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

Fulminant hepatitis, or fulminant hepatic failure, is defined as a clinical syndrome of severe liver function impairment, which causes hepatic coma and the decrease in synthesizing capacity of liver, and develops within eight weeks of the onset of hepatitis. Several independent factors influence the survival of patients: age, the cause of liver disease, the degree and the duration of encephalopathy in relation to the onset of the disease, and the prevention of complications. Over the years many intensive treatments have been practiced. Liver transplantation is expensive, and patients who survive transplantation require life-long immunosuppression, clinical care and complications management. Without transplantation fulminant hepatitis and hepatic failure might be completely recovered spontaneously, and the patient could expect a normal life. Two cases of fulminant B hepatitis with intensive care treatment, and their survival despite unfavorable prognosis are presented in this paper. The management of patients with fulminant hepatitis required intensive monitoring and therapeutic measures, including corticosteroids. The prognosis for survival without transplantation in fulminant hepatitis is limited by the measures of medical treatment and new specific therapeutic modalities which must be developed through basic research.
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PMID:[Fulminant hepatitis B]. 1289 32

Fulminant hepatitis is a severe complication of hepatitis A virus infection. Its mechanism is unknown. Liver transplantation can be necessary, but spontaneous recovery is frequent. There are no data on the level of viral replication according to the clinical form of hepatitis A. We reviewed the files of 50 patients with acute hepatitis A. Nineteen patients had fulminant hepatitis (defined by encephalopathy and factor V <50%), and, from them, 10 patients underwent transplantation. Hepatitis A virus (HAV) RNA was quantified by real-time PCR on sera obtained at admission. The genotype was determined by phylogenetic analysis of HAV RNA. HAV RNA was detected in serum by RT-PCR in 39 out of 50 patients. Encephalopathy and low factor V level were significantly related to female gender, HAV PCR negativity (9/19 vs. 5/31, respectively; P =.03), a low serum HAV RNA level (log, 3.6 +/- 0.6 vs. 4.4 +/- 0.9, respectively; P =.02), genotypes other than IA, and acetaminophen intake. In multivariate analysis, low or undetectable HAV viral load and a high bilirubin level were independently associated with both low factor V levels and fulminant hepatitis and also with death or transplantation. In conclusion, HAV-related liver failure is due to an excessive host response associated with a marked reduction in viral load. Serum HAV RNA assay could be of help in the management of severe hepatitis A.
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PMID:Viral and clinical factors associated with the fulminant course of hepatitis A infection. 1293 80

To determine the effect of swine hepatitis E virus (HEV) infection on pregnant gilts, their fetuses, and offspring, 12 gilts were intravenously inoculated with swine HEV. Six gilts, who were not inoculated, served as controls. All inoculated gilts became actively infected and shed HEV in feces, but vertical transmission was not detected in the fetuses. There was no evidence of clinical disease in the gilts or their offspring. Mild multifocal lymphohistiocytic hepatitis was observed in 4 of 12 inoculated gilts. There was no significant effect of swine HEV on fetal size, fetal viability, or offspring birth weight or weight gain. The offspring acquired anti-HEV colostral antibodies but remained seronegative after the antibodies waned by 71 days of age. Swine HEV infection induced subclinical hepatitis in pregnant gilts, but had no effect on the gilts' reproductive performance, or the fetuses or offspring. Fulminant hepatitis associated with HEV infection was not reproduced in gilts.
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PMID:Experimental infection of pregnant gilts with swine hepatitis E virus. 1462 Aug 68

Fulminant hepatitis by Epstein-Barr virus is a rare event which is predominantly due to primary infection. We report a rare case of fatal hepatic failure due to Epstein-Barr virus reactivation in a 19-year-old boy who was taking oral steroids. Transaminase peak and the fulminant course of the disease began soon after steroid interruption. Epstein-Barr virus reactivation was diagnosed on the basis of past clinical history of heterophile-positive infectious mononucleosis, a high titer of IgG anti Epstein-Barr virocapsidic antigen, slight elevation of anti-virocapsidic IgM, a high titer of anti-EA IgG antibodies and elevated viral load in serum measured by polymerase chain reaction. It is concluded that Epstein-Barr virus should be considered as a possible etiological agent of fulminant hepatitis.
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PMID:Fatal hepatitis during Epstein-Barr virus reactivation. 1506 33

Fulminant hepatitis due to herpes simplex virus (HSV) is rare in immunocompetent adults. Most reported cases have clearly established pregnancy as a condition that can predispose to disseminated HSV infection. We report a case of a 25-year-old previously healthy pregnant woman who presented with fatigue, fever, and anicteric hepatitis. Triphasic contrast-enhanced computed tomography demonstrated a miliary pattern of multiple, hypovascular, subcentimeter lesions scattered throughout the liver. Familiarity with the clinical findings and computed tomographic appearance may prompt early recognition of fulminant HSV hepatitis and allow differentiation from other hepatic disease during pregnancy.
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PMID:Fulminant herpes hepatitis in an immunocompetent pregnant woman: CT imaging features. 1518 20

