimated to be living with hepatitis B were aware of their infection, while 3% (7 million) of the people living with chronic hepatitis B were on treatment. According to latest WHO estimates, the proportion of children under five years of age chronically infected with HBV dropped to just under 1% in 2019 down from around 5% in the pre-vaccine era ranging from the 1980s to the early 2000s.

In settings with high Hepatitis B surface antigen seroprevalence in the general population (defined as  > 2% or  > 5% HBsAg seroprevalence), WHO recommends that all adults have access to and be offered HBsAg testing with linkage to prevention and care and treatment services as needed. WHO also recommends blood donor screening, routine testing for hepatitis B all pregnant women to provide the opportunity to institute measures for prevention of MTCT as well as focused or targeted testing of specific high-risk groups (including migrants from endemic regions, partners or family members of infected persons, and health-care workers PWID, people in prisons and other closed settings, MSM and sex workers, HIV-infected persons.

There is no specific treatment for acute hepatitis B. Chronic hepatitis B can be treated with medicines.

Care for acute hepatitis B should focus on making the person comfortable. They should eat a healthy diet and drink plenty of liquids to prevent dehydration from vomiting and diarrhoea.

Chronic hepatitis B infection can be treated with oral medicines, including tenofovir or entecavir.

Treatment can

• slow the advance of cirrhosis
• reduce cases of liver cancer
• improve long term survival.

Most people who start hepatitis B treatment must continue it for life.

With the updated Hepatitis B Guidelines, it is estimated that more than 50% of people with chronic hepatitis B infection will require treatment, depending on setting and eligibility criteria.

In low-income settings, most people with liver cancer present late in the course of the disease and die within months of diagnosis. In high-income countries, patients present to hospital earlier in the course of the disease and have access to surgery and chemotherapy, which can prolong life for several months to a few years. Liver transplantation is sometimes used in people with cirrhosis or liver cancer in technologically advanced countries, with varying success.

Hepatitis B is preventable with a vaccine.

All babies should receive the hepatitis B vaccine as soon as possible after birth (within 24 hours). This is followed by two or three doses of hepatitis B vaccine at least four weeks apart.

Booster vaccines are not usually required for people who have completed the three-dose vaccination series.

The vaccine protects against hepatitis B for at least 20 years and probably for life.

Hepatitis B can be passed from mother to child. This can be prevented by taking antiviral medicines to prevent transmission, in addition to the vaccine.

To reduce the risk of getting or spreading hepatitis B:

• practice safe sex by using condoms and reducing the number of sexual partners
• avoid sharing needles or any equipment used for injecting drugs, piercing, or tattooing
• wash your hands thoroughly with soap and water after coming into contact with blood, body fluids, or contaminated surfaces
• get a hepatitis B vaccine if working in a healthcare setting.

WHO response

Global health sector strategies on, respectively, HIV, viral hepatitis, and sexually transmitted infections for the period 2022–2030 (GHSSs)  guide the health sector in implementing strategically focused responses to achieve the goals of ending AIDS, viral hepatitis (especially chronic hepatitis B and C) and sexually transmitted infections by 2030.

The GHSS recommend shared and disease-specific country actions supported by actions by WHO and partners. They consider the epidemiological, technological, and contextual shifts of previous years, foster learnings across the disease areas, and create opportunities to leverage innovations and new knowledge for effective responses to the diseases. They call to scale up prevention, testing and treatment of viral hepatitis with a focus to reach populations and communities most affected and at risk for each disease, as well as addressing gaps and inequities. They promote synergies under a universal health coverage and primary health care framework and contribute to achieving the goals of the 2030 Agenda for Sustainable Development.

WHO organizes annual World Hepatitis Day campaigns to increase awareness and understanding of viral hepatitis. For World Hepatitis Day 2023, WHO focused on the theme “One life, one liver” to illustrate the importance of the liver for a healthy life and the need to scale up viral hepatitis prevention, testing and treatment to prevent liver diseases and achieve the 2030 hepatitis elimination target.

Global hepatitis report, 2024

Guidelines for the prevention, diagnosis, care and treatment for people with chronic hepatitis B infection

World Hepatitis Day

Global health sector strategy on viral hepatitis

Guidelines & manuals

• Monitoring and evaluation of hepatitis B and C
• Manual for the development of national viral hepatitis plans

More about hepatitis

• WHO's work on hepatitis 
• Global Hepatitis Programme
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