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
The latest studies, however, put the risk for those with advanced liver disease
of developing HCC at 13.4% (Gut 2000;47:131-136). As well, 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.” -
“HCV-associated liver cancer without cirrhosis”, De Mitri MS; Poussin K;
Baccarini P; Pontisso P; D’Errico A; Simon N; Grigioni W; Alberti A;
Beaugrand M; Pisi E; et al., Department of Internal Medicine, University
of Bologna, Italy, Lancet 345: 413-5 (1995 )
“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
It is thought that treatment with interferon reduces the risk of later
developing liver cancer. “The low incidence of hepatocellular carcinoma
in patients treated with interferon suggests that interferon may prevent
the development of hepatocellular carcinoma.” - “Risk Factors and the
Effect of Interferon Therapy in the Development of Hepatocellular
Carcinoma,” Journal of Gastroenterology and Hepatology 1997
Feb;12(2):149-155
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
