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VIENNA– In addition to dramatically increasing the risk of liver cancer more than 68-fold, chronic hepatitis C virus (HCV) infection more than doubled or tripled the risk of a host of other solid tumors and hematologic malignancies in a large retrospective, cross-sectional study.
Data from the Kaiser Permanente Southern California HMO accounting for more than 145,000 patient-years of follow-up for HCV-infected individuals and 14,000,000 patient-years of follow-up for non–HCV-infected individuals showed the crude rate ratio for the development of all cancers including hepatocellular carcinoma (HCC) was 2.33 (P < .0001), and excluding HCC, was 1.84.
The crude rate ratios for individual cancers in HCV-infected, compared with non–HCV-infected individuals were 68.67 for hepatocellular carcinoma (HCC); 3.59 for non-Hodgkin’s lymphoma (NHL); 3.41 for multiple myeloma; 3.05 for renal cancer; 3.03 for stomach cancer; 2.79 for pancreatic cancer; 2.56 for head and neck cancer; 2.51 for esophageal cancer; 2.44 for lung cancer; 2.05 for prostate cancer; and 1.88 for colorectal cancer.
“We need to interpret these results cautiously,” Dr. Anders Nyberg, a hepatologist at Kaiser Permanente Southern California in San Diego, acknowledged at the International Liver Congress sponsored by the European Association for the Study of the Liver.
“The strength of the study is that it is a large database in a ‘real-world’ population,” but one limitation is that it cannot establish causality and how chronic HCV infection might be linked to the increased risk of these cancers.
The link between chronic HCV infection and liver cancer is well established, and Swedish researchers have also previously reported a link with NHL and multiple myeloma (Hepatology 2005;13:652-9; doi:10.1002/hep.20608). Dr. Nyberg noted, however, that there are sporadic data on HCV and other cancer types.
The objective of the present study was therefore to look further at the possible association between HCV infection and cancer in a large population by linking the Kaiser Permanente Southern California data to the National Cancer Institute’s Surveillance, Epidemiology, and End Results (SEER) database. Patients were included if they had HCV diagnosed between 2008 and 2012 and were aged 18 years or older but excluded if they had HIV coinfection or a history of solid organ or bone marrow transplantation.
The study population consisted of 1,831 patients with a mean age of 62 years who had chronic HCV and a cancer diagnosis, 33,881 patients aged a mean of 59 years who had HCV but no cancer diagnosis, and 5,297,191 individuals aged 72 years without HCV. Dr. Nyberg noted that study subjects were predominantly male (around 50%-60%) and from white or Hispanic backgrounds.
Baseline comorbidities were more common in patients with HCV and cancer, with a Charlson Comorbidity Index of 2.1, than in those with HCV but no cancer (Charlson index of 1.5) or those in the non–HCV-infected cohort (Charlson index 0.5). There was a higher percentage of patients who smoked tobacco or with alcohol abuse in the HCV vs. non–HCV-infected cohort groups, and HCV patients were more likely to have diabetes mellitus and cirrhosis, but a lower body mass index.
When HCV and non–HCV-infected cohorts were stratified according to tobacco use, alcohol abuse, diabetes mellitus, and body weight, the increase in the cancer rate ratio for all cancer sites remained significant, as did the increase in rate of HCC and NHL.
“In the absence of alcohol abuse, tobacco use, and diabetes mellitus, there was an increase in the rate of many cancer types among those with HCV,” Dr. Nyberg said. However, when those variables were present, HCV had a more moderate effect on the cancer rates than the variables themselves, but rates were still increased.
“I interpret these data that the increased overall cancer rate is multifactorial. It may be related to hepatitis C, but it is also related to alcohol abuse, tobacco use, and diabetes mellitus,” Dr. Nyberg said at a press conference. “In the short term, my take-home message is that we can take HCV out of the equation.”
He qualified this further in an interview saying, “It is important not to just address the hepatitis C but also to address the other risk factors like stopping smoking, cutting down on drinking, reducing weight, and trying to prevent diabetes.”
This is a descriptive study, Dr. Nyberg added, and more research will be needed to further evaluate the findings.
The study was supported by a grant from Gilead Sciences paid to Kaiser Permanente Southern California. Dr. Anders Nyberg and Dr. Lisa Nyberg are employees of Kaiser Permanente Southern California but had no personal financial conflicts of interest.
VIENNA– In addition to dramatically increasing the risk of liver cancer more than 68-fold, chronic hepatitis C virus (HCV) infection more than doubled or tripled the risk of a host of other solid tumors and hematologic malignancies in a large retrospective, cross-sectional study.
