Showing papers on "Hepatitis published in 1990"
TL;DR: The nucleotide sequence of the Japanese type of hepatitis C virus (HCV-J) genome, consisting of 9413 nucleotides, was determined by analyses of cDNA clones from plasma specimens from Japanese patients with chronic hepatitis.
Abstract: The nucleotide sequence of the Japanese type of hepatitis C virus (HCV-J) genome, consisting of 9413 nucleotides, was determined by analyses of cDNA clones from plasma specimens from Japanese patients with chronic hepatitis. HCV-J genome contains a long open reading frame that can encode a sequence of 3010 amino acid residues. Comparison of HCV-J with the American isolate of HCV showed 22.6% difference in nucleotide sequence and 15.1% difference in amino acid sequence. Thus HCV-J and the American isolate of HCV are probably different subtypes of HCV. The relationship of HCV-J with other animal RNA virus families and the putative organization of the HCV-J genome are discussed.
1,295 citations
TL;DR: The slow, sequential progression from acute hepatitis C virus—related non‐A, non‐B hepatitis through chronic hepatitis and cirrhosis to hepatocellular carcinoma is suggested to support a causal association between hepatitis Cirus and hepato Cell carcinoma.
1,198 citations
TL;DR: Statohepatitis (fatty liver hepatitis), histologically identical to alcoholic disease, occurs in some obese patients after jejunoileal bypass, and incidence of steatosis and steatohePatitis correlated with the degree of obesity.
1,183 citations
TL;DR: There appears to be a strong association between HCV infection and the development of HCC, particularly in patients for which HBV infection cannot be implicated as a causative factor.
Abstract: A possible causative role for the recently discovered hepatitis C virus (HCV) in the development of hepatocellular carcinoma (HCC) was investigated by assay of sera from HCC patients in Japan for antibodies to a recombinant HCV antigen and to hepatitis B virus (HBV) antigens. Among the 253 HCC patients examined, 156 (61.7%) had no serum markers of either a previous or a current HBV infection (group I), 46 (18.2%) were negative for HBV surface antigen but positive for anti-HBV surface and/or anti-HBV core antibody, indicating the occurrence of a previous, transient HBV infection (group II), and 51 (20.2%) were chronically infected HBV carriers as evidenced by positivity for HBV surface antigen (group III). The prevalence of HCV antibody in group I (68.6%) and II (58.7%) patients was significantly higher than for group III (3.9%) or in 148 additional patients with other (non-HCC) cancers (10.1%) (P less than 0.01). Thus, there appears to be a strong association between HCV infection and the development of HCC, particularly in patients for which HBV infection cannot be implicated as a causative factor. The data also suggest an additional mode of transmission for HCV other than blood transfusion, since a history of blood transfusion was shown in only about 30% of the HCV antibody-positive HCC patients in groups I and II. A high prevalence of HCV antibody was also shown among patients with HCC whose disease was originally thought to be due to very high ethanol consumption.
1,173 citations
TL;DR: Et1.1 represents a portion of the genome of the principal viral agent, to be named hepatitis E virus, which is responsible for epidemic outbreaks of ET-NANBH, and specifically identified similar sequences in complementary DNA prepared from infected human fecal samples collected from five geographically distinct ET- NANH outbreaks.
Abstract: Major epidemic outbreaks of viral hepatitis in underdeveloped countries result from a type of non-A, non-B hepatitis distinct from the parenterally transmitted form. The viral agent responsible for this form of epidemic, or enterically transmitted non-A, non-B hepatitis (ET-NANBH), has been serially transmitted in cynomolgus macaques (cynos) and has resulted in typical elevation in liver enzymes and the detection of characteristic virus-like particles (VLPs) in both feces and bile. Infectious bile was used for the construction of recombinant complementary DNA libraries. One clone, ET1.1, was exogenous to uninfected human and cyno genomic liver DNA, as well as to genomic DNA from infected cyno liver. ET1.1 did however, hybridize to an approximately 7.6-kilobase RNA species present only in infected cyno liver. The translated nucleic acid sequence of a portion of ET1.1 had a consensus amino acid motif consistent with an RNA-directed RNA polymerase; this enzyme is present in all positive strand RNA viruses. Furthermore, ET1.1 specifically identified similar sequences in complementary DNA prepared from infected human fecal samples collected from five geographically distinct ET-NANBH outbreaks. Therefore, ET1.1 represents a portion of the genome of the principal viral agent, to be named hepatitis E virus, which is responsible for epidemic outbreaks of ET-NANBH.
