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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A great deal of interest and speculation has arisen from the discovery of a specific antigen, Australia antigen, in the serum of a high proportion of patients with viral hepatitis. This antigen has been found also in the serum of some patients with other conditions, including Down's syndrome, leukemia, leprosy, chronic renal disorders, and chronic active liver disease. It is not found in the serum of normal persons. Australia antigen has been postulated as the causative agent of viral hepatitis. In most patients the antigen can be detected for less than two weeks during the acute phase of the disease. Its persistence in other conditions may be due to an impairment of the immune response. The course of acute viral hepatitis is usually uncomplicated, full recovery of liver function taking place within four to six weeks, with restoration of normal liver histology within three to four months. Follow-up studies of patients in whom hepatitis has developed during epidemics have failed to reveal evidence of subsequent chronic progressive liver disease. This suggests that most cases of chronic active hepatitis are not the result of preceding acute viral hepatitis. However, the recent finding of Australia antigen in the serum of a small number of patients raises the possibility that sporadic viral hepatitis may be one of the causes of the chronic active hepatitis. Alternatively, the presence of the antigen may be interpreted as being due to an altered immune response. The treatment of acute hepatic coma remains unsatisfactory. Several new forms of therapy have been tried in recent years in an uncontrolled way. These include multiple exchange blood transfusions, isolated pig liver perfusion, human cross-circulation, and cross-circulation with baboons. Transient improvement may follow any of these procedures, but evidence that they influence the final outcome of the disease is lacking. The rapid fluctuations in the neurological status of individual patients makes it difficult to interpret the effects of therapy. Also, until satisfactory objective criteria of degrees of coma are universally accepted it will be impossible to compare one mode of therapy with another.
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PMID:Current concepts in viral hepatitis. 552 Jul 27

9 patients with acute hepatic necrosis following virus hepatitis or hepatic intoxication and 2 patients with acute necrosis of cirrhotic liver, all with stage IV or V hepatic coma, were treated by hemoperfusions with baboon livers. Serum levels of alpha 1-fetoprotein (AFP) were examined prae-, intra- and post perfusion by radioimmunoassay. In 4 patients who survived, the AFP-levels increased from 20 to 65 ng/ml to 180 to 480 ng/ml and remained raised for more than one week. In the patients who died of liver insufficiency, the AFP-levels were only slightly or temporarily increased. The alpha 1-fetoprotein determination is a reliable criterium for the prognosis of hepatic coma patients treated by hemoperfusion.
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PMID:[Serum concentrations of alpha 1-fetoprotein in acute hepatic failure treated by hemoperfusion with baboon livers (author's transl)]. 615 7

The results of the study of functional activity of normal killers in different liver diseases: acute virus hepatitis A (26 patients), acute virus hepatitis B (24 patients including 3 with hepatic coma), and 12 patients with chronic liver diseases including 8 with chronic persisting hepatitis and 4 with chronic active hepatitis are presented. A control group included 17 apparently normal subjects. The most marked decrease of the level of activity of normal killers was found in hepatic coma and in chronic active hepatitis. The expedience of determinations of the activity level of normal killers for prognosis of immediate and remote outcomes of viral hepatitides as well as for the development of new methods of immunocorrecting therapy is discussed.
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PMID:[Viral hepatitis and normal killers]. 649 5

560 patients with hepatic coma were treated during the years 1958 to 1982 in Homburg and Bad Kissingen . 82 patients had an endogeneous and 478 an exogeneous hepatic coma. Endogeneous hepatic coma was caused most frequently by fulminant virus hepatitis, intoxication, and hepatorenal syndrome accompanying serum hepatitis. Exogeneous hepatic coma in patients with cirrhosis of the liver was caused in most cases by gastrointestinal bleeding, by a diet too high in protein, or by excessive diuresis. Early clinical symptoms are changes in writing tests and ability to concentrate, whereas hepatic foetor occurs in coma stage III and IV. Clinical chemistry findings pointing to imminent hepatic coma are increase of arterial ammonia in exogeneous hepatic coma, and increase of free phenols in endogeneous hepatic coma. The increase of prothrombin time is prognostic for imminent hepatic coma in both types. Prognosis of endogeneous hepatic coma is still rather bad; 87% of the patients suffering from it died; in exogeneous hepatic coma prognosis has improved for stage I and II in the last 23 years, whereas however the total prognosis for all 4 stages is still unchanged, letality being 55%.
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PMID:[Causes and diagnostic criteria of hepatic coma--an analysis of 560 cases]. 667 13

The histopathological findings of the liver taken by needle biopsy before and during hepatic coma of fulminant hepatitis were studied in 3 patients; two died and one survived. In the first fatal case, massive hepatic necrosis was already present 7 days before the development of hepatic coma. In the second fatal case, submassive hepatic necrosis was seen during coma grade IV. In both cases, histological findings of the biopsy liver specimens were in accord with those of the autopsied liver. In the third survived case, diffuse degeneration and multilobular liver cell necrosis were found on the biopsy specimen taken immediately after the development of hepatic coma, grade IV.
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PMID:Histopatological findings of the liver before and during hepatic coma in fulminant hepatitis. 714 Dec

