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Last Updated: May 30, 2006
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Synonyms and related keywords: infectious hepatitis, hepatitis A virus, HAV, hepatitis B virus, HBV, hepatitis C virus, HCV, hepatitis D virus, HDV, hepatitis E virus, HEV, Picornaviridae, fulminant hepatic failure, hepatomegaly, jaundice
Section 1 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography
Author: Richard K Gilroy, MBBS, FRACP, Assistant Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center Coauthor(s): Sandeep Mukherjee, MD, Assistant Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center Editor(s): George Wu, MD, PhD, Professor, Department of Medicine, Chief, Division of Gastroenterology-Hepatology, Director, Fellowship in Gastroenterology-Hepatology, Herman Lopata Chair, Hepatitis Research, University of Connecticut School of Medicine; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Oscar S Brann, MD, FACP, Associate Clinical Professor, Department of Medicine, University of California at San Diego; Consulting Staff, Mecklenburg Medical Group; Alex J Mechaber, MD, FACP, Assistant Dean for Medical Curriculum, Associate Professor of Medicine, Division of General Internal Medicine, University of Miami Miller School of Medicine; and Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania Disclosure
Section 2 of 11
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography
Background: One of the more common causes of acute hepatitis is hepatitis A virus (HAV). The virus was isolated by Purcell in 1973. Since the application of
and vaccination and passive immunization have successfully led to some reduction in illness in high-risk groups. notification of individual cases has increased. The recent demonstration of HAV in saliva has raised questions about this exclusivity. although isolated cases of parenteral transmission have been reported. and the viral genome is copied by a viral RNA polymerase. however. Hepatocyte uptake involves a receptor. The development of an immunologic response to infection is accompanied by a predominantly portal and periportal lymphocytic infiltrate and varying degree of necrosis (see Image 2). viral replication depends on hepatocyte uptake and synthesis. clinical manifestations. drying. primarily as a result of improved reporting and diagnostic techniques. with increases in the mean age of occurrence of illness attributed to acute HAV infection in Western societies. while in contrast. and temperatures as high as 56°C and as low as -20°C. Although this phenomenon may lay a framework for potential epidemics in the future. Assembled virus particles are shed into the biliary tree and excreted in the feces. Virion proteins 1 and 3 are the primary sites of antibody recognition and subsequent neutralization. Viral proteins are synthesized. there appears to be only 1 serotype. and host ribosomes bind to form polysomes. Pathophysiology: HAV is a single-stranded. Various genotypes of the virus exist. viral RNA is uncoated. public health policies. After entry into the cell. and sanitation have had the greatest impact on this disease. the epidemiology. acid (pH 3. recently identified by Kaplan et al. and assembly occurs exclusively in liver cells. Minimal cellular morphologic changes result from hepatocyte infection. and natural history of hepatitis A have become apparent. and chlorine and iodine are similarly effective (see Image 1). on the plasma membrane of the cell. positive-sense. HAV is an icosahedral nonenveloped virus measuring approximately 28 nm in diameter. HAV can remain viable for many years. . No antibody cross-reactivity has been identified with other viruses causing acute hepatitis. Humans appear to be the only reservoir for HAV. In humans.accurate serologic investigations in the 1980s. fecal-oral transmission). linear RNA enterovirus and a member of the Picornaviridae family. public health policies and newly implemented immunization practices are likely to reduce this potential. Its resilience is demonstrated by its resistance to denaturation by ether. Reduced encounters with HAV at a young age have resulted in both a decline in herd immunity and a change to the epidemiology of the illness. Acquisition results almost exclusively from ingestion (ie. and viral replication is believed to occur exclusively in hepatocytes. Improvements in hygiene. The nadir of reported cases was in 1987. The relative frequency of HAV as a cause of acute hepatitis has declined in Western societies. Boiling water is an effective means of destroying it.0).
