Hepatitis A Clinical Presentation

Along with outlining the presenting complaint and its severity and sequelae, the history should also initiate a search for the source of exposure (eg, overseas travel, lack of immunization, intravenous [IV] drug use) and attempt to exclude other possible causes of acute hepatitis (eg, accidental acetaminophen overdose). The incubation period is 2-6 weeks (mean, 4 wk). Shorter incubation periods may result from higher total dose of viral inoculum.

Discussion focusing on excluding other potential causes should be undertaken early in order to guide further investigation. Not every patient with fever, hepatomegaly, and jaundice has hepatitis A virus (HAV) infection. Some of the important differential diagnoses for acute hepatitis warrant early and specific management.

Prodrome

In the prodrome, patients may have mild flulike symptoms of anorexia, nausea and vomiting, fatigue, malaise, low-grade fever (usually < 39.5°C), myalgia, and mild headache. Smokers often lose their taste for tobacco, like persons presenting with appendicitis.

Icteric phase

In the icteric phase, dark urine appears first (bilirubinuria). Pale stool soon follows, although this is not universal. Jaundice occurs in most (70-85%) adults with acute HAV infection; it is less likely in children and is uncommon in infants. The degree of icterus also increases with age. Abdominal pain occurs in approximately 40% of patients. Itch (pruritus), although less common than jaundice, is generally accompanied by jaundice.

Arthralgias and skin rash, although also associated with acute HAV infection, are less frequent than the above symptoms. Rash more often occurs on the lower limbs and may have a vasculitic appearance.

Relapsing hepatitis A

Relapsing hepatitis A is an uncommon sequela of acute infection, is more common in elderly persons, and is characterized by a protracted course of symptoms of the disease and a relapse of symptoms and signs following apparent resolution (see Complications).

The physical examination focuses on detecting features that support a diagnosis of acute hepatitis and should include assessment for features of chronic liver disease or, similarly, assessment for evidence of decompensation.

Hepatomegaly is common. Jaundice or scleral icterus may occur. Patients may have a fever with temperatures of up to 40°C.

Prolonged cholestasis may follow the acute infection. The frequency at which this occurs increases with age. Prolonged cholestasis is characterized by a protracted period of jaundice (>3 mo) and resolves without intervention. Corticosteroids and ursodeoxycholic acid may shorten the period of cholestasis.

The usual features of cholestatic viral hepatitis A are pruritus, fever, diarrhea, and weight loss, with serum bilirubin levels higher than 10 mg/dL. Some investigators believe that the use of corticosteroids may predispose patients to developing relapsing hepatitis A. Good data to support this hypothesis are lacking.

Acute renal failure, interstitial nephritis, pancreatitis, red blood cell aplasia, agranulocytosis, bone marrow aplasia, transient heart block, Guillain-Barré syndrome, acute arthritis, Still disease, lupuslike syndrome, and Sjögren syndrome have been reported in association with HAV. These complications are all rare.

Autoimmune hepatitis after HAV infection has received substantial discussion in the literature. A postulated mechanism involves molecular mimicry and genetic susceptibility. With this condition, as with traditional autoimmune hepatitis, steroid therapy has been associated with good clinical response and improvement in biochemical and clinical parameters. However, these findings are confined to isolated case reports, and the results of larger clinical trials are not available.

Relapsing HAV infection occurs in 3-20% of patients with acute HAV infection and uncommonly takes the form of multiple relapses. After a typical acute course of HAV infection, a remission phase occurs, with partial or complete resolution of clinical and biochemical manifestations. The initial flare usually lasts 3-6 weeks; relapse occurs after a short period (usually < 3 wk) and mimics the initial presentation, although it usually is clinically milder.

A tendency to greater cholestasis exists in these patients. Vasculitic skin rashes and nephritis may be additional clinical clues to this syndrome. During relapses, shedding of virus can be detected. IgM antibody test findings are positive. The clinical course is toward resolution, with lengthening periods between flares. The total duration is 3-9 months.

Liver transplantation has been performed in patients with this condition when signs of significant decompensation have occurred. Corticosteroid treatment has been shown to improve the clinical course, although the course is generally benign without treatment.