Some authors have even limited duration of DAA therapy to as few as 8 d, but this is not currently recommended outside a clinical trial setting[143]

Some authors have even limited duration of DAA therapy to as few as 8 d, but this is not currently recommended outside a clinical trial setting[143]. virus traverses the mucosa of the small intestinal wall. The virus particles subsequently replicate and are secreted into the biliary canaliculi, reaching back to the small intestine through the bile ducts and being re-excreted in the feces. Until the body responds with appropriate immune reaction in antibodies, the HAV enterohepatic cycle continues. Human leukocyte antigen-restricted, HAV-specific CD8+ T lymphocytes and natural killer cells have been implicated in the damage and destruction of infected hepatocytes[14-16]. Clinical presentation The usual HAV incubation period is about 2-4 wk[17]. Fever, malaise, jaundice have been described as the most common presenting symptoms for HAV contamination[18]. Other common symptoms include weakness, fatigue, nausea, vomiting, abdominal pain, arthralgias, myalgias, diarrhea and anorexia[12]. Patients rarely enter a prolonged cholestatic phase through recovery, while relapsing infections have been described as well[19]. About 10%-15% of patients present with a relapsing course within a 6-mo period of the initial contamination[20]. The symptoms during the relapse are usually less severe than the initial contamination. Notably, on extremely rare occasions a type 1 autoimmune hepatitis has been observed in genetically predisposed patients[21]. The spectrum of infections can range from asymptomatic patients without jaundice, symptomatic patients with jaundice, cholestasis with prolonged jaundice, to relapsing infections or acute liver failure[19]. Serum aminotransferases above 1000 U/dL are usually noted, with total bilirubin typically 10 mg/dL, and alkaline phosphatase below 400 U/L. Usually the serum alanine aminotransferase (ALT) is higher than the aspartate aminotransferase (AST)[22,23]. In general, older patients are more likely to have severe hepatocellular derangements, hospital admissions and higher mortality[24]. These findings can be attributed to an impaired regeneration capacity of the liver and a relatively weaker immune system in the older population[25]. In addition to old age, higher mortality has been reported in males[26]. Old age, underlying liver pathology and chronic viral hepatitis are reported risk factors for acute liver failure. In patients who develop acute liver failure, higher mortality has been associated with creatinine 2 mg/dL (strongest predictor) total bilirubin 9.6 mg/dL Pimobendan (Vetmedin) and albumin 2.5 g/L[18]. Diagnosis Specific antibodies against HAV (anti-HAV) in the serum can be detected. The diagnosis is confirmed by the presence of immunoglobulin (Ig) M anti-HAV. The antibodies can be detected at the time of onset of symptoms. Serum IgM levels peak during the acute infection and remain positive for up to 4 mo on an Pimobendan (Vetmedin) average from the onset of symptoms[27]. Immunity is usually tested with HAV total antibody to determine HAV natural exposure or secondary to vaccination[28]. The Pimobendan (Vetmedin) presence of IgM antibodies without any clinical symptoms is indicative of HAV infection in the past with persistent antibodies, asymptomatic infection or false positive test[29]. Rabbit Polyclonal to XRCC2 Liver biopsy or imaging studies are not required to make a diagnosis. If performed, a liver biopsy may show marked portal inflammation with typically a lesser degree of necrosis, Kupffer cell proliferation, acidophil bodies, or ballooning when compared to non-HAV viral hepatitis[30]. Management No specific treatment is available for HAV and the management is mainly symptomatic. The primary focus remains on improving sanitary conditions to minimize the Pimobendan (Vetmedin) transmission in the community. Historically, immunoglobulins have been used in the prevention of HAV infections. With the availability of an effective vaccine, the use of immunoglobulins has been largely abandoned except in infants below the age of 12.