however. Mexico. Frequency: • In the US: The United States is an area of low endemicity. foreign travelers (particularly those to developing nations). Over the last 40 years. in Western societies. the average age of infected persons has steadily increased. In developing nations. The contamination of the onions occurred prior to the vegetable arriving in the United States. acquisition is most frequent in persons aged 5-17 years. individuals in high-risk populations account for many sporadic cases. the age of acquisition is before age 2 years. Persons aged 5-14 years are most likely to acquire acute HAV infection. severe disease. Transmission through blood products has been described. approximately 32. and those living in poverty.000. the illness is more often mild or subclinical. In contrast. In 1988.000. The period of greatest shedding of virus is during the anicteric prodrome (14-21 d) of infection and corresponds to the time when transmission is highest. institutionalized individuals. Here was described a point source epidemic of HAV infection at a Pennsylvania restaurant where the vehicle for transmission was green onions used to make a mild salsa. The incubation period usually lasts 2-6 weeks. In this age range. Many authorities believe that hepatocyte injury is secondary to the host's immunologic response. although amounts fall rapidly. The estimated number of new infections in the United States for that same year was 61.000. The most notable report of transmission is that which appeared in The New England Journal of Medicine. This hypothesis is supported by the lack of cytotoxic activity in tissue culture and correlations between immunologic response and manifestations of hepatocyte injury. in 1995. has a high prevalence of anti-HAV antibody.000. the number of reported cases of hepatitis A was 27. the nearest southern neighbor. childcare workers.000 infections were reported. The presence of disease manifestations and the severity of symptoms following infection directly correlate with patient age. male homosexuals. Health measures implemented for these high-risk groups . Currently. Outbreaks of acute hepatitis A have received international attention. These groups include contacts of recently infected individuals. including fulminant hepatic failure does occur. and the time to onset of symptoms may be dose related. The US Centers for Disease Control and Prevention (CDC) estimated the actual number of infections in 1995 to be approximately 150.Person-to-person contact is the most common means of transmission and is generally limited to close contacts. indicating previous infection. Recognizing that active virus is shed after the development of jaundice is important. More recent data from the CDC show the number of reported acute clinical cases of HAV in 2003 to be 7653 with the estimate of actual clinical cases to be 33.
during World War II. and lack of a reliable clean water resource. • Internationally: HAV has a worldwide distribution. and South America. Virtually any food can be contaminated with HAV. Globally. class structure) of some developing nations are differing frequencies of HAV antibody in the older population. a direct correlation between increasing age and likelihood of adverse events (ie. Over the last century. Until recently. In Shanghai in 1988. Factors predisposing humans to early acquisition include overcrowding. infection is often asymptomatic and subclinical.will likely modify the evolving epidemiology. In stark contrast. Food handlers. US CDC data supported cycles of disease occurring every 510 years. • The single most important determinant of illness severity is age. certain social practices. US military personnel who served more recently in Asia or. many with jaundice. Evidence of past infection differs between adults (~40%) and children (~10%) and supports acquisition during school-aged years. This. 90% of those infected before age 2 years are asymptomatic.000 service personnel experienced symptomatic HAV infection in World War II. accordingly. improved sanitation and hygiene measures have resulted in a shift in the age group that carries the burden of disease. morbidity and mortality) is present. Approximately 75% of adults are symptomatic with infection. at the point of preparation. where evidence of past infection is nearly universal. Asia. although cases have been documented. This provided a unique opportunity to study the incubation and natural history of acute HAV infection in a large population. may result in more clinically apparent and severe disease. Acquisition in early childhood is the norm in these nations and is usually asymptomatic. poor sanitation. most cases are symptomatic. more remotely. in which people returned from areas of high endemicity. with the frequency of icteric cases approaching 80%. Within the socioeconomic framework (ie. are an infrequent source of outbreaks in the United States. this pattern has disappeared and has been associated with a decline in overall incidence of new infection. The highest seropositivity (antibody to HAV) is observed in adults in urban Africa. in turn. Some of these outbreaks correlated with the wars of the 20th century. often returned with evidence of infection acquired abroad. sporadic cases may be observed in some individuals. In recent years. As many as 200. a large shellfish-related epidemic occurred. Mortality/Morbidity: In the United States. Most deaths from acute HAV infection .