Data from the Kaiser Permanente Southern California HMO accounting for more than 145,000 patient-years of follow-up for HCV-infected individuals and 14,000,000 patient-years of follow-up for non–HCV-infected individuals showed the crude rate ratio for the development of all cancers including hepatocellular carcinoma (HCC) was 2.33 (P < .0001), and excluding HCC, was 1.84.
The crude rate ratios for individual cancers in HCV-infected, compared with non–HCV-infected individuals were 68.67 for hepatocellular carcinoma (HCC); 3.59 for non-Hodgkin’s lymphoma (NHL); 3.41 for multiple myeloma; 3.05 for renal cancer; 3.03 for stomach cancer; 2.79 for pancreatic cancer; 2.56 for head and neck cancer; 2.51 for esophageal cancer; 2.44 for lung cancer; 2.05 for prostate cancer; and 1.88 for colorectal cancer.
“We need to interpret these results cautiously,” Dr. Anders Nyberg, a hepatologist at Kaiser Permanente Southern California in San Diego, acknowledged at the International Liver Congress sponsored by the European Association for the Study of the Liver.
“The strength of the study is that it is a large database in a ‘real-world’ population,” but one limitation is that it cannot establish causality and how chronic HCV infection might be linked to the increased risk of these cancers.
The link between chronic HCV infection and liver cancer is well established, and Swedish researchers have also previously reported a link with NHL and multiple myeloma (Hepatology 2005;13:652-9; doi:10.1002/hep.20608). Dr. Nyberg noted, however, that there are sporadic data on HCV and other cancer types.
The objective of the present study was therefore to look further at the possible association between HCV infection and cancer in a large population by linking the Kaiser Permanente Southern California data to the National Cancer Institute’s Surveillance, Epidemiology, and End Results (SEER) database. Patients were included if they had HCV diagnosed between 2008 and 2012 and were aged 18 years or older but excluded if they had HIV coinfection or a history of solid organ or bone marrow transplantation.
The study population consisted of 1,831 patients with a mean age of 62 years who had chronic HCV and a cancer diagnosis, 33,881 patients aged a mean of 59 years who had HCV but no cancer diagnosis, and 5,297,191 individuals aged 72 years without HCV. Dr. Nyberg noted that study subjects were predominantly male (around 50%-60%) and from white or Hispanic backgrounds.
Baseline comorbidities were more common in patients with HCV and cancer, with a Charlson Comorbidity Index of 2.1, than in those with HCV but no cancer (Charlson index of 1.5) or those in the non–HCV-infected cohort (Charlson index 0.5). There was a higher percentage of patients who smoked tobacco or with alcohol abuse in the HCV vs. non–HCV-infected cohort groups, and HCV patients were more likely to have diabetes mellitus and cirrhosis, but a lower body mass index.
When HCV and non–HCV-infected cohorts were stratified according to tobacco use, alcohol abuse, diabetes mellitus, and body weight, the increase in the cancer rate ratio for all cancer sites remained significant, as did the increase in rate of HCC and NHL.
“In the absence of alcohol abuse, tobacco use, and diabetes mellitus, there was an increase in the rate of many cancer types among those with HCV,” Dr. Nyberg said. However, when those variables were present, HCV had a more moderate effect on the cancer rates than the variables themselves, but rates were still increased.
“I interpret these data that the increased overall cancer rate is multifactorial. It may be related to hepatitis C, but it is also related to alcohol abuse, tobacco use, and diabetes mellitus,” Dr. Nyberg said at a press conference. “In the short term, my take-home message is that we can take HCV out of the equation.”
He qualified this further in an interview saying, “It is important not to just address the hepatitis C but also to address the other risk factors like stopping smoking, cutting down on drinking, reducing weight, and trying to prevent diabetes.”
This is a descriptive study, Dr. Nyberg added, and more research will be needed to further evaluate the findings.
The study was supported by a grant from Gilead Sciences paid to Kaiser Permanente Southern California. Dr. Anders Nyberg and Dr. Lisa Nyberg are employees of Kaiser Permanente Southern California but had no personal financial conflicts of interest.
VIENNA– In addition to dramatically increasing the risk of liver cancer more than 68-fold, chronic hepatitis C virus (HCV) infection more than doubled or tripled the risk of a host of other solid tumors and hematologic malignancies in a large retrospective, cross-sectional study.
Data from the Kaiser Permanente Southern California HMO accounting for more than 145,000 patient-years of follow-up for HCV-infected individuals and 14,000,000 patient-years of follow-up for non–HCV-infected individuals showed the crude rate ratio for the development of all cancers including hepatocellular carcinoma (HCC) was 2.33 (P < .0001), and excluding HCC, was 1.84.
