1/84. Exacerbation of chronic hepatitis d during interferon alpha administration.Acute and severe impairment of liver function with jaundice and ascites occurred in two out of seven patients with chronic hepatitis d during interferon alpha administration (10 MU three times a week). Both of them were young women with histological diagnoses of moderate to severe chronic hepatitis and cirrhosis with no signs of portal hypertension. Only a slow and partial recovery was observed after interferon withdrawal. autoantibodies against basal cell layer tested positive in these two patients. In the remaining five patients with hepatitis d who did not experience liver impairment during interferon administration, basal cell layer antibodies were found only in one case. We conclude that severe decompensation of liver cirrhosis related to hepatitis d may occur during interferon administration. Positivity of basal cell layer antibodies may be associated with the risk of developing such an adverse event but our data are not sufficient to prove this association.- - - - - - - - - - ranking = 1keywords = hepatitis (Clic here for more details about this article) |
2/84. Management of liver failure in a haemophilic patient co-infected with human immunodeficiency and hepatitis c viruses.We present a case of liver failure in a haemophilic patient coinfected with transfusion acquired human immunodeficiency (hiv) and hepatitis c (HCV) viruses. The case illustrates the interaction of multiple viruses with accelerated progression to end stage liver disease and ultimately death. We report the impact on the patient management of two liver biopsies, which diagnosed an initial drug induced hepatitis and subsequently an atypical HCV related hepatitis.- - - - - - - - - - ranking = 0.875keywords = hepatitis (Clic here for more details about this article) |
3/84. Hemophagocytic syndrome presenting as acute hepatic failure in two infants: clinical overlap with neonatal hemochromatosis.Two patients with hemophagocytic lymphohistiocytosis who presented with acute liver failure are reported. Both presented with fever, hepatosplenomegaly, markedly elevated liver function tests, abnormal coagulation profiles, and an increase in serum ferritin. Both infants were diagnosed with neonatal hemochromatosis based on a clinical picture of hepatic insufficiency with hyperferritinemia and were referred for liver transplantation. The first patient died of liver failure and septicemia before transplantation. review of autopsy material revealed a hepatitis-like pattern and extensive infiltration of liver and other organs including bone marrow by histiocytes, some of which were hemophagocytic. The second patient underwent liver transplantation but died 44 days thereafter from progressive hemophagocytic lymphohistiocytosis. Examination of the resected liver demonstrated a hepatitis-like pattern, proliferation of histiocytes, and hemophagocytosis, and the bone marrow revealed hemophagocytic histiocytosis. Hemophagocytosis recurred in the allograft. Hepatic manifestations are common in hemophagocytic lymphohistiocytosis and overt hepatic failure may occur, but initial presentation as fulminant hepatic failure is not well recognized. Elevated serum ferritin can make the distinction from neonatal hemochromatosis and other forms of neonatal liver failure difficult. Hemophagocytic lymphohistiocytosis should be considered in the differential diagnosis of neonatal liver disease, especially when it is accompanied by cytopenias.- - - - - - - - - - ranking = 0.25keywords = hepatitis (Clic here for more details about this article) |
4/84. Nimesulide-induced hepatitis and acute liver failure.BACKGROUND: Nimesulide is a relatively new non-steroidal anti-inflammatory drug that is gaining popularity in many countries because it is a selective cyclooxygenase 2 inhibitor. Occasionally, treatment is associated with mild elevation of liver enzymes, which return to normal upon discontinuation of the drug. Several cases of nimesulide-induced symptomatic hepatitis were also recently reported, but these patients all recovered. OBJECTIVES: To report the characteristics of liver injury induced by nimesulide. patients AND methods: We report retrospectively six patients, five of them females with a median age of 59 years, whose aminotransferase levels rose after they took nimesulide for joint pains. In all patients nimesulide was discontinued, laboratory tests for viral and autoimmune causes of hepatitis were performed, and sufficient follow-up was available. RESULTS: One patient remained asymptomatic. Four patients presented with