Case fatality rates approach 2%. Some evidence suggests that reinfection may occur late in life in individuals in whom levels of detectable antibody have disappeared. Infection in early life occurs commonly in developing countries. Therefore. this pattern has been changing. childcare workers. Age: With increasing age of acquisition. The current older population has a large number of individuals who are immune by virtue of exposure in early life.02-0. most of those admitted to the hospital were aged 20-40 years. • Race: Immigrants from countries of high endemicity to countries of low endemicity may be responsible for some of the periodicity observed with outbreaks of infection.occur in persons older than 50 years. and a vast majority of persons who acquire infection when older than 50 years exhibit signs and symptoms of the disease. symptomatic disease is uncommon in natives and is most often observed in visitors to these countries. no sexual predilection is apparent. • Other populations with increased likelihood of adverse sequelae caused by acute HAV infection are those with significant comorbidities or concurrent chronic liver disease. as highlighted by the high incidence of hepatitis B surface antigen in persons who died in the Shanghai outbreak. male homosexuals). A rapid rise in immunoglobulin G (IgG) antibody to HAV in the absence of immunoglobulin M (IgM) is the hallmark of this event (anamnestic response). Sex: Except for persons in high-risk populations (eg. however. affected individuals tend to be infants born since the last outbreak or susceptible adults who moved to the area. CLINICAL Section 3 of 11 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography . aid workers. reinfection is not associated with clinical disease. Although reported to occur. along with case reports of acute HAV infection deaths in persons with hepatitis C. sewage workers. both symptomatic disease and adverse sequelae increase. The lower incidence of infection in the older population was related to a greater likelihood of immunity rather than to a decrease in exposure. The overall case fatality for acute HAV infection is 0. despite the fact that acute HAV infection is uncommon in this age group. In the Shanghai outbreak. In this setting. Mortality from fulminant hepatic failure increased with increasing age despite the decreasing prevalence of disease as age increased. Seropositivity for HAV antibody protects individuals against reinfection.1%.
malaise. overseas travel. and mild headache. are less frequent than the above symptoms. Smokers often lose their taste for tobacco.5°C). although less common than jaundice. myalgia. nausea and vomiting. Some of the important differential diagnoses for acute hepatitis warrant early and specific management. is generally accompanied by jaundice. and jaundice has HAV infection. is more common in elderly persons. accidental Tylenol overdose). although associated. Jaundice occurs in most (70-85%) adults with acute HAV infection. The incubation period is 2-6 weeks. although this is not universal. the history should also initiate a search for the source of exposure (eg. intravenous drug use) along with excluding other possible causes for acute hepatitis (eg. Shorter incubation periods may result from higher total dose of viral inoculum. Abdominal pain occurs in approximately 40% of patients. o o o • Relapsing hepatitis A: This is an uncommon sequela of acute infection. Not every patient with fever. Itch (pruritus). Rash more often occurs on the lower limbs and may have a vasculitic appearance. Jaundice is less likely in children and is uncommon in infants. fatigue. This phenomenon is further discussed in Complications. o • Icteric phase o o o Dark urine appears first (bilirubinuria). similar to those presenting with appendicitis. Physical: The physical examination focuses on detecting features to support a . lack of immunization. and is characterized by a protracted course of symptoms of the disease and a relapse of symptoms and signs following apparent resolution. with a mean of 4 weeks. Pale stool soon follows. along with some of the less commonly associated features of the disease. Arthralgias and skin rash. The degree of icterus also increases with age. Prodrome o • Patients may have mild flulike symptoms of anorexia.History: Along with outlining the presenting complaint and its severity and sequelae. • Discussion focusing on excluding other etiologies should be undertaken early in order to guide further investigation. low-grade fever (usually <39. hepatomegaly.
