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)

Hepatic insufficiency is generally caused by active liver cirrhosis with portal hypertension. The final stage is the exogenous hepatic coma. Much rarer is the endogenous hepatic coma caused by fulminant acute hepatitis or severe intoxications. In the treatment of hepatic insufficiency it is first necessary to eliminate all exacerbating factors such as too high protein-intake, gastrointestinal bleedings, abuse of alcohol and diuretics. Because hepatic encephalopathy is mainly produced by toxic intestinal protein metabolites no protein should be adminstered at the beginining of the disease. The production of toxic protein metabolites in the gut can be diminished as well by enemas with sodium acetate buffer (pH 4, 5) as by neomycin (6-8 gm daily). Because long-term treatment with neomycin reduces also the physiological intestinal bacteria combination with lactulose (70-100 gm daily) is better. Treatment with lactulose reduces not only significantly hyperammoniemia but also increases serum phenols. The same effect have so-called ammonia reducing amino acids such as arginine, ornithine and glutamic acid. In endogenous hepatic coma blood exchange transfusions, liver perfusions and charcoal perfusions are necessary. Nevertheless, the prognosis of hepatic insufficiency caused by fulminant hepatitis is very poor in the final stage of the disease. Therefore early diagnosis and treatment in special departments with intensive care is necessary.
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PMID:[Therapy of hepatic insufficiency]. 91 52

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

The clinical and hematological features of 100 patients with sickle cell anemia are reviewed. The heart was enlarged and a murmur was heard in nearly 80 percent of patients. Pneumonia and pulmonary infarction occurred in 43 percent and 12 percent of patients, respectively. Musculoskeletal involvement included the hand-foot syndrome (15 percent), leg ulcers (55 percent), aseptic necrosis ofbone (11 percent), and osteomyelitis (4 percent). Symptoms and signs related to the gastrointestinal system included jaundice (55 percent), hepatomegaly (50 percent), splenomegaly (23 percent), hepatitis (11 percent) and gallstones (9 percent). Three patients underwent cholecystectomy and three patients had their spleens removed. Pyelonephritis occurred in 17 patients, priapism in five and hematuria in seven. Nineteen women had 39 pregnancies, of which 35 resulted in the birth of healthy infants. At least 328 painful crises occurred in 73 patients. There were also 13 hemolytic crises, eight sequestration crises, and five aplastic crises. A trail of alkali therapy in 33 crises in children failed to produce beneficial effects greater than hydration and analgesics alone as used in the control group. Laboratory findings in the 100 patients were comparable to those previously reported in the literature. The renal concentrating defect in most patients was confirmed. There were six deaths: hepatic coma secondary to post-transfusion hepatitis, thrombosis of inferior vena cava, congestive heart failure, exsanguination from erosion of the pancreaticoduodenal artery, extensive bronchopneumonia, and pulmonary infarction.
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PMID:Sickle cell anemia- clinical manifestations in 100 patients and review of the literature. 113 Apr 36

The levels of C3, cholinesterase, albumin and prothrombin were determined in 46 patients (27 males and 19 females) - 26 with cirrhosis of the liver, 9 with acute hepatitis, 6 with chronic aggressive hepatitis, 1 with chronic persistent hepatitis and 4 with fatty liver. In all patients and, particularly in those with cirrhotic liver, it was shown that the normal or pathological level of serum C 3 is related both qualitatively and quantitatively to the normal or pathological levels of cholinesterase, albumin, and prothrombin. The percentage in which the levels of these four parameters were pathological was considerably higher in the cases with hepatic coma than in the cases without hepatic coma. The determination of the range of confidence for the 4 parameters showed that, in the patients with hepatic coma, cholinesterase reacted most sensitively to liver damage (0.5 - 0.94) followed by C3 and prothrombin (0.33 - 0.81). Also in the cases without hepatic coma, cholinesterase was the most sensitive indicator (0.05 - 0.29), followed by prothrombin (0.03 - 0.24), albumin and C3 (0.00-0.16).
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PMID:Serum levels of C3 and cholinesterase in various diseases of the liver. 125 98

By combination of continuous hemofiltration (CHF) with plasma exchange therapy we successfully treated a patient with subacute type fulminant hepatitis to keep her consciousness alert. The patient was a 55-year-old woman who admitted because of severe jaundice. On the 51st day after the onset she had consciousness disturbance and was transferred to our hospital. We started the therapy of CHF and plasma exchange at the patient's hepatic coma grade 4. On the 5th day her consciousness level recovered to grade 2 and we could keep the level for almost 2 weeks. This combination therapy seemed good not only for the improvement of consciousness of patients in hepatic coma but also to support the hepatic function of almost ahepatic patients.
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PMID:[Effective continuous hemofiltration and plasma exchange for the treatment of subacute type fulminant hepatic failure]. 139 29

