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).
1. Alter MJ (1997), Epidemiology of hepatitis C. Hepatology 26(3 suppl 1):62S-65S.
2. Alter MJ, Kruszon-Moran D, Nainan OV et al. (1999), The prevalence of hepatitis C virus in the United States, 1988 through 1994. N Engl J Med 341(8):556-562.
3. Backmund M, Meyer K, Von Zielonka M, Eichenlaub D (2001), Treatment of hepatitis C infection in injection drug users. Hepatology 34(1):188-193.
4. Bhattacharya R, Shuhart MC (2003), Hepatitis C and alcohol: interactions, outcomes, and implications. J Clin Gastroenterol 36(3):242-252.
5. Bohn MJ, Babor TF, Kranzler HR (1995), The Alcohol Use Disorders Identification Test (AUDIT): validation of a screening instrument for use in medical settings. J Stud Alcohol 56(4):423-432.
6. Bush K, Kivlahan DR, McDonell MB (1998), The AUDIT alcohol consumption questions (AUDIT-C): an effective brief screening test for problem drinking. Ambulatory Care Quality Improvement Project (ACQUIP). Alcohol Use Disorders Identification Test. Arch Intern Med 158(16):1789-1795.
7. Cook PA, McVeigh J, Syed Q (2001), Predictors of hepatitis B and C infection in injecting drug users both in and out of drug treatment. Addiction 96(12):1787-1797.
8. Corrao G, Arico S (1998), Independent and combined action of hepatitis C virus infection and alcohol consumption on the risk of symptomatic liver cirrhosis. Hepatology 27(4):914-919.
9. Dalgard O, Bjoro K, Hellum K et al. (2002), Treatment of chronic hepatitis C in injecting drug users: 5 years' follow-up. Eur Addict Res 8(1):45-49.
10. Diaz T, Des Jarlais DC, Vlahov D et al. (2001), Factors associated with prevalent hepatitis C: differences among young adult injection drug users in lower and upper Manhattan, New York City. Am J Public Health 91(1):23-30.
11. Dieperink E, Ho SB, Thuras P, Willenbring ML (2003), A prospective study of neuropsychiatric symptoms associated with interferon-alpha-2b and ribavirin therapy for patients with chronic hepatitis C. Psychosomatics 44(2):104-112.
12. Dieperink E, Willenbring M, Ho SB (2000), Neuropsychiatric symptoms associated with hepatitis C and interferon alpha: a review. Am J Psychiatry 157(6):867-876.
13. Donato F, Tagger A, Gelatti U et al. (2002), Alcohol and hepatocellular carcinoma: the effect of lifetime intake and hepatitis virus infections in men and women. Am J Epidemiol 155(4):323-331.
14. Estrada AL (2002), Epidemiology of HIV/AIDS, hepatitis B, hepatitis C, and tuberculosis among minority injection drug users. Public Health Rep 117(suppl 1):S126-S134.
15. Hernandez-Aguado I, Ramos-Rincon JM, Avinio MJ et al. (2001), Measures to reduce HIV infection have not been successful to reduce the prevalence of HCV in intravenous drug users. Eur J Epidemiol 17(6):539-554.
16. Maier I, Wu GY (2002), Hepatitis C and HIV co-infection: a review. World J Gastroenterol 8(4):577-579.
17. Okazaki T, Yoshihara H, Suzuki K et al. (1994), Efficacy of interferon therapy in patients with chronic hepatitis C. Comparison between non-drinkers and drinkers. Scand J Gastroenterol 29(11):1039-1043.
18. Saracco G, Olivero A, Ciancio A et al. (2003), Therapy of chronic hepatitis C: a critical review. Curr Drug Targets Infect Disord 3(1):25-32.
19. Sees KL, Delucchi KL, Masson C et al. (2000), Methadone maintenance vs 180-day psychosocially enriched detoxification for treatment of opioid dependence: a randomized controlled trial. JAMA 283(10):1303-1310 [see comments].
20. Thomas DL (2001), Hepatitis C. Epidemiologic quandaries. Clin Liver Dis 5(4):955-968.