Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Management of protein-calorie malnutrition found in 32 patients with severe liver diseases such as fulminant hepatitis and cirrhosis of the liver was carried out using 2 types of synthetic amino acid solution (Hep-OU and Fischer solution) for intravenous and enteral alimentations with rapid monitoring of serum aminogram. Intravenous hyperalimentation of these cases resulted in maintenance of nutritional status with improvement of nitrogen balance and normalization of impaired serum aminogram. During this study, however, nutritional support was initiated only when intractable ascites, upper gastrointestinal bleeding and hepatic encephalopathy were observed. In 2 cases of fulminant hepatitis with sepsis and 3 hepatoma patients with ascites, elemental diet containing maltose and amino acids was used to supply sufficient amounts of nutrients in a minimum volume of water. These techniques with simultaneous monitoring of urinary excretion of 3-methylhistidine and creatinine height index as nutritional parameters make nutritional management easy for patients with liver disease.
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PMID:Nutritional management of patients with severe liver disease by using intravenous hyperalimentation and elemental diet. 676 41

The authors report the case of a patient with hepatitis after the administration of dihydralazine, an analogue of hydralazine which is widely used in Europe. Hepatitis occurred during the administration of dihydralazine, quickly improved when the administration of dihydralazine was interrupted, and worsened again when it was resumed. Hepatitis was severe with hepatic encephalopathy and prolonged prothrombin time. There was centrizonal and bridging necrosis. After interruption of the drug administration, the outcome was favorable, but fibrotic sequelae were observed on a follow-up histologic examination.
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PMID:Dihydralazine hepatitis: report of a case and review of the literature. 688 86

Hepatic encephalopathy in patients with severe liver disease was associated with marked elevation of either serum methionine or blood ammonia levels or with simultaneous moderate increases in both parameters. CSF methionine levels also increased in encephalopathic patients with fulminant hepatitis and liver cirrhosis. Increased influx of methionine into the brain over the theoretical values predicted from Pardridge's equation suggested that accelerated transport of serum methionine across the blood-brain barrier was observed in these cases with hepatic encephalopathy. Hepatic encephalopathy in acute carbon tetrachloride liver injury could be obtained experimentally following intraperitoneal injection of ammonium acetate in rats, which already received intragastric administration of methionine. However, similar encephalopathy could not be observed by the administration of glycine or leucine in place of methionine. These results suggest at least that methionine and ammonia act synergistically on inducing hepatic encephalopathy.
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PMID:Impaired metabolism of methionine in severe liver diseases. II. Clinical and experimental studies on role of impaired methionine metabolism in pathogenesis of hepatic encephalopathy. 710 99

Serum amino acid patterns in patients with different types of hepatic encephalopathy were investigated. Marked elevations in most of serum amino acids observed in untreated patients with acute type of fulminant hepatitis were not remarkable in the patients who have already treated; particularly branched chain amino acids (BCAA), phenylalanine and tyrosine were much lower in the latter group. However, elevation of serum methionine levels and lower ratio of BCAA/(phenylalanine + tyrosine) were similarly observed in both groups. In encephalopathic patients with decompensated cirrhosis, many amino acids such as phenylalanine, tyrosine and methionine were elevated with a slight depressed levels of serum BCAA. Highly significant decrease in serum BCAA levels and no elevation of phenylalanine and methionine with a minimal increase of tyrosine were observed in patients with chronic type of hepatic encephalopathy; other amino acids except for glutamine and arginine were much lower as compared to those in decompensated cirrhotics and even to the control values.
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PMID:Characteristics change in serum amino acid levels in different types of hepatic encephalopathy. 711 80

Thirty-five children with G6PD deficiency, who presented with acute intravascular haemolysis, were evaluated to define its aetiology, clinical features and ultimate outcome. All were boys with ages ranging from 6 months to 12 years. Pallor of abrupt onset and passage of cola-coloured urine were universal presenting symptoms. Incriminating factors responsible for haemolysis include hepatitis (7), malaria (4), bacterial sepsis (3) and drug intake (24), with more than one predisposing condition existing in some children. Marked elevations in serum bilirubin, coinciding with intravascular haemolysis, was a feature in all the seven children with hepatitis. Azotaemia was noted in 20 patients, of whom 14 did not have oliguria. All four children with malaria presented with protracted renal failure. Therapy focused on maintaining a high urine output in those without oliguria. A total of 15 peritoneal dialyses and five haemodialyses were required in six patients with acute renal failure, all of whom were oliguric. Supportive therapy consisted of blood transfusions and treatment of the predisposing diseases. Thirty-two children recovered completely while three died, the cause of death being severe anaemia and congestive cardiac failure, malaria with oliguric renal failure and hepatic encephalopathy, respectively.
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PMID:Acute intravascular haemolysis in glucose-6-phosphate dehydrogenase deficiency. 750 89

