1/13. Fatality from hepatitis A in a child taking valproate.We report an 8-year-old boy with complex partial seizures due to congenital stroke, treated with valproate for more than 3 years (the last 2 years were on monotherapy) with no complications during that period except for transient thrombocytopenia. His sister had uncomplicated hepatitis A. One month later, the patient became jaundiced, went into fulminant hepatic failure, and quickly became encephalopathic despite discontinuation of valproate, aggressive supportive therapy, and treatment with carmitine. He then died. He had positive hepatitis A IgM; other causes for acute hepatitis were ruled out. Liver pathology revealed distended hepatocytes with cholestasis and microvesicular changes. We could find in the literature two other articles on four cases who developed liver failure with hepatitis A while on valproate. All those cases, however, recovered. In our patient a usually benign disease became deadly, probably because of the concomitant use of a hepatotoxic medication. Immunizing, with hepatitis A vaccine, all children on valproate therapy who are living in, or traveling to, endemic areas should be considered and is probably advisable.- - - - - - - - - - ranking = 1keywords = cholestasis (Clic here for more details about this article) |
2/13. thrombocytopenia in hepatitis A--an atypical presentation.Acute hepatitis due to hepatitis a virus (HAV) is usually a benign self-limiting disease during childhood. Autoimmune manifestations are rare with acute HAV, especially in children. We report an 8-year-old boy with severe thrombocytopenia as an initial manifestation of acute HAV infection. bone marrow examination suggested peripheral destruction of platelets. His clinical course was complicated by persistent severe thrombocytopenia and progressive cholestasis requiring prednisolone therapy.- - - - - - - - - - ranking = 1keywords = cholestasis (Clic here for more details about this article) |
3/13. hepatitis a virus infection presenting with seizures.Hepatitis A infection rarely causes extrahepatic manifestations. Here we present a 5-year-old patient with an initial complaint of nuchal rigidity and convulsions during the course of hepatitis A infection. Because hepatitis a virus rna was demonstrated in the cerebrospinal fluid, it was thought that convulsions might be related to this viral infection.- - - - - - - - - - ranking = 1.0510629408302keywords = extrahepatic (Clic here for more details about this article) |
4/13. Prolonged viral hepatitis type A with cholestasis: case report.We describe a clinical case of an eleven year old boy with a protracted cholestatic form of viral hepatitis type A. The role of a macrolide antibiotic in the determinism of this form of hepatitis is discussed.- - - - - - - - - - ranking = 4keywords = cholestasis (Clic here for more details about this article) |
5/13. Persistence of hepatitis a virus in fulminant hepatitis and after liver transplantation.A peroxidase-labelled, specific mouse monoclonal antibody to hepatitis a virus (HAV) and an in situ hybridization technique (streptavidin-biotin-horseradish peroxidase reaction) with an HAV-specific cDNA probe (recombinant plasmid pAWHA comprising 1.8 kb of the HAV-specific cDNA, located toward the 3' end of the genome) were used to detect HAV in liver tissues in two patients with fulminant viral hepatitis type A treated by liver transplantation after a protracted (day 40: case 1) and relapsing (day 60: case 2) clinical course. HAV antigens and HAV-specific genomic sequences were detected in the hepatectomy tissues and in serial biopsies of the liver grafts through to final follow-up at 2 months (case 2) or death at 7 months after re-grafting for chronic rejection (case 1). In the fulminant liver parenchyma, numerous degenerating and some surviving hepatocytes were positive and randomly scattered. The immunoperoxidase staining was predominantly cytoplasmic and often granular. The localization of the cDNA probe was predominantly nuclear/perinuclear but was occasionally cytoplasmic. High-titre IgM-anti-HAV antibodies persisted until death (case 1) or resolution (5 months) of an acute hepatitis (case 2), which occurred at 2 months, accompanied by HAV antigen (ELISA), in stool. Intact replicating virus particles must have been present in one or more sites in each case, including extrahepatic locations, with a viraemia as the most likely explanation for subsequent reinfection of the grafts.- - - - - - - - - - ranking = 1.0510629408302keywords = extrahepatic (Clic here for more details about this article) |
6/13. arthritis, vasculitis, and cryoglobulinemia associated with relapsing hepatitis a virus infection.hepatitis a virus, unlike hepatitis b virus, has rarely been associated with extrahepatic features. Two patients developed relapsing hepatitis A complicated by arthritis in both cases and cutaneous vasculitis in one. Both patients had cryoglobulinemia, with cryocrit values of 4.3% and 8.6%. Serologic studies showed that the cryoglobulin consisted of polyclonal IgM and IgG. The washed cryoglobulin was analyzed by sucrose density gradient ultracentrifugation under neutral (pH 7.4) and acidic (pH 2.8) conditions. enzyme-linked immunosorbent assay techniques were used to characterize the native and dissociated cryoglobulin. The cryoglobulin contained acid-dissociable IgG complexes greater than 19S, and high molecular weight rheumatoid factors of both IgG and IgM isotypes that could be dissociated to 7S and 19S forms, respectively. Dissociation of the cryoglobulin augmented 7S anti-hepatitis a virus IgG 2.27-fold, but augmented total 7S IgG only 1.12-fold, suggesting enrichment of antiviral antibody in the cryoglobulin.- - - - - - - - - - ranking = 1.0510629408302keywords = extrahepatic (Clic here for more details about this article) |
