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

We report four cases of fulminant hepatitis in children (4 to 15 years) who developed an hepatic encephalopathy grade III to IV, 4 to 13 days after the onset of their illness. Three patients recovered without sequelae. The complications were neurological: one child showed elevation of the intracranial pressure, successfully treated after monitoring of extra-dural pressure; one suffered from cerebral death. Hepatitis A was diagnosed by the presence in serum of the IgM component of hepatitis A antibody, but another etiologic factor was present in two cases: an halothane anesthesia and an Epstein Barr virus infection which could explain the severity of the hepatitis.
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PMID:[Fulminating hepatitis A in children. Apropos of 4 cases]. 358 76

Eleven patients of Chinese origin experienced spontaneous reactivation of chronic active hepatitis B. Eight HBsAg-positive patients were followed for an average of 15 months prior to, while three others presented during reactivation. Fatigue, hepatomegaly and jaundice were frequent findings. Elevation of both serum ALT (average = 1,212 units per liter) and hepatitis B virus DNA levels were noted in all patients, and reactivation lasted an average of 4.4 months. During resolution, clinical symptoms abated, serum ALT levels reverted toward normal, and in nine patients, the hepatitis B virus DNA values became undetectable. All patients lacked evidence for acute hepatitis A, Epstein-Barr Virus, cytomegalovirus or hepatitis delta virus infection. Histologic findings of liver tissue from eight patients showed piecemeal necrosis and fibrosis. Within the parenchyma, varying degrees of hepatocytolysis with cuffing, perivenular necrosis and acidophilic bodies were noted. Ground-glass cells and regenerative changes also were observed. Cirrhosis was not present in any of the liver biopsies. These findings suggest that spontaneous reactivation of hepatitis B occurs in heterosexual patients with chronic active hepatitis B and contributes to chronic inflammation and to the progression of their liver disease.
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PMID:Spontaneous reactivation of hepatitis B in Chinese patients with HBsAg-positive chronic active hepatitis. 361 49

Of the 1050 sera of acute viral hepatitis patients admitted to the Infectious Diseases Hospital in Jeddah, Saudi Arabia, over a one-year period, 40.9% were due to hepatitis A, 21.5% to hepatitis B, and 37.6% to non-A, non-B (NANB) hepatitis. The mean age for hepatitis A patients was 4 +/- 2.4 years, with no sex preponderance. The mean ages for hepatitis B and NANB were 26.1 +/- 11.9 and 28.8 +/- 14.2 years, respectively. A male to female ratio of 2:1 was noticed for both. 10% of HBsAg patients were positive for anti-delta. 32% of NANB cases were excluded on the bases of possessing specific IgM against cytomegalovirus (CMV), herpes simplex virus (HSV), Epstein-Barr virus (EBV) or Treponema pallidum. Only 9% of NANB cases had a history of blood transfusion. In conclusion, nearly all cases of acute jaundice in Saudi children are due to hepatitis A, whereas hepatitis B and NANB generally occur in adults. Other viruses such as CMV, HSV, and EBV are highly prevalent and must be excluded in all cases of NANB hepatitis.
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PMID:The aetiology of acute viral hepatitis in the western region of Saudi Arabia. 361 82

A case of Epstein-Barr virus mononucleosis with the unusual complication of exudative ascites is presented. The patient was a 22-yr-old man with the typical symptoms and physical findings of hepatitis secondary to infectious mononucleosis. Extensive evaluation including liver biopsy, failed to show another cause for the patient's ascites. The ascites and hepatitis disappeared with resolution of the acute mononucleosis infection. He is well 12 months after this illness with no evidence for chronic liver disease. This case adds to the list of causes for exudative ascites associated with acute hepatitis.
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PMID:Exudative ascites complicating infectious mononucleosis. 375 45

The risk of hepatitis B infections has been reduced by screening of blood donors for hepatitis B surface antigen (HBsAg). However, recipients remain at significant risk of developing post-transfusion hepatitis. Studies have shown that non-A, non-B hepatitis virus(es) are responsible for the majority of post-transfusion hepatitis infections. In spite of many efforts, these non-A, non-B hepatitis viruses have not yet been identified. Epidemiological studies, however, suggest that non-A, non-B hepatitis shares many features with hepatitis B. Recently, Wands et al [1982] showed, in chimpanzees infected with non-A, non-B hepatitis agents, the presence of antigenemia or viremia by radioimmunoassay with monoclonal antibodies directed toward distinct determinants of HBsAg and by molecular hybridization analysis. They suggested that non-A, non-B hepatitis agents may be related, but distinct variant(s) of hepatitis B virus (HBV). In this study, five chimpanzees were inoculated with three different agents that have been shown to transmit non-A, non-B hepatitis. The following inocula were used (I) a factor VIII preparation kindly provided by D.W. Bradley, (II) acute phase serum from a chimpanzee infected with the F strain kindly provided by A.J. Zuckerman, and (III) a DS-antigen serum previously shown by us to transmit non-A, non-B hepatitis [Duermeyer et al, 1983]. All chimpanzees developed a rise in transaminase levels between 8 and 10 weeks after inoculation. None of the chimpanzees was positive for any markers of HBV infection. No evidence was obtained of infection with hepatitis A, cytomegalovirus, or Epstein-Barr virus. One chimpanzee developed chronic liver disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Absence of detectable hepatitis B virus DNA in sera and liver of chimpanzees with non-A, non-B hepatitis. 392 Mar 54