symptoms, including fatigue, nausea and vomiting, which had developed several weeks after they began taking nimesulide (median 10 weeks, range 2-13). Hepatocellular injury was observed with median peak serum alanine aminotransferase 15 times the upper limit of normal (range 4-35), reversing to normal 2-4 months after discontinuation of the drug. The remaining patient developed symptoms, but continued taking the drug for another 2 weeks. She subsequently developed acute hepatic failure with encephalopathy and hepatorenal syndrome and died 6 weeks after hospitalization. In none of the cases did serological tests for hepatitis a, B and C, Epstein-Barr virus and cytomegalovirus, as well as autoimmune hepatitis reveal findings. CONCLUSIONS: Nimesulide may cause liver damage. The clinical presentation may vary from abnormal liver enzyme levels with no symptoms, to fatal hepatic failure. Therefore, monitoring liver enzymes after initiating therapy with nimesulide seems prudent.- - - - - - - - - - ranking = 1keywords = hepatitis (Clic here for more details about this article) |
5/84. anesthesia for cesarean delivery in a pregnant woman with acute hepatic failure.IMPLICATIONS: A case of reactivation of hepatitis B and development of fulminant hepatic failure in a pregnant hepatitis b virus carrier is reported. Although the occurrence or reactivation of hepatitis B in pregnancy are rare and usually not considered to be medical indications for termination of pregnancy, decisions regarding delivery and liver transplantation must be made if severe hepatic failure develops.- - - - - - - - - - ranking = 0.375keywords = hepatitis (Clic here for more details about this article) |
6/84. Fulminant chemical hepatitis possibly associated with donepezil and sertraline therapy.OBJECTIVE: To describe a case of fulminant hepatitis possibly related to concomitant donepezil and seratriline therapy. PATIENT AND SETTING: An 83-year-old woman treated in a dementia care facility and later in a tertiary medical center. INTERVENTION AND MANAGEMENT: Discontinuation of donepezil and sertraline therapy with subsequent improvement evidenced by liver biopsy and liver function tests. RESULTS: An older woman with Alzheimer's disease was admitted to a dementia care facility because of aggressive behavior. Treatment with sertraline was initiated in February 1998. sertraline doses were increased gradually to 200 mg daily by May 1998, and some improvement in behavior was seen. Concomitant therapy with donepezil 5 mg qhs was initiated June 26, 1998. Ten days later, confusion and jaundice were noted. Total bilirubin was 5.6 mg/dL, GGTP was 1,208 IU/L, and alkaline phosphatase was 369 IU/L. Computed tomography revealed cholelithiasis without ductal dilation. Liver, spleen, and pancreas seemed normal. Donepezil and sertraline were discontinued. The patient was admitted to our institution and treated for dehydration. A liver biopsy revealed scattered portal eosinophils and prominent cholestasis consistent with acute chemical hepatitis. The GGTP and total bilirubin of this patient peaked at 2,235 IU/L and 22.6 mg/dL, respectively. The patient improved, and her liver function tests normalized over the next 2 months.- - - - - - - - - - ranking = 0.75keywords = hepatitis (Clic here for more details about this article) |
7/84. Acute liver failure due to enalapril.This report presents a 46-year-old man who was treated for hypertension with the angiotensin-converting-enzyme (ACE) inhibitor enalapril. After 3 years of continuous treatment he presented with jaundice and progressive liver failure that continued despite withdrawal of the medication. The patient was taking no other medication. All known causes of acute liver failure could be excluded indicating a drug-induced liver damage after long-term treatment with enalapril. Analysis of liver biopsies revealed a pathomorphological pattern comparable to than observed in severe halothane hepatitis. Serological studies including T-cell stimulation with enalapril and a broad spectrum of tests for autoimmunity including autoantibodies against calreticulin, the major Ca2 and Zn2 binding protein of the endoplasmic reticulum and suggested to be involved in the pathogenesis of halothane hepatitis were negative. Thus, the mechanism of enalapril-induced liver injury remains obscure. liver failure progressed and finally led to orthotopic liver transplantation. To our knowledge, this is the longest duration of chronic treatment with an ACE inhibitor before liver failure occurred. In addition, liver failure progressed despite withdrawal of the medication. It is concluded that even after long-term treatment with an ACE inhibitor liver failure may be induced. Therefore, regular monitoring of liver enzymes should be considered.- - - - - - - - - - ranking = 0.25keywords = hepatitis (Clic here for more details about this article) |
