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Hepatitis C and Alchohol |
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August 4, 1999 Hepatitis C - caused by an RNA virus- was first identified in 1989 and represents 90+% of what we used to call? serum hepatitis?. World wide more than 100 million people are infected, in the United States there are more than 4 million. In the 1980?s and through 1993, 175,000 new cases were identified annually in the USA, since then the incidence has dropped to somewhere below 100,000 annually due to better screening of blood products. Hepatitis C is an important disease because of those infected, approximately 80% develop chronic hepatitis. Of these 80%, 20-25% will develop cirrhosis of the liver over the subsequent 20-40 years. With cirrhosis further complications occur to include; variceal bleeding, hepatoma( primary liver cell cancer) and liver failure. 1-3% of those with cirrhosis will develop hepatomas and in fact 70% of all hepatomas in the USA are associated with Hepatitis C. Chronic hepatitis C with cirrhosis is now the leading indication for liver transplantation. Extrahepatic manifestations of chronic hepatitis C infection are increasingly recognized and include glomerulonephritis and cryoglobulinemia. The identifiable sources of infection, and only about 50-60% are identifiable, include: exposure to infected blood, i.e. administration of blood and or blood products or contaminated needle use(IVDU), sexual transmission- low frequency and most commonly associated in setting of multiple partners, and vertical transmission- i.e. infected mother to new born during the birthing process- the frequency of this among those with potential transmission is low. Over the past 8 years there has been an increasing awareness that the presence of the Hepatitis C virus is disproportionately high among patients with clinical alcoholic liver disease. The incidence has been reported as high as 37%. There is no clear explanation for this high incidence although past IVDU may play a role, as well as an increased exposure to blood transfusions, perhaps secondary to increased alcohol related trauma. This observation has led to several studies to assess the effect of this co-morbidity on the development and progression of chronic liver disease. Before presenting this data it may be useful to review pertinent basics and definitions. Alcohol content of common beverages:
In the gastroenterology- liver- alcohol literature, a common definition of excess alcohol i.e. chronic alcoholism, is the average daily ingestion of 80+ gm of alcohol per day for men and 60+ gm per day for women. In the studies to be discussed the levels of daily consumption of alcohol that are used to describe moderate and excessive intake are considerably less than the above definition. In the studies reviewed, some of which will be described, from the USA, Japan, Taiwan, Sweden, France and Great Britain - some prospective, many retrospective, the overall results are the same though the numbers vary. The study of Pessione et al ( France 1998 ) is of 233 consecutive patients presenting with chronic Hepatitis C.. They were evaluated for serum HCV RNA levels, histologic activity and self-reported alcohol intake. 80% (193/233 )reported alcohol consumption of < 140gm per week. Noteworthy was that there was a highly significant direct correlation between the amount of alcohol consumed and the serum HCV RNA levels ( p<0.0001 ). There was also significant correlation between fibrosis with age ( p<0.0001 ) and alcohol consumption ( p<0.02 ). They found increases in levels of viremia and fibrosis even in those with relatively low alcohol intake. The multicenter study by Poynard et al ( France 1997 ) of 2235 untreated patients with serologic and histologic evidence for chronic hepatitis C assessed nine factors on fibrosis progression: namely, age at liver biopsy, estimated duration of infection, sex, age at infection, alcohol consumption, Hepatitis C genotype, HCV RNA level, cause of infection and histological grade of activity. They found 3 factors that were independently associated with an increased rate of fibrosis: infection after the age of 40, daily consumption of 50 gm or more of alcohol and male sex. There were similar findings in the retrospective study by Wiley et al ( USA 1998 ) comparing 86 patients with chronic hepatitis C to 90 patients with chronic hepatitis C and excess alcohol intake? ( males 60+ gm per day and females 40+gm per day). The two groups were comparable in age and duration of chronic hepatitis C, however, there were more IVDUsers and males in the alcohol group. The time period to grade 3 fibrosis was half that in the ? excess alcohol? group compared to the control group. Complications in the alcohol group to include those secondary to cirrhosis and hepatoma were 3 times more common when compared to the control group. These findings are not dependent on the patients sex, the genotype of the hepatitis C virus or route of transmission of the C virus. Also noteworthy is that those patients with histologic features of alcoholic liver disease along with the chronic hepatitis C have an even less efficacious response to interferon therapy. The risk of hepatoma is 8.3x in those with alcolic liver disease with cirrhosis and chronic hepatitis C versus those with cirrhosis due HCV alone, where the incidence is 1+%. Several additional studies are confirmatory. The mechanism of injury and the effect of alcohol on HVC replication is summarized in the Figure 1 as hypothesized by Schiff. Pertinent is that high serum virus levels as seen in habitual alcohol users correlates with the rate of progression of the liver disease and a poor response to interferon / ribavarin therapy, the only current therapeutic modality available. The bottom line is that for patients with chronic hepatitis C who are even moderate users of alcohol ( 20-30 gm per day ) have an accelerated form of chronic liver disease leading to cirrhosis and its complications. Although there are suggestions that up to 10gm of alcohol per day may be relatively safe, perhaps the best advice for this group of patients is abstinence. Remember that patients with chronic liver disease secondary to alcohol and or viral causes, especially with cirrhosis, are relatively free of coronary artery disease- so that the med medical indications of daily wine use are not pertinent. REFERENCES: 1. Pessione et al: Effect of alcohol consumption on serum hepatitis C virus RNA and histologic lesions in chronic hepatitis C. HEPATOLOGY 1998: 27: 1717-1722 2. Poynard et al: Natural history of liver fibrosis progression in patients with chronic hepatitis C. THE LANCET 1997; 349: 825-832 3. Wiley et al: Impact of alcohol on the histological and clinical progression of hepatitis C infection. HEPATOLOGY 1998; 28: 805-809 4. Schiff E R : Hepatitis C and alcohol. HEPATOLOGY 1997; 26(Suppl 1): 39S-42S 5. Serfaty et al: Risk factors for cirrhosis in patients with chronic hepatitis C virus infection: Results of a case control study. HEPATOLOGY 1997; 26: 776-779 6. Frieden et al: Chronic liver disease in central Harlem: The role of alcohol and viral hepatitis. HEPATOLOGY 1999; 29: 883-888
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