Alpha-methyldopa-induced histologic alterations were investigated in 21 patients with hepatic injury after short- and long-term exposure. Seven patients developed liver injury within 6 months and 24 after several years (mean, 5 years) of exposure. Histologic findings and clinical and biochemical data differed significantly in the two groups. Morphologic analysis of the short-term-treated group revealed marked parenchymatous degeneration, focal, confluent and massive necrosis, and inflammation. Fatty accumulation and increased fibrous trabeculae were characteristic for the patients treated for long term. All patients in the short-term-exposed group had acute and severe hepatitis. Four of them had icterus. Two patients died of hepatic coma. Patients in the long-term-treated group had for several months initially mild but increasing discomfort, dyspepsia, nausea, and colics. Liver function tests in these groups revealed differences in serum albumin, bilirubin, and transferase levels. No changes were observed in alkaline phosphatase and Thrombotest. Fat accumulation and fibrous trabeculae suggest that the alterations precede the clinical symptoms and biochemical signs of hepatitis. The findings show that alpha-methyldopa may induce hepatocellular injury after short- and long-term exposure.
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PMID:Morphologic alterations in patients with alpha-methyldopa-induced liver damage after short- and long-term exposure. 732 15

A 10 year old boy, in grade IV hepatic coma, was treated by combination of XAD-4 resin hemoperfusion (HP), activated charcoal HP (Adsorba 300C, Gambro), exchange transfusion by up to 12.0 liters of fresh whole blood, and regular dialysis. Serum free amino acids' values were consecutively assessed during 4 days of treatment. The liver was 490 gr in weight at autopsy and histologic examination revealed cellular necrosis compatible with fulminant hepatitis. Pre-treatment values of alanine, lysine, proline, phenylalanine, arginine, threonine, tyrosine and methionine were increased by 2 to 38 times of normal control, while those of cystine, glutamic acid, serine and glycine were minimally increased up to 1.7 times. Histidine, isoleucine, leucine and valine, on the other hand, were decreased by 20 to 30% and aspartic acid was the lowest at 14% of normal control. The effect of XAD-4 resin HP and exchange transfusion was rather non-specific by decreasing the total amount of amino acids. The molar ratios of branched chain amino acids vs. aromatic amino acids or essential amino were elevated by activated charcoal HP, but, did not reach to normal range.
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PMID:[Variation of serum free amino acids in fulminant hepatitis treated with hepatic assists (author's transl)]. 740 29

The prognosis of fulminant hepatitis due to non-A, non-B virus infection and acute reactivation of hepatitis B virus in HB carriers is generally poor, and the treatment of choice in Western countries is recognized as liver transplantation. In countries such as Japan where liver transplantation is not readily available, however, these intractable types of fulminant hepatitis have to be treated medically. Based on the assumption that persistent replication of causal viruses and enhanced host immune responses, especially cellular immunity, to eradicate the viruses are the key mechanism in progressive liver cell destruction and the poor prognosis, we attempted a combination treatment with interferon and cyclosporin A for these types of fulminant viral hepatitis. Subjects in the present study consisted of 1 patient with acute severe hepatitis without coma and 13 patients with coma (13 with fulminant hepatic failure) due to non-A, non-B virus and acute reactivation of hepatitis B virus. The patients were given interferon-beta, 300 x 10(4) U daily, and cyclosporin A, at an initial dose of 3 mg/kg, with tapering. Fourteen patients with coma received artificial liver support that we devised. The patient with acute severe hepatitis survived, showing histologically remarkable liver regeneration. Eight of the 14 patients with hepatic coma, all of whom were indications for liver transplantation according to the criteria of the King's College group, survived. Decreased transaminase level, increased liver volume, and histological liver regeneration were observed in all the survivors. The combination of interferon and cyclosporin A is worth attempting in fulminant hepatitis caused by non-A, non-B virus and acute reactivation of hepatitis B virus in HB carriers.
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PMID:Interferon and cyclosporin A in the treatment of fulminant viral hepatitis. 771 17

After undergoing withdrawal treatment for alcoholism as an in-patient for one year a 49-year-old woman was started on disulfiram, 250 mg daily, her liver function tests being normal. Except for vitamin B1 she received no further medication. Jaundice developed 13 days after onset of treatment and acute liver failure was diagnosed on the 18th day after a total disulfiram dose of 4.5 g (Quick value < 10%; bilirubin 460 mumol/l; GPT 5099 U/l; GOT 4142 U/l), as well as early renal failure (creatinine 300 mumol/l). An acute viral infection, autoimmune hepatitis and a metabolic liver disease were excluded by biochemical, serological and molecular biology tests. All toxicological tests were negative. The patient died 25 days after the onset of disulfiram treatment in hepatic coma due to a fulminant hepatitis with hepatorenal syndrome. Both a liver biopsy and the autopsy showed the signs of an acute hepatic dystrophy without cirrhosis. The temporal relationship between the disulfiram intake and onset of the illness, the exclusion of other causes of the fulminant hepatitis and the liver histology, which was compatible with a chemical-toxic hepatitis, indicate that this was a case of disulfiram-induced hepatitis. The hepatotoxicity of disulfiram is a very rare idiosyncratic reaction which is often fatal. Disulfiram administration must be discontinued at once if there is a rise in liver enzyme activity or jaundice occurs.
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PMID:[Fulminant hepatitis caused by disulfiram]. 840 76

We report two cases of ischemic hepatitis in patients with alcoholic cirrhosis. In both, hepatic ischemia was induced by hemorrhagic shock and severe sepsis. Despite control of the bleeding and restoration of normal hemodynamics, liver failure deteriorated to hepatic coma and death in both cases. Ischemic hepatitis occurred in 1.5% of 130 consecutive cases of cirrhosis admitted for hemorrhage on our medical intensive care unit. Although cirrhotic patients run an increased risk of ischemic hepatitis, our experience and our review of the literature indicate that this condition is rare in these patients.
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PMID:Ischemic hepatitis in cirrhosis. Rare but lethal. 840 9


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