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

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

To elucidate the risk factors for hepatocellular carcinoma (HCC) among women, we made a combined analysis of the data from three case-control studies conducted in high-risk areas of Japan. A total of 120 cases and 257 controls were included in the analysis. After adjustment for the study category, age, and other potential confounders, significantly increased risks were associated with chronic hepatitis-B virus infection (odds ratio [OR] = 42.4, 95 percent confidence interval [CI] = 11.2-160.2), a past history of blood transfusion (OR = 3.7, CI = 1.8-7.5), and a history of smoking (OR = 2.2, CI = 12-4.1). In addition, women with a history of heavy drinking experienced an elevated risk of borderline significance (OR = 4.2, CI = 0.9-20.4, P = 0.07). When these ORs were compared with the corresponding estimates among males from the same case-control studies, no significant differences were observed between the two genders. Among the factors examined in this analysis, drinking and smoking habits--which are more common among Japanese men than women--may partly account for a large male-predominance in the incidence of HCC. Further studies are needed to clarify the roles that sex-hormones and hepatitis-C virus infection might play in the large gender difference of HCC occurrence.
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PMID:Risk factors for hepatocellular carcinoma among Japanese women. 774 57

Urticaria has been described only rarely in patients with hepatitis A virus infection, although its association with acute hepatitis B virus infection is well recognized. A young male homosexual presented with hepatitis and urticaria, which proved to be an acute hepatitis A virus infection. In one study of a foodborne outbreak of hepatitis A virus, 2/130 patients developed hives. A few other isolated cases of presumed hepatitis A virus infection and urticaria have been reported, but this is the first detailed description of a serologically proven hepatitis A virus infection associated with the development of urticaria, in which no other risk factor could be implicated.
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PMID:Urticaria and acute hepatitis A virus infection. 838 Sep 51

Attempts at antiviral therapy of patients with active liver disease as a consequence of chronic hepatitis B virus infection have been moderately successful. The molecular and cellular basis for a successful outcome in these patients is not understood and the same therapies do not appear to benefit carriers that still have fairly normal livers and only a moderate hepatitis as a result of the immune response to the infection. Most carriers fall into this latter classification, at least during the early years of infection, and a therapy that could be successfully applied before extensive liver damage had occurred would presumably reduce the risk of subsequent liver damage and the progression to primary hepatocellular carcinoma. Traditionally, it has been assumed that the primary reason that individuals become chronically infected is that the cytotoxic T-cell response and/or antibody-dependent killing of infected hepatocytes is insufficient to clear the infection. Less attention has been focused on the role of the antibody response in the generation of virus-neutralizing antibodies as the possible major deficiency predisposing some individuals to become carriers. However, carriers normally are antigenemic for HBsAg and virus, and carriers with only antibodies to these structures in their circulation are virtually unknown. In addition, it is usually assumed that the hepatocyte, the major target of infection, does not spontaneously turn over and that, in the absence of an immune response to the infected cell, hepatocellular viability is unaffected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The problem of antiviral therapy for chronic hepadnavirus infections. 850 29

A program of twice yearly testing of Alaska Native carriers of hepatitis-B surface antigen (HBsAg), for alpha-fetoprotein elevations as an indicator of early hepatocellular carcinoma has been established in Alaska. Because many HBsAg carriers live in remote regions of Alaska, logistical and cost considerations complicate the efficiency of this program. We evaluated the feasibility of using blood spotted onto mail-in cards as a system of blood collection and commercial assays for alpha-fetoprotein and HBsAg testing. We compared alpha-fetoprotein levels and the detection of HBsAg in both plasma and blood spots from HBsAg-positive carriers, normal volunteers, and pregnant females. There was good correlation between serum and blood spot AFP levels (r = 0.94, p < 0.001) over a wide range of serum alpha-fetoprotein levels. alpha-fetoprotein and HBsAg remained detectable in blood spots stored at room temperature for more than 8 weeks. The sensitivity of detection of HBsAg in blood spots was not as great in blood spots when compared to plasma levels. This system has been incorporated into the hepatocellular carcinoma screening program in Alaska. It should also prove feasible and economical for such screening to be undertaken in developed countries and possibly make alpha-fetoprotein screening affordable in those developing countries where the prevalence of hepatitis-B virus infection is high.
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PMID:Detection of alpha-fetoprotein and hepatitis-B surface antigen in blood spotted on filter paper: use as a screen for hepatocellular carcinoma in Alaska Natives. 888 34

We studied the relationship between hepatocyte proliferation and hepatitis delta virus (HDV) replication at the single cell level. The proliferating cell nuclear antigen (PCNA) (by immunohistochemistry) and the HDV RNA (by in situ hybridization) were stained in neoplastic and non-neoplastic liver tissues of 19 patients with chronic HDV infection, including four cases of cirrhosis with superimposed hepatocellular carcinoma (HCC). As controls, we assessed the hepatocyte proliferation of liver tissues from 16 patients with chronic hepatitis B and on three normal livers. The hepatocyte PCNA labelling index of HDV-infected tissues was comparable with that seen in chronic hepatitis B-infected livers but was significantly higher than that observed in normal livers. Although cirrhotic tissues had lower hepatocyte proliferating fractions than non-cirrhotic tissues, the difference was not statistically significant. The hepatocyte proliferation rate did not correlate with the level of intrahepatic HDV replication or with the histological activity. In double-labelling experiments, PCNA and HDV RNA staining did not co-localize, with the exception of two of three cirrhotic tissues associated with HCC, where the association between the two markers was statistically significant. This co-localization was not observed, however, in the adjacent tumorous tissues. In patients with chronic HDV infection the hepatocyte proliferation was increased with respect to normal liver tissue, but was comparable with that observed in patients with chronic hepatitis B virus infection and did not correlate with the level of HDV replication or the histological activity. In the cirrhotic tissue of patients with HCC (but not in the tumour counterpart), HDV RNA may occasionally co-localize with the marker of hepatocyte proliferation. Whether this association between viral replication and cell division is related to liver carcinogenesis remains to be established.
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PMID:Relationship between hepatocyte proliferation and hepatitis delta virus replication in neoplastic and non-neoplastic liver tissues. 909 64