789 citations
TL;DR: Findings show that anti-C100-3-positive patients with chronic post-transfusion NANBH are likely to be viraemic; confirm that antibodies to C 100-3 are a marker for infectivity; and suggest that the prevalence of HCV infections may be underestimated from the frequency of antibodies to cDNA/polymerase chain reaction alone.
711 citations
TL;DR: Patients with no history of transfusions were just as likely to be positive for antibody to hepatitis C virus as patients with transfusion-associated hepatitis, indicating that hepatitis Cirus is the major causative agent of all non-A, non-B hepatitis in the United States.
Abstract: The Centers for Disease Control conducted intensive surveillance for acute non-A, non-B hepatitis in four sentinel counties over a 7-year period. Testing for antibody to hepatitis C virus was performed with the newly developed enzyme immunoassay. The incidence of non-A, non-B hepatitis remained relatively stable (average, 7.1 cases per 100 000), but there were significant changes in disease transmission patterns. The proportion of patients with a history of blood transfusion declined from 17% to 6%, but the proportion with a history of parenteral drug use increased from 21% to 42%. The proportion of patients with histories of sexual exposure (6%), household exposure (3%), occupational exposure to blood (2%), or hemodialysis (0.6%) did not change over time. Antibody to hepatitis C virus was found in 45% of patients within 6 weeks of onset of illness and in 68% of patients followed up for at least 6 months. Patients with no history of transfusions were just as likely to be positive for antibody to hepatitis C virus as patients with transfusion-associated hepatitis, indicating that hepatitis C virus is the major causative agent of all non-A, non-B hepatitis in the United States. ( JAMA . 1990;264:2231-2235)
583 citations
TL;DR: Stored serum samples from blood donors who had been involved in three episodes of post-transfusion NANBH in 1981 also contained hepatitis C viral sequences, which seem to be a better predictor of infectivity than the presence of anti-C100 alone.
546 citations
Journal Article•
TL;DR: The results indicate HBV-infected subjects who develop a self-limited acute hepatitis show a vigorous PBMC response to hepatitis B core Ag and HBeAg, as expression of T cell activation, which may reflect immune events of pathogenetic relevance with respect to evolution of disease and viral clearance.
Abstract: The proliferative response of PBMC to hepatitis B virus (HBV) envelope, core, and e Ag was analyzed prospectively in 21 patients with acute self-limited HBV infection and compared with the response of patients with chronic HBV infection and different levels of HBV replication (i.e., hepatitis e Ag (HBeAg)- or anti-HBe-positive) and liver damage (i.e., chronic active hepatitis or chronic asymptomatic carriers). Our results indicate that: 1) HBV-infected subjects who develop a self-limited acute hepatitis show a vigorous PBMC response to hepatitis B core Ag and HBeAg, as expression of T cell activation; 2) appearance of a detectable lymphocyte response to HBV nucleocapsid Ag is temporally associated with the clearance of HBV envelope Ag; 3) in patients with chronic HBV infection the level of T cell responsiveness to hepatitis B core Ag and to HBeAg is significantly lower than that observed during acute infection; 4) T cell sensitization to HBV envelope Ag in acute and chronic HBV infection is usually undetectable and when measurable is expressed transiently and at low levels. These results may reflect immune events of pathogenetic relevance with respect to evolution of disease and viral clearance.
485 citations
TL;DR: Evaluation of the relation between tumor necrosis factor and plasma levels of endotoxin and interleukin-1 beta in patients with acute severe alcoholic hepatitis suggested that tumor Necrosis factor plays a role in the pathogenesis.
Abstract: Study Objective:To determine whether elevated tumor necrosis factor levels contribute to the clinical manifestations and complications of severe acute alcoholic hepatitis and to evaluate t...
438 citations
TL;DR: The decline in the number of hepatitis B cases among homosexual men probably results from the modification of high-risk sexual behavior; the decline among health care workers is due mostly to hepatitis B immunization.
Abstract: To determine trends in the incidence and epidemiology of acute hepatitis B in the United States we conducted intensive surveillance for viral hepatitis in four sentinel counties from October 1, 1981, to September 30, 1988. The overall incidence of hepatitis B remained relatively constant throughout the study period (average, 13.2 cases per 100 000 population), but disease transmission patterns changed significantly. The proportions of hepatitis B cases accounted for by homosexual activity and health care employment decreased 62% and 75%, respectively; the proportions of cases accounted for by parenteral drug use and heterosexual exposure increased 80% and 38%, respectively. The percentage of patients for whom no risk factor was identified (30% to 40%) did not change over time. These patients tended to belong to minority populations, and their socioeconomic level was low. The decline in the number of hepatitis B cases among homosexual men probably results from the modification of high-risk sexual behavior; the decline among health care workers is due mostly to hepatitis B immunization. The current strategy for prevention of hepatitis B, which targets high-risk groups for immunization, has failed to have a significant impact on the incidence of disease. (JAMA. 1990;263:1218-1222)
TL;DR: The findings suggest that serum from AI-CAH patients may contain a component that gives false-positive results in the assay, and this component may be associated with immunosuppressant therapy.
