Relevance of anti-HCV reactivity in patients with alcoholic hepatitis

Cl, Mendenhall; Möritz, Thomas; Chedid, Antonio; Aj, Polito; Quan, Stella; Rouster, Susan D.; Roselle, Gary A.

doi:10.1007/bf02989216

Cited by 20 publications

(9 citation statements)

References 12 publications

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“…One possible explanation is that it is not using regression analysis seem to target alcohol as a major factor in inducing progression of liver disease in persons the result of a host difference, but rather the difference in the predominant viral genotype in Japan compared with the with chronic HCV infection, 58-63 although others are less convincing. 64,65 The question is whether these are independent United States. However, as already noted, the role of the genotype in defining outcome is far from clarified.…”

Section: Of Hcv-related Chronic Liver Diseasementioning

confidence: 99%

Natural history of hepatitis C

1997

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Approximately 85% of persons with acute hepatitis C de-Infection with the hepatitis C virus (HCV) is a problem of much current concern. Although acute hepatitis C is comvelop chronic hepatitis as determined by persistently abnormal serum enzymes and/or viremia (hepatitis C virus [HCV] monly an asymptomatic and seemingly mild illness, the viral infection nearly always persists, resulting in the development RNA). Both the acute and chronic illnesses are predominantly asymptomatic. For this reason and because the chronic illness of chronic hepatitis. By convention, chronic hepatitis is believed to have developed when the serum enzymes remain runs an extremely protracted course, it has been difficult to accurately define the frequency and rate of progression to abnormal for at least 6 months. An additional subgroup continue to show persistent infection (HCV RNA reactivity) in symptomatic or end-stage liver disease, specifically cirrhosis and hepatocellular carcinoma (HCC). Three evaluation strate-the absence of increased serum enzyme levels. Unfortunately, these events usually take place in an oblivious host who gies have been used. The first, prospective studies beginning from disease onset, have identified over 8 to 14 year follow-up generally continues to remain asymptomatic. Once chronicity ensues, it is believed that the disease may range through periods that morbidity (symptoms, cirrhosis) and mortality (hepatic failure, HCC) are modest in frequency. The second, incrementally advancing stages of histologically defined chronic hepatitis, progress to cirrhosis, and culminate in the prospective studies of subjects with already established chronic liver disease, have demonstrated high rates of devel-development of hepatocellular carcinoma (HCC). Some authorities believe that these sequentially progressive changes opment of cirrhosis, HCC, and mortality over relatively short follow-up periods. The third, retrospective/prospective (non-are inevitable and will occur in most chronically infected persons provided they do not die first from another lethal concurrent prospective) studies, has consisted of follow-up of recipients of HCV-contaminated immunoglobulin and of illness. Others believe that only a proportion of infected persons will develop progressive disease and that attention transfusion recipients from five enzyme-monitored transfusion studies of the early 1970s. The former study identified should therefore focus on establishing as early as possible who is likely to show advancing disease and on attempting to no mortality, trivial morbidity, and minimal cirrhosis 17 years after infection. The latter, involving hepatitis cases and define factors that might be responsible for such progression.These contradictory views can be resolved only by conductmatched nonhepatitis controls studied over a 20-year period, demonstrated no increase in all-cause but a slight increase in ing appropriate long-term studies of the natural history of the disease. liver-related mortality. Clinically evident chronic liver disease was ...

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Section: Of Hcv-related Chronic Liver Diseasementioning

confidence: 99%

Natural history of hepatitis C

1997

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“…The presence of HCV RNA was associated with more severe deSeveral studies have demonstrated a high prevalence of grees of periportal and bridging necrosis, intralobular degenanti-HCV among alcoholic patients with liver disease. [1][2][3][4][5] Testeration, focal necrosis, and portal inflammation. In yet aning with supplemental assays such as recombinant immuother study from Japan of 252 patients with a diagnosis of noblot assays has confirmed that 8% to 45% of alcoholic alcohol-induced liver disease, HCV RNA detection was highpatients with liver disease have anti-HCV.…”

Section: In Alcoholic Patientsmentioning

confidence: 99%

“…Injection drug use is the most common risk factor identified. 3 Yet there has not been a good explanation for the disproportionately high prevalence of HCV among alcoholic patients with liver disease without a history of drug use. 13 Caldwell et al 14 found no difference in the prevalence of anti-HCV among patients with alcohol-induced liver disease who had high risk factors as compared with those without identifiable modes of parenteral transmission.…”