8/84. Acute liver failure in pregnancy. A case report.BACKGROUND: Liver disease in pregnancy can be grossly divided into those disorders coincidentally occurring during the pregnant state and hepatic diseases limited to pregnancy. Numerous infectious agents can result in acute hepatitis and include not only the hepatitis viruses--A, B, C and E--but herpesvirus and cytomegalovirus as well. Coxsackie B viruses can cause several clinical presentations, ranging from asymptomatic to mild febrile illness to myocarditis and meningitis. Rarely has coxsackievirus infection been associated with fulminant hepatic failure. CASE: A Coxsackie B virus infection resulted in acute liver failure in a gravid woman. The patient was managed expectantly, with resolution of the liver disease and delivery five weeks after discharge. CONCLUSION: The onset of hepatic disease is insidious, with only vague symptoms or minor complaints often heralding the progression to liver failure. A careful history, physical examination and appropriate diagnostic tests can help determine the etiology of hepatic disease and help decide whether expectant management of the gravid patient or immediate delivery is appropriate.- - - - - - - - - - ranking = 0.25keywords = hepatitis (Clic here for more details about this article) |
9/84. A case of cholestatic autoimmune hepatitis and acute liver failure: an unusual hepatic manifestation of mixed connective tissue disease and sjogren's syndrome.Although hepatomegaly is reported to occur occasionally in patients with mixed connective tissue disease (MCTD) or sjogren's syndrome (SS), autoimmune liver diseases such as primary biliary cirrhosis, sclerosing cholangitis, and autoimmune hepatitis in association with MCTD or SS have rarely been described. We report a case of severe cholestatic autoimmune hepatitis presenting with acute liver failure in a 40-yr-old female patient suffering from MCTD and SS. The diagnosis of MCTD and SS was made at the age of 38. The patient presented severe jaundice and elevation of conjugated bilirubin. The patient denied alcohol and drug use and had no evidence of viral hepatitis. On the 8th day of her hospitalization, the patient developed grade III hepatic encephalopathy. She was diagnosed as autoimmune hepatitis presenting with acute liver failure based on clinical features, positive FANA and anti-smooth muscle antibodies, negative anti-mitochondrial antibodies, high titers of serum globulin, liver biopsy findings, and a good response to corticosteroid therapy, The patient was managed with prednisolone and the clinical symptoms, liver function test results, and liver biopsy findings showed much improvement after steroid therapy.- - - - - - - - - - ranking = 1keywords = hepatitis (Clic here for more details about this article) |
10/84. Fatal acute hepatic failure induced by danazol in a patient with endometriosis and aplastic anemia.We describe a 47-year-old woman with severe aplastic anemia with genital bleeding who developed acute severe hepatitis after the administration of danazol while she was receiving cyclosporin. She had been diagnosed with severe aplastic anemia 1 year previously and, while hospitalized, had received methyl prednisolone pulse therapy, which was not successful. She was then referred to our hospital. She was treated with antithymocyte globulin, cyclosporin, granulocyte colony-stimulating factor, and methyl prednisolone; a good response was achieved after 3 months of this therapy. Subsequently, oral administration of cyclosporin was continued, but she was readmitted to our hospital when pancytopenia gradually developed and the genital bleeding recurred. danazol was administered for pancytopenia and endometriosis. Four days after the first administration of danazol, epigastric pain occurred, and the danazol was stopped. Eighteen days after the first danazol administration, very severe hepatic injury occurred abruptly. The patient died of hepatic failure. Postmortem examination revealed centrilobular massive necrosis of the liver. danazol was implicated as the agent responsible for causing the hepatic failure. drug interactions between danazol and cyclosporin may cause adverse effects.- - - - - - - - - - ranking = 0.125keywords = hepatitis (Clic here for more details about this article) |
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