TL;DR: Data obtained indicate that this agent, termed the hepatitis C virus (HCV), is the major cause of post-transfusion, community-acquired and cryptogenic, NANB and many asymptomatic but infectious blood donors can now be detected using this antibody assay.
Abstract: A 'blind' recombinant immunoscreening approach, of general application to studies of infectious diseases, was used to clone and identify the genome of the previously uncharacterized non-A, non-B hepatitis (NANB) virus. This agent is a positive-stranded RNA virus that appears to be distantly related to the flaviviridae family. A recombinant viral antigen (C100-3) was used to develop a capture assay for circulating antibody. Data obtained using this assay indicate that this agent, termed the hepatitis C virus (HCV), is the major cause of post-transfusion, community-acquired and cryptogenic, NANB. Anti-C100-3 antibody appears to be directed towards dominant, non-structural viral epitopes. It is a non-neutralising antibody that develops generally late in infection and is a particularly good marker of chronic, persistent viraemia. Many asymptomatic but infectious blood donors can now be detected using this antibody assay. HCV is associated with the development of hepatocellular carcinoma and possibly, other liver diseases.
TL;DR: The screening of blood donors for anti- HCV antibody should prevent about half the cases of transfusion-associated hepatitis, but the donors with infectious virus who are anti-HCV-negative may remain seronegative for prolonged periods.
Abstract: Background. The hepatitis C virus (HCV) is now known to be the chief cause of transfusion-associated non-A, non-B hepatitis, but the prevalence of HCV among blood donors and the frequency of transmission by blood transfusion are unknown. Methods. To assess the sensitivity and specificity of a test for antibody to HCV, we tested serum samples from participants in a large study of transfusion-associated hepatitis. Samples were obtained prospectively from consecutive adults undergoing open-heart surgery in Spain, but were tested retrospectively, after the antibody enzyme immunoassay for anti-HCV became available. Results. Of 280 transfusion recipients given a total of 1109 units of blood, 27 (9.6 percent) had transfusion-associated non-A, non-B hepatitis (mean follow-up, 52 weeks) and 24 of the 27 seroconverted to anti-HCV—positive, whereas only 2 (0.8 percent) of the remaining transfusion recipients seroconverted. Among the 1044 donor specimens available for testing, 16 (1.5 percent) had anti-HCV a...
TL;DR: Sequence analysis of amplified 400 bp cDNA fragments encoding a portion of NS5 gene suggested that HCV can be classified into two types (named K1 and K2) in Japan.
TL;DR: HCV infection appears to play a relatively minor role in HBsAg-positive liver disease in Taiwan but is strongly associated with HBs Ag-negative chronic liver disease and HCC.
Abstract: To assess the contribution of hepatitis C virus (HCV) in liver disease in Taiwan, antibody to HCV (anti-HCV) was studied by radioimmunoassay in 392 patients with chronic liver disease and in 440 healthy adults and 444 subjects at risk. The anti-HCV prevalence was 0.95% in 420 volunteer blood donors, 90% in 100 hemophiliacs, and 81% in 58 parenteral drug abusers. Anti-HCV was present in 6 (7.7%) of 78 hepatitis B surface antigen (HBsAg)-positive and 28 (65%) of 43 HBsAg-negative patients with chronic hepatitis, 3 (10%) of 31 HBsAg-positive and 13 (43%) of 30 HBsAg-negative cirrhotics, and 7 (17%) of 42 HBsAg-positive and 15 (63%) of 24 HBsAg-negative patients with hepatocellular carcinoma (HCC). An outbreak of non-A, non-B hepatitis revealed 18% of 57 patients to be positive for anti-HCV, and in 29 patients with posttransfusion hepatitis prospectively followed, 7 (24%) developed anti-HCV. Thus, HCV infection appears to play a relatively minor role in HBsAg-positive liver disease in Taiwan but is strongly associated with HBsAg-negative chronic liver disease and HCC. The infection is extremely common in hemophiliacs and parenteral drug abusers.
TL;DR: It is concluded that the presence of elevated plasma TNF alpha is a significant predictor of decreased long-term survival in patients with severe alcoholic hepatitis.
