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)

Previous work from this laboratory has suggested that the plasma amino acid pattern, known to be deranged in hepatic encephalopathy, may be related causally. In order to test this hypothesis, 23% dextrose and a special amino acid solution whose components were calculated to normalize the plasma amino acid pattern were infused in 11 patients, eight with chronic cirrhosis and acute exacerbation (Group 1) and three patients with fulminant hepatitis (Group 2), in amounts of up to 120 Gm. of protein equivalent per 24 hours. Plasma amino acids were abnormal but different in both groups. In Group 1 (cirrhosis) changes in plasma amino acid pattern including elevated phenylalanine, tyrosine, glutamate, aspartate, and methionine and decreased valine, leucine, and isoleucine. In Group 2 all amino acids were elevated, with the exception of the branched chains which were normal. Hepatic encephalopathy improved in all patients in Group 1 and in one of three patients in Group 2 following the infusion. The ratio (see article) showed an excellent correlation with a grade of encephalopathy. When this ratio, previously 1.0 in the presence of encephalopathy, returned to the normal value near 3.0 to 3.5, encephalopathy improved. An excellent correlation was obtained between the ratio and the grade of encephalopathy and was dose related as well. The results suggest that different amino acid patterns in hepatic encephalopathy of differing etiologies require treatment modalities which may differ for the two types of encephalopathy. Whereas amino acid infusion appears to be a valuable, efficacious way of providing nutrition in treating hepatic encephalopathy in patients with cirrhosis and acute deterioration and coma, other means of therapy such as plasms "laundering" appear to be necessary in patients with fulminant hepatitis.
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PMID:The effect of normalization of plasma amino acids on hepatic encephalopathy in man. 81 29

The ammonia hypothesis is the most likely explanation for the pathogenesis of hepatic encephalopathy in cirrhosis patients. Reduction of hyperammonemia is therefore the most consistent therapy. From this point of view, the antibiotics have a central significance for the reduction of ammonia formation in the intestinal tract. Equally important is the correction of the hypopotassemia, which may lead to a renally induced hyperammonemia. At the same time, disorders which favor the cerebral toxicity of ammonia, especially anemia and hypoxias, must be compensated. These various measures have improved the prognosis for hepatic encephalopathy of the cirrhosis patient, but were without effect on the course of the coma in severe toxic hepatitis. During the last toxic hepatitis. During the last 10 years, many treatment methods have been reported whose efficacy, however, could not be proved.
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PMID:[Present-day therapy of hepatic encephalopathy (author's transl)]. 82 98

Within 5 to 14 days of onset of grade 3 or 4 coma, liver biopsies were obtained in 14 of 15 consecutive patients who recovered from fulminant hepatitis. In 9 patients, follow-up biopsy was obtained 6 to 60 months after acute hepatitis and autopsy was performed in 2 patients who died in 4 months from complications of hepatitis (aplastic anemia) or of corticosteroid therapy (sepsis). During fulminant illness the biopsy findings were: multilobular necrosis in 4 patients, confluent (bridging) necrosis in 9, and only portal inflammation in 1. The duration or the grade of coma did not correlate with the severity of necrosis on the biopsy. Follow-up biopsy showed development of chronic (active) hepatitis in 3 of 9 patients (with cirrhosis in one of these). Chronic liver disease was not found in the two autopsies. If fulminant hepatitis is the result of vigorous cell-mediated immune attack on hepatocytes, then this process cannot always eradicate chronic hepatitis B surface antigenemia, nor can it always prevent the development of chronic (active) hepatitis or cirrhosis.
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PMID:The liver during and after fulminant hepatitis. 89 67

Extracorporeal pig liver perfusion was adopted in 2 patients with acute hepatic coma due to fulminant hepatitis. Exchange transfusion was used in a third patient, while a fourth was subjected to both procedures. A marked haematological improvement was noted in all cases. Yet, three patients died without showing any clinical benefit. In the fourth case, coma regressed and gradual improvement to the point of complete recovery was achieved. Liver perfusion and exchange transfusion in the same patient were attended by very different clinical effects, though each procedure produced a comparable improvement at the blood chemistry data. Careful analysis of the data suggests that the difference was attributable to discrepancies between the degree of tissue purification achieved.
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PMID:[Experience with the treatment of acute hepatic coma using extracorporeal perfusion of heterologous liver and exchange transfusion]. 94 19

Clinic and histologic characteristics in fulminant hepatitis are pointed out, participation of other organs is reported. Coma, bleeding and renal failure are complications and often are followed by death. Conservative treatment prophylacting complications is described. Newer methods in treatment of coma are exchange-transfusion, liver-perfusion and -grafting. They showed success in some cases. Success, however is less due to the method than to ability of regeneration of the remaining liver tissue. Despite the newer methods of treatment the rate of mortality is yet 80 to 90%.
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PMID:[Fulminant hepatitis. Complications and therapeutic possibilities]. 122 28