Fulminant hepatitis is characterized by massive or submassive liver necrosis. Massive liver necrosis can be induced by activated macrophages infiltrating into the liver. Osteopontin, an extracellular matrix, is a secretory glycoprotein as well essential for Th1 immune response, contributing to macrophage activation and infiltration. To know the significance of osteopontin in the development of fulminant hepatitis, plasma osteopontin levels were measured in patients with fulminant hepatitis. The levels were significantly greater in patients with fulminant hepatitis than in those with acute or chronic hepatitis as well as healthy adults. Among patients with fulminant hepatitis except one in whom bacterial infection was complicated, plasma osteopontin levels were elevated especially in the patients who developed hepatic encephalopathy of grade II or more within 10 days of the disease onset, a clinical type characteristic of massive liver necrosis. Immunohistochemical examination revealed that osteopontin was stained in macrophages positive for CD68, a marker for macrophages, in necrotic areas of the liver in a patient with fulminant hepatitis. In conclusion, plasma osteopontin levels were elevated in patients with fulminant hepatitis, probably reflecting production of osteopontin in Kupffer cells and hepatic macrophages, which might be involved in the development of massive liver necrosis in fulminant hepatitis.
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PMID:Plasma osteopontin levels in patients with fulminant hepatitis. 1528 11

Fulminant hepatitis is a rare complication of adenoviral infection that has not previously been reported in children receiving standard chemotherapy for acute leukemia. The authors have observed fatal adenovirus hepatitis in three children receiving first-line chemotherapy for acute lymphoblastic leukemia (ALL). The patients presented 10, 17, and 8 months into therapy according to the UKALL XI (third intensification), UKALL 97/99 (maintenance), and pilot UKALL 2003 (delayed intensification II) protocols, respectively. All patients received aggressive supportive care and intravenous immunoglobulins. The second and third patients were also treated with intravenous cidofovir. Despite these measures, all three children deteriorated rapidly and died of fulminant liver failure. Although rare, adenovirus infection should be considered in the differential diagnosis of acute hepatitis in children receiving standard chemotherapy for ALL.
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PMID:Fatal adenovirus hepatitis during standard chemotherapy for childhood acute lymphoblastic leukemia. 1570 79

Fulminant hepatitis is a rare complication of acute hepatitis A infection. Nevertheless, the seroepidemiology of the infection is rapidly changing with the developing world, rendering more adults susceptible to the infection, in particular with more severe course. We report here fulminant hepatitis A infection with a mortal course during an epidemic period in two siblings. Although it causes a self-limited mild disease, hepatitis A virus may have a severe course including fulminant hepatitis and may lead to mortality, especially in older ages. Hence, the risk of hepatitis A virus infection and its complications should be reduced with measures of immunization and sanitation.
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PMID:Two siblings with fulminant viral hepatitis A: case report. 1664 33

Genotypes of hepatitis B virus (HBV) were determined in 485 patients with acute hepatitis B from all over Japan. They were A in 92 (19%), Ba in 26 (5%), Bj in 32 (7%), C in 330 (68%) and D in 5 (1%). Sexual contacts were the main route of transmission in them. Overall, HBV persisted in only 5 of the 464 (1%) followed patients. Genotypes C accounted for more than 68% in northern as well as southern areas, contrasting with genotype A accounting for 34% in and around the Metropolitan areas. During 24 years from 1982 to 2005, genotype A increased from 5% to 33%, while genotype B gradually decreased from 26% to 8%. Fulminant hepatitis was significantly more frequent in infection with genotype Bj (41%) than those with the other genotypes (p<0.01). The core-promoter double mutation (T1762/A1764) and precore stop-codon mutation (A1896) were more frequent in patients with fulminant than acute self-limited hepatitis (57% versus 15% and 58% versus 10%, respectively, p<0.01 for both). In conclusion, genotype A distributes unevenly over Japan, prevails in younger patients through sexual transmission and has increased with years. Furthermore, fulminant outcome was more frequent in patients with genotype Bj than those with the other genotypes.
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PMID:Spatial and chronological differences in hepatitis B virus genotypes from patients with acute hepatitis B in Japan. 1695 89

A 40-year-old man, who had suffered from general malaise and brown urine during his stay in China, was admitted with remarkable jaundice and hepatocellular disorders soon after he returned to Japan. Because his coagulation test results worsened, he was transferred to our hospital. No evidence of hepatitis A-D virus infection, autoimmune hepatitis, or metabolic disorders was noticed. His prothrombin time was extended (18%), grade II encephalopathy appeared on the second hospital day, and fulminant hepatitis was diagnosed. Artificial liver support was introduced, and his hepatic coma and coagulation parameters gradually recovered. Genotype IV hepatitis E virus RNA was detected in his early phase sera and also both IgG and IgM type anti-hepatitis E virus antibodies were detected. Fulminant hepatitis E resulting from infection in China was diagnosed.
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PMID:[A case of fulminant hepatitis E treated with artificial liver support]. 1728 17


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