Diphenylhydantoin-induced hepatitis and mononucleosis are uncommon in children. The occurrence of these two diseases in the same individual, with progression to hepatic failure is rare and has not been reported in infants. This report represents a 6-month-old male infant who developed an infectious mononucleosis-like syndrome and hepatic failure 16 days after diphenylhydantoin administration. He took this anticonvulsant for controlling seizures after a head injury. Fever, skin rash, hepatosplenomegaly, lymphadenopathy, and atypical lymphocytosis led to the initial diagnosis of infectious mononucleosis. However, negative heterophil antibody did not support the diagnosis. Jaundice ensued in the following course and became more and more profound. Meanwhile, physical examination showed shrinking in liver size. Negative virology studies, including Epstein-Barr virus, cytomegalovirus, and hepatitis B virus, excluded them as causative agents. The patient lapsed into a stage I hepatic coma, but gradually recovered clinically and biochemically after eight successive exchange transfusions and supportive care. Two liver biopsies were performed 20 and 50 days after the onset of disease, respectively. Remarkable hepatic parenchymal loss, cholestasis, and fatty change were found on histologic examination of the first biopsy specimen, and portal fibrosis was noted on the second.
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PMID:Mononucleosis and hepatic failure associated with diphenylhydantoin treatment in an infant. 167 17

Human hepatocyte growth factor (hHGF) was purified from the plasma of six patients with fulminant hepatic failure due to hepatitis B in two and non-A, non-B hepatitis in four. The purified hHGF from each patient contained two major protein bands having molecular weights of 79,000 and 86,000 and several minor bands having molecular weights between 76,000 and 92,000 on sodium dodecyl sulfate-polyacrylamide gel electrophoresis performed under nonreduced conditions. After reduction with 2-mercaptoethanol, three major bands having molecular weights of 58,000, 34,500, and 31,500 were evident. In addition, a band having a molecular weight of 21,000 was detected. hHGF activity was destroyed by its reduction. The hHGF purified from patients demonstrated a dose response in terms of an increase in DNA synthesis using cultured hepatocytes. The hHGF concentration in the plasma of the patients with grade III-IV hepatic coma was calculated to be in the range of 1.8-3.0 nM. Finally the heavy chain of hHGF was not recognized by an anti-human albumin antibody, indicating that hHGF is not biliprotein, an albumin-bilirubin complex, that has been reported to be a putative liver growth factor.
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PMID:Human hepatocyte growth factor in blood of patients with fulminant hepatic failure. Basic aspects. 182 62

A 49 year old female was started on disulfiram. Six weeks later she was given naproxen because of epicondylitis. After 5 days' treatment with naproxen she complained of nausea, anorexia and jaundice. At admission, bilirubin was 452 mumol/l, aspartate aminotransferase (ASAT) 1925 U/I, alanine aminotransferase (ALAT) 2815 U/I and prothrombin time measured as Normotest was 27%. The patient developed a fulminant hepatitis and died in hepatic coma almost four weeks after the introduction of naproxen. Postmortem examination disclosed a small liver (1,100 g) and histological examination showed massive necrosis and collapse of the lobules. The naproxen was the most probable cause of death, but it is impossible to exclude disulfiram as causative agent.
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PMID:[Fulminating hepatitis after treatment with naproxen and/or disulfiram?]. 200 Jun 13

Serum complement hemolytic activities (CH 50) and plasma prothrombin time (PTT) of patients with fulminant hepatitis (FH, 11 cases of acute type and 11 cases of subacute type), severe acute hepatitis (AH-S, 9 cases) and typical acute hepatitis (AH-T, 20 cases) were examined. AH-S was diagnosed as AH patients with PTT under 40% and without hepatic coma. Survival rates were 100% in AH-S, 45.5% (5/11) in acute type of FH and 9.1% (1/11) in subacute type of FH. The mean levels of CH 50 on their admission were 42.6 U/ml in AH-T, 28.8 U/ml in AH-S and 13.1 U/ml in FH. CH50 levels in acute hepatitis decreased in parallel to the severity of the disease and correlated with PTT (r = 0.809). In many cases of FH and almost all cases of AH-S, CH50 levels changed more slowly than those of PTT. The patients with AH-S and subacute type of FH showed a prolonged PTT and the normal levels of CH 50 in their acute phase. These results indicate that CH50 and PTT could be useful markers differentiating subacute type from acute type of fulminant hepatitis.
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PMID:[Parameter in fulminant hepatitis]. 200 37

Two fatal cases of amiodarone-induced acute, confluent, necrotic hepatitis are described. The patients, aged 28 and 60, had received a high loading dose of amiodarone. After the first and second day respectively following the administration of amiodarone, the patients developed jaundice, hepatomegaly, high serum transaminases, a prolonged prothrombin time and low cholesterol concentration. They died of hepatic coma and acute renal failure on the fourteenth and fourth day respectively. Needle liver biopsy, performed immediately after death, revealed lesions of acute drug-induced hepatitis with confluent and bridging necrosis. It is proposed that rapid administration of a high loading dose of amiodarone can cause acute confluent necrotic hepatitis. The mode of administration and the dosage of the drug should be re-considered.
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PMID:Acute amiodarone-induced hepatitis. 202 92


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