Treating Co-Occurring Substance Use Disorders and Hepatitis C

Treating Co-Occurring Substance Use Disorders and Hepatitis C

Chronic infection with the hepatitis C virus (HCV) is frequently complicated by the presence of coexisting substance use disorders (SUDs) and mental illnesses. Patients experience multiple barriers to evaluation and treatment services, and health care providers often experience uncertainty and frustration in trying to provide those services. Chronic hepatitis C is the leading cause of liver failure and subsequent liver transplantation, a trend that will rapidly rise in the next decade as the largest group of patients with chronic HCV infection develops cirrhosis, hepatocellular carcinoma and liver failure (Alter, 1997). Furthermore, antiviral treatment is now achieving viral elimination in a substantial proportion of patients, and efforts to improve treatment outcomes are continuing (Saracco et al., 2003).

Alcohol Consumption and HCV

Alcohol consumption is considered a cofactor in the natural history of hepatitis C, although some consider that not enough emphasis has been placed on its importance. Drinking eight to 12 or more drinks per day for many years clearly accelerates the progression of chronic hepatitis C to cirrhosis and to hepatocellular carcinoma (HCC), as well as mortality (Bhattacharya and Shuhart, 2003). The risk for developing HCC is particularly high for heavy drinkers who are infected with HCV. The evidence regarding less extreme drinking levels is not as clear and is limited by retrospective designs relying on remote recall of drinking over several decades and the use of different measures and cutoff levels for analysis. However, it has been shown that the relationship between drinking and risk of cirrhosis may be additive at lower levels (<3 drinks/day) and synergistic at higher levels (>8 drinks/day) (Corrao and Arico, 1998). Some studies have reported a relationship between light-to-moderate drinking and development of cirrhosis in the context of HCV, while others have found a relationship only with heavy drinking (Donato et al., 2002). The resolution of this question awaits further research.

The effect of alcohol consumption on response to interferon-based treatments is similarly in question. Several small, mostly retrospective studies found that lifetime alcohol use reduces the response to interferon (Okazaki et al., 1994). In addition to the methodological problems already mentioned, most studies were conducted on Japanese patients treated with interferon monotherapy. Methods for collecting information about alcohol consumption are poorly described, and many studies lack information about genotype or compliance. More recently, however, a history of problematic alcohol use (and almost certainly some ongoing drinking) was not found to affect outcomes in a small sample of male veterans treated with interferon and ribavirin (Virazole, Rebetol) (Dieperink et al., 2003). At this point, it is not possible to develop firm conclusions about the effect of alcohol use on HCV treatment response.

Injection Drug Use and HCV

Injection drug use (IDU) is the primary mode of HCV transmission. Among people attending drug treatment programs, HCV seroprevalence ranges from 30% to >90%, with 65% to 85% being common (Diaz et al., 2001). Intranasal and crack cocaine use have also been reported to be risk factors for HCV, but this could be due to unreported IDU by these individuals (Thomas, 2001). Risk of exposure to HCV is greatest during the first period of drug use and increases to >60% after five years of IDU (Cook et al., 2001). Sharing other types of drug-using equipment such as cookers and cotton may transmit HCV. The transferring of drug from one syringe to another (known as frontloading) is another potential mode of transmission. Although the incidence of HCV in people who inject drugs has been declining, there is evidence that educational prevention efforts such as those used for HIV are ineffective (Hernandez-Aguado et al., 2001) and that new prevention methods are needed.

There is no evidence that IDU by itself alters the course of HCV infection, but IDU is frequently coupled with heavy drinking of ethanol, which increases the rate of fibrosis. Co-infection with HIV ranges from 5% to >30%, depending on the overall prevalence of HIV in the area, and HIV co-infection appears to increase the rate of fibrosis in HCV (Maier and Wu, 2002). Co-infection with the hepatitis B virus and other hepatitis viruses is common in individuals who inject drugs (Estrada, 2002).


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