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

The case reported here is that of a girl with presumably viral non A, non B, acute hepatitis with a very unusual course. Fulminant hepatitis with submassive and bridging hepatic necrosis and a 17-day coma began during the 7th week of evolution. Prolonged chronic active hepatitis followed. Treatment was initiated 6 months after the beginning of the affection and was maintained for more than 2 years, with an apparent cure persisting after follow-up period of 6 months; fibrous scars were the only abnormalities demonstrable on histologic examination of liver biopsy. It is possible that such type of fulminant hepatitis with unusual course will become more frequent, as survival of the initial acute episode increase.
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PMID:[Chronic active hepatitis with a favorable course, after fulminant hepatitis]. 12 40

In the majority of instances acute viral hepatitis resolves totally without sequelae. Fulminant hepatitis is a highly lethal lesion but 20 to 25 per cent of patients, principally young patients, survive. Survivors do not appear to develop chronic liver disease. Persistent viral hepatitis follows acute icteric hepatitis, both type B and non-B, in 10 to 12 per cent of patients. Six long-term HBs Ag carriers demonstrated HBs Ag clearance after 14-73 months. Chronic active viral hepatitis often progresses to cirrhosis. This progressive hepatitis appeared as a sequelae of acute icteric type B hepatitis in 3 per cent of 429 patients. In patients with chronic active type B hepatitis, low titers of HBs Ag are common.
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PMID:Viral hepatitis: clinical aspects. 17 56

The authors report the cases of 3 patients who died from fulminant hepatitis after receiving iproclozide, a hydrazine-containing monoamine oxidase inhibitor. Fulminant hepatitis in these patients resembled that reported in patients receiving other hydrazine-containing monoamine oxidase inhibitors: (1) the 3 patients were women; (2) the monoamine oxidase inhibitor has been ingested for 1 month or more; (3) the main clinical manifestations were jaundice and disorders of consciousness; (4) hypersensitivity manifestations were absent; (5) the predominant liver lesion was necrosis; (6) all 3 patients died. In our 3 patients, jaundice occurred 7 to 10 days after the adjunction to iproclozide of a microsomal enzyme inducer. These observations suggest that concomitant administration of iproclozide and of microsomal enzyme inducers may produce fulminant hepatitis in man. It is speculated that iproclozide could be, like iproniazid, transformed into a hepatotoxic metabolite, the production of which would be increased by microsomal enzyme induction.
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PMID:Iproclozide fulminant hepatitis. Possible role of enzyme induction. 68 May 6

The clinical course of acute viral hepatitis may vary from asymptomatic to fulminant, and the final outcome can be complete recovery, chronic hepatitis or cirrhosis. The two main challenges this generally benign, self limiting infection has presented for may years have been to understand 1) the progression to fulminant hepatitis, and 2) the progression to chronic hepatitis or cirrhosis. Fulminant hepatitis may appear infrequently (1-2 % of patients with clinical hepatitis) in both type A and type B infections. Nearly 10% of patients with acute viral hepatitis type B develop either chronic hepatitis or cirrhosis. The exact figures for progression to chronicity in patients with type A infections are probably less,but are still not fully known. During the acute phase of the disease, the patients with later progression to chronicity differ significantly from those with subsequent resolution in a number of serological, biochemical and morphological variables. Persistence of HBS antigenaemia for more than 13 weeks, a high concentration of circulating Dane particles, and the presence in the serum of the "e" antigenic determinant seem to be reliable prognostic markers for pregression to chronic hepatitis or cirrhosis. Such markers are prerequisites for therapeutic trials with potent drugs which are only justified for patients with fulminant hepatitis and patients with progression to chronicity. If the different outcome of viral hepatitis is a result of the individual T-cell function, these two categories of patients may represent the opposite extremes in lymphocytic function. Controlled clinical trials are required to evaluate the clinical effect of immunosuppression in fulminant hepatitis and immunostimulation in chronic hepatitis.
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PMID:Clinical course and prognosis of acute hepatitis. 79 97

The authors report 6 cases of fulminant hepatitis in patients treated with isoniazid and rifampin. In 4 of these patients, the treatment had been started within 3 days after a general anesthesia. The course of the disease was remarkably similar in all 6 patients: (1) the time interval from the beginning of the isoniazid-rifampin administration to the onset of jaundice was 6 to 10 days; (2) disorders of consciousness appeared less than 3 days after the onset of jaundice; (3) serum transaminases were 26 to 80 times the upper limit of normal; (4) the main liver lesion was centrilobular necrosis; (5) hypersensitivity manifestations were absent; (6) all 6 patients recovered. Fulminant hepatitis might be attributable to a hepatotoxic metabolite of isoniazid, the production of which would be attributable to a hepatotoxic metabolite of isoniazid, the production of which would be increased as a consequence of the enzyme-inducing effect of rifampin and, possibly, other drugs administered for general anesthesia.
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PMID:Isoniazid-rifampin fulminant hepatitis. A possible consequence of the enhancement of isoniazid hepatotoxicity by enzyme induction. 83 May 77