Section: Epidemiology Of Hepatitis C Among Alcoholic Patientsmentioning

confidence: 99%

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Hepatitis C and alcohol

1997

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Chronic alcoholism in patients with chronic hepatitis C alcoholics with anti-HCV and liver disease also have HCV RNA (65% to 94%) detectable in serum; indeed, this marker appears to cause more severe and rapidly progressive liver is detected in some alcoholic patients with liver disease who disease leading more frequently to cirrhosis of the liver and are anti-HCV negative. hepatocellular carcinoma. The primary risk factor for acquiring hepatitis C among alcoholics is injection drug use. How-ASSOCIATION OF ALCOHOL USE AND SEVERITY ever, the epidemiology is not well defined, and other sources OF HEPATITIS C of spread must be important. Alcohol intake in excess of Alcoholic patients with anti-HCV confirmed by immu-10 g/d has been associated with increased serum hepatitis C noblot are also likely to have HCV RNA detectable in serum, viral RNA and aminotransferase levels, the mechanism of indicating active viral infection. The presence of HCV RNA which is poorly understood. The histological picture of hepati-usually is associated with some degree of necroinflammatory tis C in patients with chronic alcoholism is typically indistin-changes with or without fibrosis in the liver regardless of guishable from chronic hepatitis C in nonalcoholic patients. serum alanine aminotransferase (ALT) levels. Furthermore, Interferon therapy is less effective among alcoholic than non-alcoholic patients with anti-HCV have, on average, more sealcoholic patients, even after a period of abstinence. Patients vere liver disease than antibody-negative patients. In a large with chronic hepatitis C should restrict their alcohol intake Veterans Administration study, confirmed anti-HCV positivto less than 10 g/d, and if cirrhosis is present or interferon ity in serum correlated positively and significantly with the therapy is planned, abstinence from alcohol should be encour-presence of cirrhosis, cellular unrest, periportal inflammation, aged. Future research efforts should focus on the epidemiol-and piecemeal necrosis on liver biopsy in alcoholic subjects. 6 ogy and pathogenesis of combined chronic hepatitis C and In contrast, antibody to hepatitis B core antigen did not correalcoholism. (HEPATOLOGY 1997;26(Suppl 1):39S-42S

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“…Uniformly similar results were obtained in the three parts of the study. Chronic alcohol intake had tion compared to anti-HCV-negative alcoholics [12,13,[15][16][17], although these findings have not been substanti-no effect on serum HCV titers: (a) there was no difference in virus levels between alcoholics and nonalcoholics; ated in other studies [9,10,[18][19][20]. One possible mechanism for the synergy between alcohol and HCV is the (b) no correlation was observed between the amount of daily ethanol consumption and virus titers in the blood, potentiating effect of ethanol on viral replication, either directly or by reducing the host immune response to the and (c) there was no consistent change in HCV levels over a 6-month period, regardless of whether the subject infection.…”

Section: Discussionmentioning

confidence: 65%

Influence of Chronic Alcohol Abuse on Hepatitis C Virus Replication

Anand

Velez²

2000

Dig Dis

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Background: Patients with alcoholic liver disease have a high prevalence of hepatitis C virus (HCV) infection. Several workers have shown that HCV-infected alcoholics have more severe biochemical and histological evidence of liver disease than anti-HCV-negative patients. One possible mechanism for the increased liver damage is that alcohol may have a stimulatory effect on HCV replication. The present study was carried out to examine this issue in detail. Methods: Sixty-eight HCV-infected patients, comprising of 50 chronic alcoholics, consuming 80 g or more of alcohol daily for at least 5 years, and 18 completely abstinent subjects were included in the study. Quantitative HCV-RNA was performed by the branched chain DNA (bDNA) technique. Results: There was no significant difference in the mean serum HCV titers in chronic alcoholics compared to nonalcoholic subjects. Linear regression analysis showed no correlation between the daily ethanol consumption and HCV titers. Seven of the chronic alcoholics, 4 of whom were continuing to drink and 3 who had become abstinent, were retested after 6 months. There was no definite trend in the viral titers, either in abstinent individuals or in those who continued to drink. Conclusions: These findings suggest that chronic alcohol abuse does not influence the HCV load in the serum. Therefore, the observation that alcoholics with HCV infection have more severe liver damage requires some other explanation than increased HCV viral titers.

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Relevance of anti-HCV reactivity in patients with alcoholic hepatitis

Cited by 20 publications

References 12 publications

Natural history of hepatitis C

Natural history of hepatitis C

Hepatitis C and alcohol

Influence of Chronic Alcohol Abuse on Hepatitis C Virus Replication

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