• • • Hepatomegaly is common. Tylenol. Viral Other Problems to be Considered: Acute drug-induced liver injury (eg. ecstasy) Acute HIV infection Drug-induced hypersensitivity reactions (eg. Epstein-Barr virus [EBV]) . Causes: Most patients have no defined risk factors. Patients may have a fever with temperatures of up to 40°C. Jaundice or scleral icterus may occur. cytomegalovirus [CMV]. Risk factors for acquisition include the following: • • • • • • Personal contacts Institutionalization Occupation (eg. daycare) Foreign travel Male homosexuality Illicit parenteral drug use Section 4 of 11 DIFFERENTIALS Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography Budd-Chiari Syndrome Cytomegalovirus Hepatitis. sulfasalazine hypersensitivity) Viral hepatitis (eg.diagnosis of acute hepatitis and should include assessment for features of chronic liver disease or similarly assessment for evidence of decompensation.
which increases dissipation of body heat via vasodilation and sweating.Used to treat nausea and vomiting. not to exceed 5 doses in 24 h Documented hypersensitivity. hydantoins. Acts centrally on chemoreceptor triggers in the floor of the fourth ventricle. 5-10 mg PO tid/qid 5-20 mg IV/IM tid Not established Drug Name Adult Dose Pediatric Dose . severe or recurrent pain or high or continued fever may indicate a Precautions serious illness. Hepatotoxicity possible in persons with chronic alcoholism following various dose levels. Relieves mild to moderate pain. Drug Category: Analgesic agents -.Usually safe but benefits must Pregnancy outweigh the risks.Pain control is essential to quality patient care. caution in Contraindications G-6-PD deficiency or PKU Rifampin can reduce analgesic effects.6 g/d Pediatric Dose >12 years: 325-650 mg PO q4h. Acetaminophen is useful for pain and/or fever. Adult Dose not to exceed 4 g/d <12 years: 10-15 mg/kg/dose PO q4-6h prn. coadministration with barbiturates. Metoclopramide (Reglan) -.The goals of pharmacotherapy are to reduce morbidity and to prevent complications. not to exceed 2. Interactions carbamazepine.Dopamine antagonist that stimulates acetylcholine release in the myenteric plexus. which provides important antiemetic activity. and isoniazid may increase hepatotoxicity B . Feverall) -.Reduces fever by acting directly on hypothalamic heat-regulating Drug Name centers. contained in many OTC products and combined use with these products may result in cumulative doses exceeding recommended maximum dose Drug Category: Antiemetics -. Tempra. Acetaminophen (Tylenol. 325-650 mg PO q4-6h or 1 g PO tid/qid.
Derived from large pools of human plasma and is composed of 4 . Havrix: 1440 U IM once. duration of effect has not been fully established. or E viruses Drug Category: Immune globulins -. pheochromocytoma. Caution in acute infection or febrile illness. Pediatric Dose 720 U day 0 and 720 U booster dose at 6-12 mo Vaqta: 25 U IM once. booster dose at 618 mo Documented hypersensitivity.Purified preparation of gamma globulin. booster dose at 6-12 mo Adult Dose Vaqta: 50 U IM once. Caution in history of mental illness and Precautions Parkinson disease Drug Category: Vaccines. or perforation. efficacy >85%. vaccine does not protect against hepatitis B. booster dose at 6 mo <2 years: Not recommended >2 years: Havrix: 360 U IM days 0 and 30. IV/SC/ID Contraindications administration May decrease effects of Interactions immunosuppressive agents C . history of seizure disorders Anticholinergic agents antagonize Interactions effects. Contraindications obstruction. GI hemorrhage. Vaqta) -. Hepatitis A vaccine.Usually safe but benefits must Pregnancy outweigh the risks. inactivated (Havrix. C. 360 U booster dose at 6-12 mo.May be administered with Drug Name immunoglobulin injections without affecting efficacy. alternatively.Hepatitis A vaccine is used for active immunization against disease caused by HAV.Documented hypersensitivity. viral -. caution Precautions in individuals taking anticoagulant therapy.Safety for use during pregnancy has Pregnancy not been established. opiate analgesics may increase CNS toxicity B .