A radioimmunoassay for human alpha1-acid glycoprotein has been developed. 97.8% of 125I-alpha1-acid glycoprotein prepared for the assay were immunoprecipitable with specific anti-sera against the protein. alpha1-acid glycoprotein concentration in sera from normal adults was found to range between 70 and 114 mg/100 ml, with a mean of 93. Fulminant hepatitis, liver cirrhosis or chronic active hepatitis with sublobular necrosis caused a significant lowering of alpha1-acid glycoprotein concentration. Sera obtained from patients with acute hepatitis in convalescence, chronic inactive hepatitis or primary biliary cirrhosis gave normal concentration of the glycoprotein.
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PMID:Serum glycoproteins in the liver diseases. II. Radioimmunoassay of alpha-1 acid glycoprotein. 101 93

Hepatitis A is an acute, necroinflammatory disease of the liver which results from infection by the hepatitis A virus (HAV). The mean incubation period is approximately 30 days. Although the disease is usually self-limited, the severity of illness is age-dependent. In children, hepatitis A is usually asymptomatic, while in adults, symptomatic infection is characteristic and jaundice is common. Fulminant hepatitis A is rare and is also age-dependent. The onset of hepatitis A is often abrupt and characteristic prodromal symptoms are followed, within a few days to a week, by dark urine and jaundice. Mild to moderate tenderness over an enlarged liver is usually detected. Serum alanine and aspartate aminotransferase levels usually both rise rapidly during the prodromal period, reach peak levels and then decrease by approximately 75% per week. Serum bilirubin concentrations reach peak levels later and decline less rapidly than serum aminotransferases. Nonetheless, the period of jaundice persists for < 2 weeks in approximately 85% of cases. Nearly all adult patients with clinically apparent disease experience complete clinical recovery with restoration of normal serum bilirubin and aminotransferase values by 6 months. Relapses and prolonged cholestasis are unusual manifestations of hepatitis A, and even in these circumstances, recovery is the rule and chronic hepatitis is not seen. The diagnosis of hepatitis A requires the detection of immunoglobulin M antibody to HAV in a patient who presents with, or has recently had, clinical features of hepatitis (icteric or anicteric disease) or in an individual with inapparent, asymptomatic infection in whom serum aminotransferase elevations may be detected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical manifestations and diagnosis of hepatitis A virus infection. 133 49

Fulminant hepatitis shows characteristic imbalance of amino acid levels; increased aromatic amino acid (AAA) and methionine. Elevated plasma AAA may cause hepatic encephalopathy and BCAA-enriched amino acids solution (BCAAs). Glucagon-Insulin (G-I) therapy and artificial liver support system have been proposed to correct the imbalance of amino acids. BCAAs and G-I therapy correct the aberrant amino acid patterns and artificial liver support system, including plasma pheresis, and charcoal haemoperfusion has also been used to reduce plasma amino acids levels. While imbalance of amino acids level in fulminant hepatitis is a result of acute necrosis of a large proportion of hepatocytes, careful and sufficient management of the disease is essential to normalize amino acid profiles.
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PMID:[Imbalance of amino acid metabolism in fulminant hepatitis and its management]. 140 90

Viral A hepatitis is a self-limited infection occurring predominantly among children usually as an anicteric often subclinical illness. Adults afflicted with this virus are more likely to develop icteric hepatitis. This is exemplified in developed countries when a common source outbreak occurs among non-immune adults. Fulminant hepatitis is uncommon in the USA and hepatitis A has never been documented to evolve into chronic hepatitis. However, prolonged cholestasis and relapsing hepatitis are well described. The usual features of cholestatic viral hepatitis A are pruritus, fever, diarrhoea, and weight loss. Serum bilirubin levels are > 10 mg/dl and the clinical course lasts at least 12 weeks. Cholestasis will spontaneously resolve, although corticosteroids will hasten the resolution but may predispose the patient to develop a relapse of the hepatitis. A biphasic or relapsing form of viral hepatitis A occurs in 6 to 10% of cases. The initial episode lasts 3 to 5 weeks and is followed by a period of remission characterized by normal liver chemistries lasting 4 to 5 weeks. Relapse may mimic the initial episode of the acute hepatitis. The full duration of the illness ranges from 16 to 40 weeks from the onset and immunoglobulin M antibody to hepatitis A virus persists throughout the clinical course. Hepatitis A virus has been recovered from stools during the relapse. Extrahepatic manifestations of hepatitis A include evanescent skin rash and transient arthralgias. Documented cases of arthritis and cutaneous vasculitis have been associated with cryoglobulinaemia and are rare.
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PMID:Atypical clinical manifestations of hepatitis A. 147 99

There is a paucity of data on the incidence of sporadic viral hepatitis in Indian children. Clinical, biochemical and etiological profile of 54 patients with acute viral hepatitis was evaluated. Of these, 32 (59.25%) patients had Hepatitis A, 18 (33.33%) had NANB, 2 (3.7%) had Hepatitis B and 2 (3.7%) concurrent Hepatitis A and B infection. It was not possible to distinguish the etiological agents on the basis of the clinical and biochemical profile. Fulminant hepatitis was documented in 8 (14.8%) cases. Children with NANB infection were at a greater risk (p less than 0.05) of developing fulminant hepatitis as compared to Hepatitis A infection.
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PMID:Clinical and etiological profile of acute viral hepatitis. 150 Jan 10


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