Disseminated clostridial infection and gallbladder infection with gas-producing organisms may lead to air in the liver and biliary system. Elevation of serum aminotransferase enzymes are common and usually in the range of ∼100-500 U/L for AST/ALT.2, 7 Since the advent of antiviral drugs, the frequency of viral infection http://www.selleckchem.com/products/Methazolastone.html as a cause of acute elevation of serum ALT/AST after HCT has plummeted.23 An extreme rise in ALT is now mostly due to a noninfective cause such as zone 3 hepatocyte

necrosis in SOS, hypoxic hepatitis, drug-induced liver injury, or a hepatitic presentation of GVHD.23, 37 Acute hepatitis caused by HSV, varicella zoster virus (VZV), adenovirus, and hepatitis B virus can lead to fatal fulminant hepatic failure after HCT1 and Epstein-Barr virus (EBV)-lymphoproliferative disease can be rapidly progressive (Fig. 3B–F), whereas hepatic

infections caused by cytomegalovirus and hepatitis C virus are seldom severe.7 With routine use of prophylactic acyclovir or valacyclovir, acute hepatitis due to HSV and VZV is now rare23; human herpesvirus 6 (HHV-6) and HHV-8 reactivation causing hepatitis despite antiviral prophylaxis has been reported. When there is uncertainty about the cause of rising serum ALT levels, DNA blood tests for herpesviruses, adenovirus, and HBV should be performed. Transvenous measurement of the wedged hepatic venous pressure gradient and biopsy can exclude hepatocyte necrosis caused by SOS and may demonstrate a specific viral diagnosis.25, 26 Acyclovir should be started empirically, particularly if the patient presents with abdominal HCS assay complaints typical of VZV infection.39 Adenovirus hepatitis Phloretin should be suspected if the patient has concomitant pulmonary, renal, bladder, or intestinal

symptoms; the most effective treatment is cidofovir when given early.40 Detection of EBV DNA by polymerase chain reaction in patients receiving immune suppressive drugs has allowed pre-emptive therapy with anti-B cell therapy. Fulminant hepatitis B may develop during immune reconstitution in patients at risk, but can be prevented with prophylactic antiviral agents.1, 4 If severe hepatitis B reactivation does occur, usually because a diagnosis of HBV was not made prior to HCT,10 antiviral therapy should be initiated immediately. Fulminant hepatitis B has also been reported following premature discontinuation of prophylactic antiviral therapy in oncology patients. Anti-HBV drugs should be not be discontinued until 6 months after full immune reconstitution.1 All patients, particularly those with high pretransplant HBV DNA levels, should be monitored by HBV DNA and serum ALT tests following antiviral drug withdrawal. Chronic hepatitis C in HCT recipients usually results in asymptomatic elevation of ALT from days +60-120, coinciding with the tapering of immunosuppressive drugs.7 Severe HCV hepatitis has only rarely been reported; antiviral therapy for HCV is not indicated early after HCT.