7/13. Functional causes of the ductal obstructive pattern on hepatobiliary scans.Hepatobiliary imaging with Tc-99m IDA derivatives has proven value for evaluation of biliary disease. Prompt hepatocellular uptake with persistent nonvisualization of the common bile duct and bowel is usually indicative of a high-grade common bile duct obstruction, but is not pathognomonic. A functional abnormality due to hepatocyte dysfunction resulting in intrahepatic cholestasis can also cause this pattern. Two cases of hepatocellular excretory dysfunction, one due to E. coli endotoxemia with intrahepatic cholestasis and the other due to acute hepatitis A that produces ductal obstructive patterns on Tc-99m disofenin scintigraphy in patients with documented patent biliary ducts, are reported. Transhepatic cholangiography or endoscopic retrograde cholangiography may be useful when the diagnosis of biliary ductal obstruction is in doubt.- - - - - - - - - - ranking = 2.0003710640439keywords = cholestasis, bile (Clic here for more details about this article) |
8/13. serum levels of secretory immunoglobulin a in liver disease.Secretory immunoglobulin a (sIgA) in serum was measured in patients with various liver diseases using enzyme immunoassay specific to sIgA. Marked elevation of the serum sIgA concentrations was found in liver diseases especially in intrahepatic or extrahepatic cholestasis. In chronic hepatitis and liver cirrhosis serum sIgA correlated significantly with leucine aminopeptidase (r = 0.69), GOT (r = 0.66), alkaline phosphatase (r = 0.55), and direct bilirubin (r = 0.42). In acute hepatitis their levels correlated significantly with total bilirubin (r = 0.59) and GPT (r = 0.55). In acute hepatitis and acute exacerbation of chronic hepatitis the major peaks of serum sIgA were observed later than those of liver enzymes. These results suggest two mechanisms working to elevate the serum sIgA levels in liver diseases. In chronic hepatitis, liver cirrhosis, and intrahepatic and extrahepatic cholestasis the raised serum sIgA probably reflects reflux of bile, a rich source of secretory component and sIgA, into circulation. In acute or chronic massive liver necrosis elevation of sIgA may be associated with liver regeneration. Serial measurement of serum sIgA with other conventional parameters will contribute much to the understanding of the pathophysiology of liver diseases.- - - - - - - - - - ranking = 4.1023114136823keywords = extrahepatic, cholestasis, bile (Clic here for more details about this article) |
9/13. Prolonged intrahepatic cholestasis secondary to acute hepatitis A.Viral hepatitis characterized by prolonged cholestasis has not been associated with a specific serologic marker. We report the cases of six patients presenting with a clinical syndrome typical of cholestatic hepatitis who were subsequently found to have acute hepatitis A. Usual features include pruritus, fever, diarrhea, and weight loss with serum bilirubin levels greater than 10 mg/dL, and a clinical course lasting at least 12 weeks. All patients recovered completely without sequelae. knowledge of this unusual manifestation of hepatitis A may help avoid potentially invasive procedures involved in the evaluation of suspected obstructive jaundice and facilitate appropriate immunoprophylactic measures.- - - - - - - - - - ranking = 5keywords = cholestasis (Clic here for more details about this article) |
10/13. Fulminant hepatic failure with massive necrosis as a result of hepatitis A infection.Fulminant hepatic failure as a result of hepatitis A is a rarely diagnosed complication entity in developed countries. With the advent of specific serologic markers for acute hepatitis a virus infection, the incidence and pathology of fulminant hepatitis A can be more clearly defined. We describe four patients (one adult, three children; two males and two females, ages 2 1/2-58 years) referred to our institution for orthotopic liver transplantation subsequent to fulminant hepatic failure following hepatitis A infection. All of these patients had a history of residence in or travel to hepatitis A endemic areas. Hepatitis A infection was documented by the presence of serum IgM against hepatitis a virus prior to transplantation. infection with hepatitis b virus, cytomegalovirus, Epstein-Barr virus, and herpes simplex virus was excluded by clinical and specific serologic examinations. All patients presented with varying degrees of encephalopathy, progressing to coma. Coagulopathy in the form of prolonged prothrombin time and partial thromboplastin time was present in all patients. Peak liver parenchymal enzymes increased to greater than ten times the upper limit of the normal range. Total and direct bilirubin levels increased to > 20 and 10 mg/dl, respectively. Histologic evaluation of the explanted livers showed a spectrum of changes ranging from periportal hepatocellular necrosis with focal parenchymal collapse and prominent bile duct proliferation to massive necrosis with complete loss of hepatic architecture.(ABSTRACT TRUNCATED AT 250 WORDS)- - - - - - - - - - ranking = 0.00018553202194243keywords = bile (Clic here for more details about this article) |
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