Safety for use during pregnancy has Pregnancy not been established. eg. Used for postexposure prophylaxis or when inadequate time is available for immunization to be effective before potential exposure.06 mL/kg IM q4-6mo for travelers staying >3 mo Pediatric Dose Not established Documented hypersensitivity. promotes remyelination. urticaria. blocks complement cascade. pruritus.02-0. intramuscular (BayGam 15-18%) -. blocks Fc receptors on macrophages. approximating the distribution of human serum. including INF-gamma. IgA Contraindications deficiency. do not administer within 3 mo of vaccine C . aseptic meningitis (10%). 0. For situations in which exposure is likely to occur before vaccination would be effective. If likely to be returning to areas of high endemicity. may increase Drug Name CSF IgG (10%). both may be administered without reducing the efficacy of HAV vaccine. infusions may increase risk of migraine attacks. Gammagard S/D). anti-IgE/IgG antibodies Increases toxicity of live virus vaccine Interactions (MMR). Immune globulin. Effective when administered within 14 d of exposure. suppresses inducer T and B cells and augments suppressor T cells.Neutralizes circulating myelin antibodies through anti-idiotypic antibodies. increases risk of renal tubular necrosis in elderly patients and in . where hepatitis A is common) 0. Precautions First check serum IgA (use an IgAdepleted product. down-regulates proinflammatory cytokines.subclasses of antibodies.06 mL/kg IM for exposed contacts or individuals traveling to areas for up to 6 mo. infusions may increase serum viscosity and thromboembolic events. use higher dose if subject will be Adult Dose in the area for up to 6 mo (ie. or petechiae (2-5 d postinfusion to 30 d). concurrent vaccination is recommended.
safe food sources) is also important. Approximately 20% of individuals with acute HAV infection may require hospitalization. volume depletion. the dose should be no greater than 4 g/d. and apparent hyponatremia FOLLOW-UP Section 8 of 11 Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography In/Out Patient Meds: • Tylenol may be safely used to treat some of the symptoms associated with the illness. The vaccine is not yet licensed for use in persons younger than 2 years. o • In the United States. Transfer: • Refer patients with fulminant hepatic failure to facilities with expertise in liver transplantation. Vaccine efficacy ranges from 80-100% after 1-2 doses compared to placebo. The current dosing recommendations for the available vaccinates are provided in Medication. hand washing. Global immunization appears to be prohibitively expensive. vaccination programs targeting children during urban outbreaks have demonstrated significant benefits. o o o .patients with diabetes. which increases herd immunity and reduces the likelihood of further outbreaks in high-risk communities. Long-term secondary goals include immunization. Immunization programs applied to high-risk groups show morbidity and cost benefits. Education about transmission and prevention of transmission (eg. laboratory study result changes associated with infusions include elevated antiviral or antibacterial antibody titers for 1 mo. However. with treatment of contacts to prevent further cases of disease is the primary goal. and preexisting kidney disease. The efficacy of immunization has been clearly demonstrated in high-risk groups. Deterrence/Prevention: • Control at the source. 6-fold increase in ESR for 2-3 wk.
• • Notify the appropriate public health authority following diagnosis.8% among adults older than 50 years and is also higher in persons with chronic liver diseases. Complications: • Generally. • • Annually. postexposure prophylaxis). where overall the mortality is estimated at approximately 0. o Death is more frequent in elderly patients and in those with underlying liver disease. Although the case-fatalities from fulminant HAV have been reported in all age groups. high endemicity) is longer than 3 months or when repeat travel to the area (ie. In children. Both the vaccination and intramuscular immunoglobulin should be administered to provide long-term immunity. >2 visits outside a 3-mo period) is likely. HAV infection elicits no lasting sequelae. Passive immunization with Gammagard reduces infection when administered within 14 days of exposure (ie. preexposure prophylaxis has been somewhat replaced by immunization. Immunization is indicated for individuals traveling to areas of high endemicity who have less than 2 weeks before departure. an estimated 100 people die in the United States as a result of acute liver failure due to HAV. particularly in persons who intend to travel to these areas repeatedly.3%. Vaccination in some low-risk groups who are potential sources of larger outbreaks of infection (eg. 10% of cases of fulminant failure in children are caused by HAV infection. occurring in fewer than 0. the rate is 1. liver transplantation has been performed for fulminant hepatic failure. The potentially disastrous outcome of acute HAV infection in this group cannot be overemphasized. Response rates in patients with advanced liver disease and in those on immunosuppressive therapies are likely to be lower. food handlers) has been implemented by some employers. Death is rare. although cost-benefit analysis for the employer does not seem to support such measures. Initiate contact tracing after diagnosis. o o o In many instances. The frequency of acute hepatitis appears more common in states neighboring Mexico. Postexposure prophylaxis is recommended for nonimmunized close contacts of those recently diagnosed with acute HAV infection. cost-benefit analysis suggests that vaccination is preferred over gamma globulin when an extended stay in the area of risk (ie. In France.o o People with chronic liver disease of any cause should consider vaccination. For travelers.2% of cases. The outcomes from transplantation are the same as for others with .
