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INTRODUCTION
Hepatitis C is a growing medical illness that has vast implications in that patients can develop chronic liver disease and, potentially, liver malignancies. The hepatitis C virus (HCV) is an RNA virus classified in the Flaviviridae family of viruses. Before the characterization of the virus, the diagnosis was one largely of exclusion (i.e. non-A, non-B hepatitis). Early studies demonstrated that non-A, non-B hepatitis was associated with blood transfusions. Population-based surveillance conducted demonstrated that this disease accounted for 15% to 20% of community-acquired viral hepatitis in the United States in 1998. Studies using first generation serological assays for antibody to the hepatitis C virus demonstrated that HCV was primarily responsible for the majority of cases of community-acquired non-A, non-B hepatitis in the United States.
The Third National Health and Nutrition Survey (1988-1994) estimate that there are approximately 3.9 million non-institutionalized Americans who have been infected with HCV. Of these, 2.7 million have chronic infection, indicating that HCV infection is the most common chronic blood-borne infection in the United States. The majority of those infected are unaware of their infection because they do not currently have signs or symptoms of disease. The highest prevalence of infection is found among those with repeated, direct percutaneous exposures to blood (e.g., injection drug users, recipients of blood transfusions from HCV-positive donors, and persons with hemophilia who were treated with clotting factor concentrates before 1987). The estimated prevalence of infection varies greatly among different geographic locations and selected populations in the United States according to the varying prevalence of risk factors for infection.
Incidence
The overall incidence of hepatitis C infection has been falling steadily during the 1990s. Public health interventions to reduce HIV transmission by needle exposure and the introduction of widespread blood donor screening have greatly reduced the occurrence of new hepatitis C infections. However, this fortunate public health development has limited the understanding as well as treatment of acute hepatitis C. It has reduced an identifiable group of patients in whom to study the possible benefits of treatment for acute hepatitis C infection.
Risk factors and Transmission
Some modes of transmission of hepatitis C virus are well documented and widely accepted; others are less well defined and require further study. It is clear that HCV is most frequently transmitted through large or repeated direct percutaneous exposures to infected blood. The two most common exposures associated with transmission of HCV are blood transfusion and injection drug use. Early case-control studies of patients with newly acquired symptomatic non-A, non-B hepatitis found a significant association between disease acquisition and a history six months prior to illness of blood transfusions, injection drug use, health care employment with frequent exposure to blood, personal contact with others who had hepatitis, multiple sexual partners or low socioeconomic status. Today, HCV is rarely transmitted by blood transfusion or transplantation of organs due to thorough screening of the blood supply for the presence of the virus and inactivation procedures that destroy bloodborne viruses. Viral inactivation procedures have largely eliminated clotting factor concentrates as a source of HCV infection.
Studies of injection drug users have demonstrated that the prevalence of HCV infection is extremely high. . Duration of injecting is the strongest single predictor of risk of HCV infection among injection drug users. Injection drug use has been the principal mode of transmission of HCV since the 1970's. In comparison to other viral infections, HCV is more rapidly acquired after initiation of intravenous drug use. In addition, rates of HCV among young, injection drug-users are four times higher than HIV infection. However, sexual transmission of HCV has been controversial. It is believed that HCV can be transmitted via some sexual behaviors, but these are inefficient routes of transmission. The likelihood of infection increases with the number of lifetime sexual partners. A history of a sexually transmitted disease, sex with a prostitute, more than five sexual partners per year, or a combination of these has been independently associated with positive HCV serology. Stable, monogamous sexual activity is rarely associated with HCV transmission. The frequency of HCV transmission between monogamous sexual partners is less than 5% according to the United States Public Health Service.
Alcohol is also important in the management of patients with HCV infection in that those that use alcohol have an increased prevalence of HCV infection plus excess alcohol accelerates HCV liver damage and impairs effectiveness of HCV therapy. Multiple studies have demonstrated a high prevalence of HCV antibodies among patients with a history of alcoholism. Ten percent of all alcoholics test positive for HCV, and this increases to 30 percent in alcoholics with clinically overt liver disease. One must realize that this increased prevalence may reflect polysubstance abuse, and/or unmeasured risk behavior. The mechanism of alcohol-induced injury in patients with HCV remains unclear. Several mechanisms have been suggested to explain the effect of alcohol on HCV infection. Alcohol is known to cause increased levels of reducing equivalents in the liver altering hepatic metabolism. Exactly how this impacts HCV remains ill-defined. Still, one should be aware that alcohol may compromise the immune response to HCV. Alcoholics are known to have an impaired humoral response to virus specific antigens, as exhibited by a decreased response to the hepatitis A and hepatitis B peptide vaccines.
In summary, most studies have shown that heavy alcohol contributes to serious liver disease in patients with chronic hepatitis C. The therapy (i.e. the use of interferon) response seems to be reduced in heavy drinkers and the risk for the development of liver cancer is increased. The mechanisms for these effects are still not clearly understood. Clearly, further investigation is needed to clarify the role of alcohol on HCV-related liver disease.
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