Posttransfusion hepatitis of the non-A, non-B variety continues to be a significant problem in current hemotherapy. This disorder is many times more common than transfusion-associated disease caused by hepatitis B virus, cytomegalovirus, and Epstein-Barr virus, and also seems to be viral in origin. Several potential etiological agents have been implicated, but none has been identified with certainty, despite concerted efforts at doing so. Clinical disease is usually attended by few symptoms and signs, but evolution to chronic liver disease is distressingly common; over 50 percent of all cases of non-A, non-B posttransfusion hepatitis manifest this transition. Efforts at prevention of non-A, non-B hepatitis associated with blood transfusion have thus far been hampered by the lack of reliable laboratory markers for carriers of this disease, and controversy exists over the implementation of screening tests on blood donors, using such nonspecific indicators of possible viral carriage as serum alanine aminotransferase levels. It is probable, however, that simple measures such as more restrained blood usage, encouraged by greater educational efforts within the medical community, could be beneficial in minimizing the number of new cases of non-A, non-B posttransfusion hepatitis seen each year in the United States.
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PMID:Non-A, non-B hepatitis associated with blood transfusion. 392 Jul 92

Molecular hybridization was employed to detect HBV DNA in sera of patients with acute or chronic hepatitis, by a simplified version of the spot hybridization technique. HBV DNA was found in 21 out of 50 sera obtained in acute hepatitis B. Determination of HBV DNA was negative in sera of patients with hepatitis A, Epstein-Bar virus infections or other HBsAg-negative liver diseases. There was no cross-hybridization between HBV DNA and sera of patients with non-A, non-B hepatitis.
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PMID:Determination of HBV DNA by a simplified method of spot hybridization. 392 15

Three asymptomatic chronic carriers of hepatitis B surface antigen, who had normal serum aminotransferase levels and no detectable hepatitis B e antigen in serum, developed icteric, symptomatic acute hepatitis. Serologic evidence of acute infection with hepatitis A virus, delta hepatitis virus, cytomegalovirus, or Epstein-Barr virus was absent. However, hepatitis B virus DNA and DNA polymerase activity, which were not detectable before the exacerbation, appeared in the serum of all three patients during the acute illness, confirming the diagnosis of spontaneous reactivation of chronic type B hepatitis. Thus, acute exacerbations of chronic type B hepatitis may present as an acute hepatitis superimposed on the chronic carrier state.
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PMID:Reactivation of chronic type B hepatitis presenting as acute viral hepatitis. 399 87

Seven hundred and sixty-eight patients were seen and tested at frequent intervals after transfusion of whole blood. Eight patients were judged to have developed icteric or anicteric post-transfusion viral hepatitis, an incidence of 1%. Five were icteric and four of these were hepatitis B antigen (HB Ag) positive; two of these four died. One of the fatal cases and one non-fatal HB Ag positive case had received HB Ag positive blood. Two other antigen-positive patients had received blood or plasma or both which had not been tested for antigen.Thirty-five patients showed conspicuous or sustained elevations of alanine transaminase without clinical features of hepatitis.Four were positive for HB Ag but had not received antigen positive blood.Two who had received antigen positive blood remained antigen negative, but one developed hepatitis B antibody (HB Ab).Two other patients were also transfused with plasma.Five had serological evidence of cytomegalovirus (CMV) infection accompanying the enzyme changes.One patient who had received HB Ag positive blood remained antigen-negative and showed no abnormalities.Five patients who became HB Ag positive, although they had been given antigen-negative blood, remained clinically and biochemically well.Cytomegalovirus primary infection or reactivation occurred in another 32 patients; five had isolated, transient enzyme rises, one other was associated with a drug-induced focal liver necrosis and 26 showed no enzyme changes. Epstein-Barr virus infections, one of which was associated with a transient upset of enzyme activity, were detected in five patients. There were no cases of post-perfusion syndrome.
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PMID:Post-transfusion hepatitis in a London hospital: results of a two-year prospective study. A report to the M.R.C. Blood Transfusion Research Committee by the Medical Research Council Working Party on Post-Transfusion Hepatitis. 437 Jun 14

We report a patient with icteric hepatitis and abdominal pain caused by Epstein-Barr virus in the absence of other common features of infectious mononucleosis. The peak alanine aminotransferase was 289 IU/I. Hemolytic anemia and urinary retention complicated the patient's course. Patients with infectious mononucleosis commonly have hepatic involvement but isolated symptomatic hepatitis is unusual. Although rare cases of liver failure have been reported, there is no evidence that Epstein Barr virus causes chronic liver disease. The clinical and histological features of Epstein Barr virus-induced hepatitis are reviewed.
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PMID:Epstein-Barr viral hepatitis: an unusual case and review of the literature. 608 55


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