Abstract: Plasma tumor necrosis factor alpha (TNF alpha), interleukin 1 alpha (IL-1 alpha), and interleukin 1 beta (IL-1 beta) were measured in plasma samples obtained from 23 patients with severe alcoholic hepatitis on admission and after 30 days of hospitalization. Over a 2-year follow-up period, 14 patients died at a mean time of 8 months following discharge. The presence of elevated plasma TNF alpha either at admission or discharge from the hospital was associated with death in 82% (14/17) of patients. By contrast absence of elevated plasma TNF alpha was associated with survival in 100% (6/6). The difference in survival with and without detectable plasma TNF alpha was significant at p = 0.0022. Plasma TNF alpha was not elevated in alcoholic patients without clinically apparent liver disease, with alcoholic cirrhosis, or in nonalcoholic healthy controls. Plasma IL-1 alpha was also significantly increased in alcoholic hepatitis whereas IL-1 beta was not. Neither IL-1 alpha nor beta was correlated with outcome in the alcoholic hepatitis group. It is concluded that the presence of elevated plasma TNF alpha is a significant predictor of decreased long-term survival in patients with severe alcoholic hepatitis.
TL;DR: Sixty of the hepatitis B surface antigen-positive Alaska natives were followed up prospectively over a period of 7815 carrier years for the development of sequelae related to chronic hepatitis B virus infection, with the leading cause of death being malignant neoplasms compared with accidents in the general Alaska native population.
Abstract: • A total 1400 hepatitis B surface antigen–positive Alaska natives, 824 men and 576 women of all ages, were followed up prospectively over a period of 7815 carrier years for the development of sequelae related to chronic hepatitis B virus infection. During the observation period, 20 cases of hepatocellular carcinoma, 14 cases of chronic active hepatitis, 8 cases of cirrhosis, and 1 case of glomerulonephritis developed in this cohort. The annual incidence of hepatocellular carcinoma was 387 per 100 000 for men and 63 per 100 000 for women. The incidence of chronic active hepatitis and cirrhosis was 193 and 107 per 100 000 in men and 158 and 95 per 100 000 in women, respectively. No cases of either essential mixed cryoglobulinemia or necrotizing vasculitis were seen. Sixty of the hepatitis B surface antigen–positive carriers died, with 13 (21.7%) of the deaths due to hepatocellular carcinoma. The leading cause of death in this group was malignant neoplasms compared with accidents in the general Alaska native population. ( Arch Intern Med . 1990;150:1051-1054)
TL;DR: Accumulating evidence suggests that a high proportion of this non-A, non-B hepatitis (NANB) is enterically transmitted and is caused by one virus or class of serologically related viruses.
Abstract: More than 50% of acute viral hepatitis occurring in some developing countries appears to be unrelated to infection by HAV or HBV and accumulating evidence suggests that a high proportion of this non-A, non-B hepatitis (NANB) is enterically transmitted. Epidemics or outbreaks of enterically-transmitted NANB (ET-NANB) have been documented in the Soviet Union, Nepal, Burma, Pakistan, India, Borneo, Somalia, Sudan, Ivory Coast, Algeria, and Mexico. These outbreaks primarily affect young to middle-age adults and are often associated with a high mortality rate in infected pregnant women, approaching 20% in most reported epidemics. Several investigators have reported finding 27 to 34 nm virus-like particles (VLPs) in stools of acutely infected cases. Stools containing these small, non-enveloped VLPs have been shown to cause NANB in experimentally infected cynomolgus macaques, African green monkeys, chimpanzees, rhesus monkeys, and Saguinus mystax monkeys (tamarins). Infected primates have been shown to seroconvert to 27-34 nm VLPs recovered from stools of cases occurring in the Soviet Union, India, Nepal, Burma, Pakistan and/or Mexico, suggesting that ET-NANB is caused by one virus or class of serologically related viruses. The morphological features and physicochemical properties of one candidate virus are very similar to those of some human caliciviruses, a group of viruses that is normally associated with outbreaks of severe diarrhoea.
TL;DR: Use of anti-HCV screening to prevent post-transfusion NANBH was compared with measurement of alanine aminotransferase concentrations: a corrected efficacy of 63% and 65%, a specificity of 93% and 64%, and a positive predictive value of 16.6% were found.
TL;DR: The prevalence of serum antibodies to hepatitis C virus (HCV) was assessed by an enzyme-linked immunosorbent assay in 46 patients seropositive for liver-kidney microsomal antibody (anti-LKM1), the marker of autoimmune hepatitis type 2, with similar prevalence to that reported in patients with chronic non A, non B posttransfusion hepatitis.
