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2.9.10 Does HCV Increase the Likelihood of Cancer?



2.9.10 Does HCV increase the likelihood of cancer?

Chronic infection by HCV is associated with an increased risk of liver cancer. The prevailing concept is that hepatocellular carcinoma (HCC) occurs against a background of inflammation and regeneration associated with chronic hepatitis over the course of approximately 3 or more decades. Most cases of HCV-related HCC occur in the presence of cirrhosis. Earlier statistics put the risk for a person with chronic HCV hepatitis developing HCC at 1-5 percent after 20 years, with striking variations in rates in different geographic areas of the world. Once cirrhosis is established, the rate of development of HCC is 1-4 percent per year. (National Institutes of Health Consensus Statement on Hepatitis C 1997)

Later studies, however, put the risk for those with advanced liver disease of developing HCC at 13.4% (Gut 2000;47:131-136). Cirrhosis is NOT a necessary precursor to HCC: it can develop at any time, as the study below shows:
“Chronic infection with hepatitis C virus (HCV) is regarded as a risk factor for hepatocellular cancer, mostly in patients with liver cirrhosis. We looked for HCV genomes in the livers of patients with hepatocellular cancer who did not have cirrhosis to see whether HCV was directly oncogenic. Cancerous and non-cancerous liver tissue and serum samples from 19 patients negative for hepatitis B surface antigen were analysed by polymerase chain reaction for the presence of HCV genome, HCV replication, HCV genotyping, and HBV genome. 13 of 19 patients were HCV RNA-positive in cancerous and non-cancerous liver tissue; 8 of 17 tested were anti-HCV positive.”

“Among the 13 HCV RNA-positive patients, 11 had genotype 1b and 2 had genotype 2a. 7 of 13 serum samples were HCV RNA positive.”

“7 of 19 patients were HBV DNA positive in cancerous and non-cancerous liver tissue, 5 of them anti-HBc positive. 4 patients were both HCV RNA and HBV DNA positive and 3 were both HCV RNA and HBV DNA negative. The results provide evidence for the association of HCV, mostly genotype 1b, with hepatocellular cancer without the intermediate step of cirrhosis.”
(De Mitri MS, et al. Lancet 345: 413-5, 1995, “HCV-associated liver cancer without cirrhosis”)

“Previously, we reported the high prevalence of hepatitis C virus (HCV) infection in patients with oral cancer or oral lichen planus in Kyushu, Japan. We now report a 61-year-old man with chronic hepatitis C and no oral lesions who developed oral cancer 6 months after interferon therapy (interferon alpha, 6 million units (MU) daily for 2 weeks and then 3 times a week for 14 weeks). This case emphasizes the need for periodic oral cavity examinations of hepatitis C patients and contributed to the investigation of oral cancer and HCV.”
(“Oral cancer and hepatitis C virus [HCV]: can HCV alone cause oral cancer?--a case report.” Kurume Medical Journal, 1996 Vol 1, Issue 43, pp 97-100)

An association between chronic hepatitis C infection and non-Hodgkin’s lymphoma has been reported. “HCV Infection and Extrahepatic Malignancies,” Journal of Clinical Gastroenterology 1997 Mar;24(2):87-89

The statistics are worse for those with HCV who smoke.

Researchers studying the Swedish HCV population looked at whether or not people with HCV were at greater risk for different types of cancer other than liver cancer. Of all the different types they looked at, they found that the danger of non-Hodgkin’s lymphoma and multiple myeloma were higher than for people without HCV—for non-Hodgkin’s lymphoma, 1.99 times higher, and for multiple myeloma, 2.54 times higher. The bulk of the people with HCV having one of the above cancers were estimated to have had HCV for greater than 15 years. Researchers propose that the danger for HCV-related cancers goes up with the length of time one is infected with HCV. (Ann-Sofi Duberg, et al, Hepatology; 41:3; March 2005, "Non-Hodgkin's Lymphoma and Other Nonhepatic Malignancies in Swedish Patients With Hepatitis C Virus Infection,")

A study from Japan followed 75 patients, 38 with SVR, and 37 who normalized their ALT but still had detectable HCV, for 12 years. After 12 years, there were still 15 patients available for testing in each group. Four of the SVRs developed liver cancer, found 1 month to 5 1/2 years after treatment. None of the non-SVR group did. = “SVR Can Last for Years, Doctors Claim” (John C. Martin, Hepatitis Neighborhood 11-24-04, http://www.hepatitisneighborhood.com/content/inthenews/archive2152.aspx )

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