Cases reported "Hepatic Encephalopathy"

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21/468. Fulminant hepatic failure caused by adenovirus infection following bone marrow transplantation for Hodgkin's disease.

    Adenoviruses are increasingly realised to be responsible for serious morbidity and mortality following allogeneic bone marrow transplantation. We describe a case of fulminant hepatic failure due to adenovirus serotype 2 in a 39-year-old woman who received a matched sibling allogeneic bone marrow transplant for multiply relapsed Hodgkin's disease. Isolated fulminant hepatic failure caused by this serotype of adenovirus has not previously been described.
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22/468. Paracetamol-induced fulminant hepatic failure in a child after 5 days of therapeutic doses.

    We report the case of a two and a half year-old girl who developed fulminant hepatic failure following 5 days of regular oral ingestion of paracetamol, approximately 90 mg x kg-1 x day-1. She presented with the typical findings of hepatomegaly, encephalopathy, high ammonia levels, high transaminases, hypoglycaemia and lactic acidosis. After stabilization, she was transferred to a specialist paediatric liver failure unit and fortunately she made a full recovery with intensive medical management.
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23/468. Kikuchi's disease with multisystemic involvement and adverse reaction to drugs.

    Kikuchi's disease (KD), or histiocytic necrotizing lymphadenitis, was initially described in japan in 1972. In the following years, several series of cases involving patients of different ages, races, and geographic origins were reported, but pediatric reports have been rare. The etiology of KD is unknown, although a viral or autoimmune hypothesis has been suggested. The most frequent clinical manifestation consists of local or generalized adenopathy, although in some cases, it is associated with more general symptoms, multiorganic involvement, and diverse analytic changes (leukopenia, elevated erythrocyte sedimentation rate, and c-reactive protein, as well as an increase of transaminases and serum lactic dehydrogenase). diagnosis is based on characteristic pathologic findings that permit differentiation of this disease from lymphoma, systemic lupus erythematosus, and infectious lymphadenopathies. We present here the case of a 14-year-old boy who presented with severe systemic manifestations and transient fulminant hepatic failure in response to treatment with antituberculosis drugs. Kikuchi's disease, lymphadenitis, liver failure, antituberculosis drugs.
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24/468. Subclinical portal-systemic encephalopathy in a child with congenital absence of the portal vein.

    A 6-year-old girl with congenital absence of the portal vein (CAPV) who had persistent hyperammonemia due to a congenital portosystemic shunt is reported. The patient only exhibited mild intention tremor, without any apparent neurological manifestations of portal-systemic encephalopathy. However, magnetic resonance imaging of the head showed white matter atrophy with ventricular dilatation, which is thought to represent subclinical brain damage caused by chronic hyperammonemia. This is the first report of subclinical portal-systemic encephalopathy in a patient with CAPV. The present case suggests that the effect of a congenital portosystemic shunt on the central nervous system is serious, but can be clinically latent in children with CAPV.
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25/468. Fatal fulminant hepatic failure due to cyproterone acetate.

    cyproterone acetate is a normally well-tolerated drug that is used widely for the treatment of prostatic carcinoma. Liver toxicity due to its use is not well known. We describe two cases of fatal fulminant hepatitis related to the use of cyproterone acetate.
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ranking = 328.27841268172
keywords = hepatitis, b
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26/468. Fatal fulminant hepatitis associated with bromfenac use.

    OBJECTIVE: To report a case of fulminant hepatic failure associated with the use of bromfenac, a new analog of the phenyl acetate class of nonsteroidal antiinflammatory drugs. CASE SUMMARY: A 60-year-old white woman with liver failure who had no known history of chronic liver disease was transferred to the liver transplant unit for evaluation. For three months preceding her illness, the patient was treated with bromfenac 25 mg po qid for arthritic pain. Prior to the initiation of bromfenac, her liver function test results were normal. Etiologic evaluation at presentation was unremarkable. The patient's condition continued to deteriorate, with the development of hepatic encephalopathy and worsening liver function test results while awaiting liver transplantation. Progressive hepatic and renal dysfunction along with respiratory decompensation ensued, and the patient died 48 days after initial presentation. CONCLUSIONS: Fulminant hepatic failure associated with the prolonged use of bromfenac appears to be an idiosyncratic response consistent with experience with other agents of its class. This case along with other cases of serious hepatotoxicity associated with the use of this agent ultimately resulted in bromfenac's removal from the market.
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ranking = 1313.5025396158
keywords = hepatitis, b
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27/468. Hypercalcaemia secondary to hepatocellular carcinoma.