Good data to support this hypothesis are lacking. Vasculitic skin rashes and nephritis may be additional clinical clues to this syndrome. Following a typical acute course of HAV infection. o o o o . Acute renal failure. with partial or complete resolution of clinical and biochemical manifestations. Still disease. relapse occurs after a short period (usually <3 wk) and mimics the initially presentation. A postulated mechanism involves molecular mimicry and genetic susceptibility. and weight loss. with lengthening periods between flares. o Prolonged cholestasis may follow the acute infection. acute arthritis. However. agranulocytosis. The usual features of cholestatic viral hepatitis A are pruritus. although it usually is clinically milder. IgM antibody test findings are positive. These complications are all rare. Recurrent disease does not occur following transplantation despite immunosuppression. o o • Relapsing HAV infection o This complication occurs in 3-20% of patients with acute HAV infection and uncommonly takes the form of multiple relapses. lupuslike syndrome. A tendency to greater cholestasis exists in these patients. pancreatitis. and the results of larger clinical trials are not available. and Sjögren syndrome have been reported in association with HAV infection. these findings are confined to isolated case reports. Corticosteroids and ursodeoxycholic acid may shorten the period of cholestasis. Autoimmune hepatitis following HAV infection has received substantial discussion in the literature. During relapses. interstitial nephritis. The clinical course is toward resolution. a remission phase occurs.fulminant disease. diarrhea. The frequency at which this occurs increases with age. The total duration is 3-9 months. transient heart block. in much the same way as that proposed in type 1 diabetes. Guillain-Barré syndrome. shedding of virus can be detected. Prolonged cholestasis is characterized by a protracted period of jaundice (>3 mo) and resolves without intervention. with serum bilirubin levels greater than 10 mg/dL. The initial flare usually lasts 3-6 weeks. bone marrow aplasia. fever. red blood cell aplasia. in a way similar to that of traditional autoimmune hepatitis. Steroid therapy for this condition was associated with good clinical response and improvement in biochemical and clinical parameters. Some investigators believe that the use of corticosteroids may predispose patients to developing relapsing hepatitis A.
visit eMedicine's Hepatitis Center. Travelers should avoid uncontrolled water sources. Recurrence and chronic hepatitis does not usually occur. in selected cases. which comes from a combination of careful history and subsequent examination. safe water supplies. is an option if the patient has fulminant failure. Advice should be provided regarding the benefits of immunization. Long-term immunity accompanies infection. Also. Finally. For excellent patient education resources. and Pancreas Center. Omitting these measures may place the practitioner in a vulnerable situation. Boiling water or adding iodine inactivates the virus. although the course is generally benign without treatment.o Liver transplantation has been performed in patients with this condition when signs of significant decompensation have occurred. Liver. and Public Health Center. particularly in high-risk individuals. Patient Education: • Travelers should be educated about good hygiene and clean. raw shellfish. always exclude drugs. tracing contacts and notifying local public health authorities are important steps for preventing further cases. Section 9 of 11 • • MISCELLANEOUS Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Pictures Bibliography Medical/Legal Pitfalls: • Central to the prevention of any legal problem is establishing the correct diagnosis. All fruit should be washed and peeled. Corticosteroid treatment has been shown to improve the clinical course. • . remember that transplantation. Gallbladder. therefore. After establishing a diagnosis. Prognosis: • Prognosis is excellent. and uncooked food. particularly Tylenol. see eMedicine's patient education articles Hepatitis A and Foreign Travel. Appearances may be deceiving. People with HAV infection who are treated at home and those around them should follow strict enteric precautions. as a cause of acute liver injury.
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