Extracorporeal perfusion of pig liver lasting 4 hr, followed by isovolaemic exchange (6 litres in 1 hr) were employed in the management of coma in a case of acute virus hepatitis. Liver perfusion led to temporary regression of coma, whereas transfusion was followed by gradual improvement in the clinical picture; this was apparently not a direct consequence of the procedure adopted. Assessment of the degree of purification obtained with these two methods offers an explanation for the difference in their clinical effectiveness.
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PMID:[Success in a case of fulminant hepatitis treated with extracorporeal liver perfusion and exchange transfusion]. 124 7

Thirteen out of 18 patients with fulminant hepatitis developed cerebral edema macroscopically confirmed at autopsy. Cerebral bleeding and herniation were also observed in 38 and 8% of edema cases, respectively. No significant difference was found in the clinical backgrounds (age, sex, laboratory data) of patients with and without cerebral edema. Respiratory distress (100% of edema cases, p less than 0.05), abnormal pupils (89%, p less than 0.10), convulsions (61%) and tachycardia unrelated to fever (60%) were more frequently observed in cerebral edema cases than in those without edema. The frequency of convulsions increased as hepatic encephalopathy progressed, and the frequency of respiratory distress and abnormal pupils in edema cases was significantly higher at the coma grade V of hepatic encephalopathy. Tachycardia was detected early, even at the mild grades of hepatic encephalopathy. These results suggest that symptoms due to cerebral edema such as convulsions, abnormal pupils and respiratory distress should be distinguished from those due to hepatic encephalopathy in fulminant hepatitis patients.
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PMID:Cerebral edema during hepatic encephalopathy in fulminant hepatic failure. 157 40

The value of coagulation factor V and VIII/V levels as prognostic indicators was assessed in 27 patients with fulminant hepatic failure and compared with other predictive indices. Admission factor V levels were significantly reduced in 22 patients with paracetamol induced hepatic failure compared with a healthy control group (median 9.5% v 103%, respectively; p less than 0.001) and with lower values in non-A non-B hepatitis (median 2.7%). Values in the seven patients who died after paracetamol overdose, considered together with the four who underwent liver transplantation (group median 5.1%), were significantly lower than in the 11 who survived (median 11.8%; p less than 0.01). Median admission factor VIII was higher in those who died or received a transplant than in those who survived (298% v 162%; p less than 0.05), with both results higher than in healthy volunteers (median 104%; p less than 0.01) but lower than in non-A non-B hepatitis (median 340%). The ratio of factor VIII/V on admission was less than 30 in all patients who survived paracetamol overdose (median 17) with corresponding values greater than 30 in 10 of 11 of those who died (median 39). A factor V result less than or equal to 10% on admission predicted an adverse outcome in 10 of 11 fatal cases, a 91% sensitivity which was greater than for the previously defined indicator of an arterial blood pH less than 7.30 on admission (sensitivity 82%). Prothrombin time at admission or on day 4 did not usefully predict outcome in our series. Predictive accuracy was 73% and 82% for factor V and admission acidosis respectively and 95% for factor V in conjunction with admission coma grade III or IV and factor VIII (ratio > 30). These criteria may be useful in selecting patients with paracetamol induced fulminant hepatic failure for transplantation.
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PMID:Coagulation factor V and VIII/V ratio as predictors of outcome in paracetamol induced fulminant hepatic failure: relation to other prognostic indicators. 174 Feb 85

The purpose of the present paper was to asses the values of plasminogen (PLg) as severity index in viral hepatitis (VH). The results were compared with serum bilirubin (SB) and prothrombin time. The following groups of patients were investigated: I- VH (n-672); II- Fulminant hepatitis (FH)(n-53); III-Liver cirrhosis (n-52); IV- Cholangiohepatitis (21); Toxic hepatitis (n-22); V- Gall stone (n-56) VI- Neoplasms with jaundice (n-56); VII- Healthy subjects (n-137). PLg was found to be diminished in parenchymal liver diseases, especially in VH's patients according to the severity and the stage of the diseases. The most impressive decline was observed in FH--more than 50% of the tests showed Plg activity less than 10% (reverence values 83-126% activity). In VH, PLg was superior to SB and prothrombin time when evaluating the severity of the disease at the time of admission in the hospital. We proposed PLg as valuable criterion for the severity of VH. The range being as follows: Light forms of VH- PLg activity above 70%; Medium forms-from 69 to 50%; Severe forms-from 49 to 20% and patients with high risk of liver coma-PLg activity below 20%.
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PMID:Bilirubin or plasminogen--which is better in the assessment of the severity of viral hepatitis? 175 47

From 1979 to 1988 in the GDR the number of patients with alcoholic liver cirrhosis increased from 2,387 to 3,958 (61.2%). An evident decrease of patients with acute virus hepatitis was observed (from 7,037 in 1979 to 1,578 in 1989). In future a further increase of alcoholic liver diseases with the resulting complications (e.g. coma, bleeding varices and withdrawal symptoms) has to be expected.
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PMID:[Epidemiology of liver diseases in the GDR, 1979-1989]. 181 56


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