    Many syndromes reflecting impaired metabolism have been described in association with primary neoplastic diseases. Hypercalcaemia secondary to malignancy without bone metastases and with normal parathyroid glands has been described as "pseudohyperparathyroidism". Differentiation from primary hyperparathyroidism is difficult and care should be taken to exclude an occult malignancy prior to surgical exploration for a parathyroid adenoma. Hypercalcaemia associated with hepatocellular carcinoma is not uncommon. Nevertheless, we describe a rare case of coma with persistent hypercalcaemia in a cirrhotic patient not previously known to have hepatocellular carcinoma.
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28/468. Hepatic decompensation in patients with cirrhosis during infection with influenza A.

    BACKGROUND: patients with chronic liver disease can develop hepatic decompensation during systemic infections. Although gram-negative and gram-positive bacteria are well recognized as causes of decompensation, the effect of influenza virus infection on patients with chronic liver disease is poorly documented. methods: Retrospective analysis of patients with positive viral cultures who were seen at a liver transplantation clinic in a tertiary care referral center during the 1997-1998 influenza A (H3N2) epidemic in San Diego, Calif. RESULTS: Three patients with end-stage liver disease (1 with Wilson disease and 2 with alcoholic liver disease) developed hepatic decompensation and required hospitalization during infection with influenza A. Two patients had biochemical and clinical evidence of hepatic decompensation, including ascites, hepatic encephalopathy, and peripheral edema, and the third had acute hepatocellular damage, with elevated levels of aminotransferases. Viral hepatitis serologic test results, acetaminophen levels, drug and alcohol screening findings, and bacterial and fungal cultures were negative in all 3 patients. Hepatic decompensation resolved without the need for transplantation in the 2 patients with liver failure, and all patients recovered to their baseline liver function levels within 1 month of onset of acute illness. CONCLUSIONS: Influenza A infection can cause hepatic decompensation and hospitalization in patients having cirrhosis or who are awaiting liver transplantation. Effective prevention with vaccination and early recognition and treatment of influenza are strongly recommended in these individuals.
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keywords = hepatitis, b
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29/468. Long-term treatment of portosystemic encephalopathy with oral branched-chain amino acids--a case report.

    We treated a 68-year-old male patient of hepatic encephalopathy with oral branched chain amino acids-enriched formula (Aminoleban EN) in addition to lactulose. His encephalopathy was successfully controlled with this therapy for more than a year despite the high blood ammonia levels. Repeated amino acids analyses demonstrated that the deranged branched chain to aromatic amino acids ratio was attenuated with long-term Aminoleban EN administration both in plasma and in cerebrospinal fluid. Oral branched-chain amino acid supplement was very useful in improving the chronic portosystemic or hepatic encephalopathy in this patient.
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30/468. Fatal hepatitis and renal failure during treatment with nimesulide.

    A healthy 70-year-old woman who took nimesulide for 5 days, presented 2 weeks later with jaundice for which no other cause was found. Laboratory evidence of coagulopathy, hypoalbuminaemia and hypoglycaemia were present on admission, and liver biopsy showed massive necrosis of hepatocytes and severe inflammatory infiltrate. Despite supportive and corticosteroid treatment, her jaundice deepened and progressive acute renal failure developed, characterized by a 'prerenal' profile changing into irreversible acute tubular necrosis pattern, coma, occult Gram-negative sepsis and death. Although rare, nimesulide-associated hepatotoxicity and nephrotoxicity may occur and should be recognized as early as possible, to ensure immediate drug withdrawal and treatment.
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ranking = 1313.3358729491
keywords = hepatitis, b
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