"Ecstasy" or 3,4-methylenedioxymethylamphetamine, is a synthetic amphetamine which is increasingly consumed in Spain as a "recreational" drug. It has been associated with serious medical and psychiatric side effects, though, it is popularly considered, as a non dangerous drug. The development of acute hepatitis associated with the use of "ecstasy" has been reported by other authors from areas where its use is widely spread. We report the development of acute hepatitis associated with use of "ecstasy" in a young man with successful recovery and spontaneous resolution. In other cases the acute hepatitis may have a torpid evolution with slow resolution, fulminant liver failure, and death with hepatic encephalopathy, disseminated intravascular coagulation and adult distress syndrome. An idiosyncratic toxic hepatitis might be due to either 3,4-methylenedioxymethylamphetamine or a metabolite, a contaminant in 3,4-methylenedioxymethylamphetamine manufacture, or to an additive in tablet or capsule formulation.
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PMID:[Acute hepatitis due to ingestion of Ecstasy]. 757 30

In 19 acute hepatitis patients with severe coagulopathy who were fully alert and oriented without any changes of mood or behavior, the P300 latency and the arterial blood ketone body ratio (KBR) were assessed as predictors of fulminant hepatitis. All 5 patients developing fulminant hepatitis had a corrected P300 latency longer than 345 msec and 4 of them had a KBR below 0.6. There was a significant negative correlation between the KBR and the blood ammonia level and between the KBR and the corrected P300 latency, while there was a positive correlation between the blood ammonia level and the corrected P300 latency. These data suggest that hepatic encephalopathy develops when loss of hepatic detoxifying activity allows toxic substances to reach the brain and induce cerebral edema. Our findings also suggest the clinical value of using the P300 latency combined with the KBR as predictors of fulminant hepatitis.
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PMID:Long-latency event-related potentials in acute hepatitis patients with severe coagulopathy. 768 66

While typhoid is quite common in our environment, presentation in association with severe hepatitis and hepatic encephalopathy is uncommon. The case of a 14 year old male with typhoid who presented with jaundice and severe hepatitis with encephalopathy is presented. The first symptoms occurred one week before presentation. The clinical features and laboratory investigations confirmed typhoid fever. The associated severe hepatitis could have been related to a direct liver involvement by Salmonella typhi, drug toxicity or hepatitis B infection from previous indiscriminate parenteral drugs. The specific cause of the hepatitis could not be confirmed. The patient is presented to illustrate a rare association and possible complication of typhoid fever, inappropriate self and other medication in the place of proper hospital presentation and assessment and the diagnostic difficulties confronting many centres in the developing environment.
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PMID:Typhoid fever associated with severe hepatitis. 783 18

The prognosis of patients with severe hepatitis is related to the severity of the disease when they are admitted to hospital. We retrospectively analyzed the clinical and laboratory data of 201 cases of severe hepatitis with the method of logistic regression and had obtained 8 independent variables strongly affecting the prognosis to form the multiple regression discriminant equation. The eight independent variables are Pa, A/G, SB, BUN, Cr, hepatic encephalopathy, infection and digestive tract bleeding. We can get the values of care fatality rates from the equation. The degree of severity can be classified with the value. Treatment plans can be drawn out and clinical research grouping can be improved on the basis of the values.
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PMID:[Evaluation of surveillance on the case fatality rates in patients with severe hepatitis and of its clinical application]. 814 18

A 14-year-old girl with acute lymphoblastic leukemia in second remission received an allogeneic marrow graft from her HLA identical brother. Cyclosporine A and short term methotrexate were given for prophylaxis against graft versus host disease. On day 42 post transplantation elevation of SGOT and SGPT was recognized, rising the next day to 8,560IU and 2,590IU, respectively. Prothrombin activity dropped below 10%. HCV antibody and HBs antigen were both negative. Fulminant hepatitis was diagnosed, therefore plasma exchange was initiated. However, hepatic encephalopathy developed and she died on day 57. The postmortem liver appearance was consistent with early changes of veno-occlusive disease. Such atypical cases of VOD with late onset are difficult to distinguish from fulminant hepatitis but should be kept in mind.
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PMID:[Fulminant hepatitis-like veno-occlusive disease of the liver after allogeneic bone marrow transplantation in acute lymphoblastic leukemia]. 831 37


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