TL;DR: In southern Africa, HCV is associated with hepatocellular carcinoma but HBV is present in a higher proportion of patients, and the average age is higher and women and urban dwellers are more likely to be infected.
TL;DR: It is suggested that corticosteroids reduce short-term mortality in patients with acute alcoholic hepatitis who have hepatic encephalopathy, that the protective effect depends on the exclusion criterion of acute gastrointestinal bleeding and is influenced by trial quality, and that cortiosteroids are of no benefit in patients without hepaticEncephalopathy.
Abstract: Purpose To determine whether corticosteroids affect short-term mortality from alcoholic hepatitis. Data identification Studies published from 1966 to 1989 were identified through a MEDLINE computer search and an extensive manual search of the bibliographies of identified articles. Study selection We found 11 randomized studies (10 of which were placebo controlled) that assessed mortality in hospitalized patients diagnosed with acute alcoholic hepatitis and treated with corticosteroids. Data extraction Two critical appraisers independently evaluated trial quality and abstracted quantitative data on clinical characteristics of the populations, interventions, and all-cause mortality. Results of data synthesis Overall, the protective efficacy (or percent reduction in mortality) of corticosteroids was 37% (95% CI, 20% to 50%). Protective efficacy was higher among trials with higher quality scores and trials that excluded subjects with active gastrointestinal bleeding. In subjects with hepatic encephalopathy, protective efficacy was 34% overall (CI, 15% to 48%). It was also higher among trials with higher quality scores and trials excluding subjects with acute gastrointestinal bleeding, but was not present among trials with lower quality scores or trials that did not exclude subjects with acute gastrointestinal bleeding. In subjects without hepatic encephalopathy, corticosteroids had no protective effect, and this lack of efficacy was consistent across all trial subgroups. Conclusions These results suggest that corticosteroids reduce short-term mortality in patients with acute alcoholic hepatitis who have hepatic encephalopathy, that the protective effect depends on the exclusion criterion of acute gastrointestinal bleeding and is influenced by trial quality, and that corticosteroids are of no benefit in patients without hepatic encephalopathy.
TL;DR: The detection of anti-HCV in donors who have neither an elevation of alanine aminotransferase level nor presence of antibody to hepatitis B core antigen suggests that donor screening for anti- HCV will further reduce the risk of transfusion-associated hepatitis.
Abstract: In a survey carried out from 1985 through 1986, volunteer blood donors to The Greater New York Blood Program were tested for two surrogate markers for nonA, non-B hepatitis—elevation of alanine aminotransferase level and presence of antibody to hepatitis B core antigen. Stored serum samples from selected donors were also recently tested for antibody to hepatitis C virus (anti-HCV). Anti-HCV was detected in 0.9% to 1.4% of donors and was higher in black and Hispanic donors than in white donors. Anti-HCV prevalence increased with increasing age through the fourth decade of life, but decreased thereafter, possibly reflecting the disappearance of detectable antibody with time. Anti-HCV correlated with both alanine aminotransferase level and the presence or absence of antibody to hepatitis B core antigen. These associations suggest that donor screening for elevation of alanine aminotransferase level and presence of antibody to hepatitis B core antigen was, as expected, at least partially effective in preventing transfusion-associated non-A, non-B hepatitis. The detection of anti-HCV in donors who have neither an elevation of alanine aminotransferase level nor presence of antibody to hepatitis B core antigen suggests that donor screening for anti-HCV will further reduce the risk of transfusion-associated hepatitis. ( JAMA . 1990;263:49-53)
TL;DR: Transmission of non-A, non-B hepatitis through parenteral exposures, including drug abuse, blood transfusion, and occupational injury with a needle contaminated with blood is well documente...
Abstract: Excerpt Transmission of non-A, non-B hepatitis through parenteral exposures, including drug abuse, blood transfusion, and occupational injury with a needle contaminated with blood is well documente...
TL;DR: HCV appears to be the major predisposing factor for most non-A, non-B hepatitis and chronic liver disease in haemophilia.
TL;DR: Logistic regression analysis showed that HBeAg positivity, elevated ALT levels (greater than 200 IU/l) at presentation, and male sex were associated with a significantly higher probability of developing exacerbations.
TL;DR: The prevalence of hepatitis C virus antibody and its relationship to the severity of liver disease in chronic alcoholic patients has been assessed, using a recently developed enzyme immunoassay and confirmed by a recombinant immunoblot assay.
TL;DR: Data suggest that a viable precore minus mutant of hepatitis B virus is responsible for the lack of HBeAg in the serum of these patients, which may explain the peculiar geographic distribution of anti-HBe positive hepatitis.