This study was conducted to determine serum levels of trace metals in young adult patients in the early icteric phase of acute hepatitis B virus infection. There were 15 patients (10 males, 5 females) and 15 healthy volunteers (11 males, 4 females). The age distribution of both groups ranged from 15-40 years and were comparable [mean (SD) = 28(6) vs 31(7) years; p = 0.12]. Compared to the healthy controls, the patients had significantly decreased serum zinc but elevated serum copper levels [means (SD) of zinc = 118(22) vs 97(20) micrograms/dl, p = 0.012; and of copper = 82(15) vs 135(40) micrograms/dl, p < 0.001]. The overall serum levels of calcium, magnesium and phosphorus in the studied patients were within normal ranges. Serum zinc concentrations of these patients correlated with albumin (r = 0.69, p = 0.005) and their serum calcium correlated with alkaline phosphatase (r = 0.61, p = 0.015). These results demonstrate that alterations of zinc and copper metabolism occur early during the acute icteric phase of uncomplicated hepatitis. These changes may be of pathophysiological significance in acute hepatitis, in particular in patients with pre-existing zinc deficiency.
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PMID:Serum trace metal levels in patients with acute hepatitis B. 918 56

Interleukin-12 is produced by antigen-presenting cells and regulates the balance between TH1/TH2 lymphocyte subsets, promoting cell-mediated immune reactions. Amongst patients with chronic hepatitis B undergoing interferon-alpha treatment, only those who clear hepatitis B virus show a substantial increase in the production of biologically active IL-12 and an inverse ratio between serum levels of IL-12p40 subunit and IL-12. The peak of serum IL-12 occurs after the hepatitis flare and precedes or coincides with the time of HBe seroconversion. These data indicate that IL-12 is an important element for establishing the host immune control on hepatitis B virus replication in patients with chronic hepatitis B virus infection.
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PMID:Studies of interleukin-12 in chronic hepatitis B virus infection. 942 15

Hepatitis-associated aplastic anemia (HAAA) is an uncommon disorder that usually is not due to hepatitis A or B virus infection. Hepatitis C virus (HCV) seropositivity is infrequently observed in aplastic anemia (AA) patients who have not been extensively transfused. However, HCV seropositivity may not be detected until several weeks or months after viral infection and AA patients may exhibit defective humoral immunity. Therefore, we evaluated sera from AA patients for the presence of HCV viremia using a reverse transcriptase polymerase chain reaction (RT-PCR) based assay and several serologic assays for HCV antibodies. Serum samples from 90 AA patients who presented to the UCLA Medical Center between March 1984 and February 1990 were analyzed. Overall, 17 patients were found to have HCV viremia by RT-PCR assay, of whom 14 had a positive second-generation HCV enzyme immunoassay (EIA-2) and only 6 were EIA-1 reactive. The frequency of HCV viremia increased with the duration of time between diagnosis and sample procurement, and the number of blood products transfused prior to sampling (P = 0.026). No patient who received fewer than 20 U of blood products or who was sampled less than 20 days after diagnosis had a positive HCV RT-PCR result. Of four patients with hepatitis-associated AA (HAAA), one who was sampled 23 days after diagnosis had hepatitis C viremia and a reactive EIA-2 assay. Therefore, the high frequency of HCV viremia in this patient population is most likely due to transfusion with contaminated blood products prior to the introduction of routine blood donor screening for HCV.
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PMID:Hepatitis C virus infection in acquired aplastic anemia. 962 79

Fibrosing cholestatic hepatitis is a histological variant of hepatitis B virus infection with a high rate of mortality. We describe a patient who acquired acute hepatitis B virus infection 8 months after renal transplantation. Clinical features of rapidly progressive liver failure, indicated by prolonged prothrombin time (57 seconds) and increased bilirubin (40.4 mg/dL) and ammonia (129 mumol/L) concentrations, were accompanied by an extremely high serum HBV DNA level (2.153 x 10(6) pg/mL). Liver biopsy specimen showed fibrosing cholestatic hepatitis with widespread balloon degeneration of hepatocytes, focal hepatocyte loss, bile stasis, periportal fibrosis, mild lymphocytic infiltration, and strongly positive immunohistochemical staining for hepatitis B surface antigen (HBsAg) and hepatitis B core antigen. Lamivudine therapy suppressed HBV DNA to < 10 pg/mL within 4 weeks, which was followed by gradual recovery of liver function from a state of hepatic precoma. Twenty-four months after the onset of hepatitis, the patient had normal prothrombin time and bilirubin, transaminase, and albumin levels. She remained HBsAg positive and hepatitis B e antigen negative. Renal allograft function was stable, with a creatinine level of 1.52 mg/dL. HBV DNA remained suppressed after 22 months of lamivudine therapy. Our experience shows that fibrosing cholestatic hepatitis and liver failure caused by HBV infection can be successfully treated with lamivudine.
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PMID:Treatment of fibrosing cholestatic hepatitis with lamivudine. 964 74


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