The crude rate ratios for individual cancers in HCV-infected, compared with non–HCV-infected individuals were 68.67 for hepatocellular carcinoma (HCC); 3.59 for non-Hodgkin’s lymphoma (NHL); 3.41 for multiple myeloma; 3.05 for renal cancer; 3.03 for stomach cancer; 2.79 for pancreatic cancer; 2.56 for head and neck cancer; 2.51 for esophageal cancer; 2.44 for lung cancer; 2.05 for prostate cancer; and 1.88 for colorectal cancer.
“We need to interpret these results cautiously,” Dr. Anders Nyberg, a hepatologist at Kaiser Permanente Southern California in San Diego, acknowledged at the International Liver Congress sponsored by the European Association for the Study of the Liver.
“The strength of the study is that it is a large database in a ‘real-world’ population,” but one limitation is that it cannot establish causality and how chronic HCV infection might be linked to the increased risk of these cancers.
The link between chronic HCV infection and liver cancer is well established, and Swedish researchers have also previously reported a link with NHL and multiple myeloma (Hepatology 2005;13:652-9; doi:10.1002/hep.20608). Dr. Nyberg noted, however, that there are sporadic data on HCV and other cancer types.
The objective of the present study was therefore to look further at the possible association between HCV infection and cancer in a large population by linking the Kaiser Permanente Southern California data to the National Cancer Institute’s Surveillance, Epidemiology, and End Results (SEER) database. Patients were included if they had HCV diagnosed between 2008 and 2012 and were aged 18 years or older but excluded if they had HIV coinfection or a history of solid organ or bone marrow transplantation.
The study population consisted of 1,831 patients with a mean age of 62 years who had chronic HCV and a cancer diagnosis, 33,881 patients aged a mean of 59 years who had HCV but no cancer diagnosis, and 5,297,191 individuals aged 72 years without HCV. Dr. Nyberg noted that study subjects were predominantly male (around 50%-60%) and from white or Hispanic backgrounds.
Baseline comorbidities were more common in patients with HCV and cancer, with a Charlson Comorbidity Index of 2.1, than in those with HCV but no cancer (Charlson index of 1.5) or those in the non–HCV-infected cohort (Charlson index 0.5). There was a higher percentage of patients who smoked tobacco or with alcohol abuse in the HCV vs. non–HCV-infected cohort groups, and HCV patients were more likely to have diabetes mellitus and cirrhosis, but a lower body mass index.
When HCV and non–HCV-infected cohorts were stratified according to tobacco use, alcohol abuse, diabetes mellitus, and body weight, the increase in the cancer rate ratio for all cancer sites remained significant, as did the increase in rate of HCC and NHL.
“In the absence of alcohol abuse, tobacco use, and diabetes mellitus, there was an increase in the rate of many cancer types among those with HCV,” Dr. Nyberg said. However, when those variables were present, HCV had a more moderate effect on the cancer rates than the variables themselves, but rates were still increased.
“I interpret these data that the increased overall cancer rate is multifactorial. It may be related to hepatitis C, but it is also related to alcohol abuse, tobacco use, and diabetes mellitus,” Dr. Nyberg said at a press conference. “In the short term, my take-home message is that we can take HCV out of the equation.”
He qualified this further in an interview saying, “It is important not to just address the hepatitis C but also to address the other risk factors like stopping smoking, cutting down on drinking, reducing weight, and trying to prevent diabetes.”
This is a descriptive study, Dr. Nyberg added, and more research will be needed to further evaluate the findings.
The study was supported by a grant from Gilead Sciences paid to Kaiser Permanente Southern California. Dr. Anders Nyberg and Dr. Lisa Nyberg are employees of Kaiser Permanente Southern California but had no personal financial conflicts of interest.
AT THE INTERNATIONAL LIVER CONGRESS 2015
Key clinical point: Chronic hepatitis C virus (HCV) infection raises the risk of all types of cancer, not just liver cancer.
Major finding: The rate ratio for the development of all cancers, excluding liver cancer, was 1.84 (P < .0001) and including liver cancer was 2.33 comparing HCV- vs. non–HCV-infected individuals.
Data source: Retrospective, cross-sectional study of data collected from 2008 to 2012 involving more than 145,000 patient-years of follow-up in the chronic HCV cohort and almost 14,000,000 patient-years of follow-up in the non-HCV cohort.
Disclosures: The study was funded by a grant from Gilead Sciences paid to Kaiser Permanente Southern California. Dr. Anders Nyberg and Dr. Lisa Nyberg are employees of Kaiser Permanente Southern California but had no personal financial conflicts of interest.