International Liver Congress 2015

VIENNA – Delaying hepatitis C virus (HVC) treatment can have a detrimental effect on the outcomes of some patients, according to the results of a large 10-year retrospective analysis involving more than 187,000 U.S. veterans.

Indeed, waiting until a patient with HCV infection develops advanced cirrhosis, as measured by the Fibrosis-4 (FIB4) index, can reduce the chances that treatments will be effective and significantly increases morbidity and mortality. Health economist Jeffrey McCombs, Ph.D., of the University of Southern California, Los Angeles, presented data from a 10-year retrospective analysis of the Department of Veteran’s Affairs Veterans Health Administration HCV clinical registry involving more than 187,000 U.S. veterans with detectable HCV levels.

Jezperklauzen/ThinkStock.com

The caveat is that older treatments rather than newer all-oral direct-acting agents were used in the study population at the time of data analyses.

The analysis built on three previous analyses of data from the VA System, the first of which found that viral load suppression reduced the risk of liver events by around 27% and death by 45% (JAMA Intern. Med. 2014;174: 204-12). This analysis also found that relative to patients with genotype 1 (GT1), patients with GT2 were at lower risk and patients with GT3 were at higher risk of liver events and death.

The second analysis looked at treatment timing and found that treatment effectiveness was significantly reduced if treatment was started after common laboratory tests to detect liver changes became abnormal.

The third analysis looked at using the FIB4 index to monitor the risk of long-term morbidity and mortality and found that a FIB4 in excess of 3.4 was associated with a significantly increased risk for liver events and death, whereas a FIB4 of 1.45 was associated with moderate risk.

“This brought us to the last research question, looking at the relationship between treatment efficacy and exceeding certain FIB4 levels,” Dr. McCombs said at the meeting sponsored by the European Association for the Study of the Liver. The analysis compared treating early versus treating late, based on FIB4 levels – FIB4 of 1.0, FIB4 of 1.45, and FIB4 of 3.25.

Initiating treatment early before patients’ FIB4 exceeded 1.0 was associated with a 41% reduction in morbidity and a 36% reduction in mortality. Waiting until the FIB4 exceeded 1.0 resulted in a 30% reduction in liver events and 40% in mortality.

Treating patients early before exceeding a FIB4 of 1.45 was associated with morbidity and mortality reductions of 39% and 40% and waiting until the FIB4 exceeded this threshold was associated with reductions of 27% and 39%, respectively.

Using the FIB4 threshold of 3.25 showed even smaller reductions in morbidity and mortality. When treating early, the reductions were 36% and 45%; when treating late, the reductions were 11% and 25%.

“This is the kind of information you need when you talk with your payers,” Dr. McCombs said. “If you restrict access to treatment, you are not going to be as effective.”

Treating early or late appeared to have a similar effect on viral load and the number needed to treat (NNT) increased using the FIB4 3.5 threshold. Indeed, if treatment is initiated before the FIB4 rises above 3.25, the NNT is 180 patients to prevent one death, Dr. McCombs said, but if treatment is delayed, then the NNT jumps to 325 patients.

In patients with low FIB4 a ‘watch and wait strategy’ could potentially be feasible, he acknowledged in an interview. “The bottom line is that we can’t afford to treat everybody now,” he said.

“The FIB4 is a parameter we can probably watch, but it is unknown exactly how long we can wait,” Dr. McCombs said.

The data were derived from a study that was supported by a grant from Bristol-Myers Squibb. Dr. McCombs had no disclosures.

VIENNA – Delaying hepatitis C virus (HVC) treatment can have a detrimental effect on the outcomes of some patients, according to the results of a large 10-year retrospective analysis involving more than 187,000 U.S. veterans.

Indeed, waiting until a patient with HCV infection develops advanced cirrhosis, as measured by the Fibrosis-4 (FIB4) index, can reduce the chances that treatments will be effective and significantly increases morbidity and mortality. Health economist Jeffrey McCombs, Ph.D., of the University of Southern California, Los Angeles, presented data from a 10-year retrospective analysis of the Department of Veteran’s Affairs Veterans Health Administration HCV clinical registry involving more than 187,000 U.S. veterans with detectable HCV levels.

Jezperklauzen/ThinkStock.com

The caveat is that older treatments rather than newer all-oral direct-acting agents were used in the study population at the time of data analyses.

The analysis built on three previous analyses of data from the VA System, the first of which found that viral load suppression reduced the risk of liver events by around 27% and death by 45% (JAMA Intern. Med. 2014;174: 204-12). This analysis also found that relative to patients with genotype 1 (GT1), patients with GT2 were at lower risk and patients with GT3 were at higher risk of liver events and death.

The second analysis looked at treatment timing and found that treatment effectiveness was significantly reduced if treatment was started after common laboratory tests to detect liver changes became abnormal.

The third analysis looked at using the FIB4 index to monitor the risk of long-term morbidity and mortality and found that a FIB4 in excess of 3.4 was associated with a significantly increased risk for liver events and death, whereas a FIB4 of 1.45 was associated with moderate risk.

“This brought us to the last research question, looking at the relationship between treatment efficacy and exceeding certain FIB4 levels,” Dr. McCombs said at the meeting sponsored by the European Association for the Study of the Liver. The analysis compared treating early versus treating late, based on FIB4 levels – FIB4 of 1.0, FIB4 of 1.45, and FIB4 of 3.25.

Initiating treatment early before patients’ FIB4 exceeded 1.0 was associated with a 41% reduction in morbidity and a 36% reduction in mortality. Waiting until the FIB4 exceeded 1.0 resulted in a 30% reduction in liver events and 40% in mortality.

Treating patients early before exceeding a FIB4 of 1.45 was associated with morbidity and mortality reductions of 39% and 40% and waiting until the FIB4 exceeded this threshold was associated with reductions of 27% and 39%, respectively.

Using the FIB4 threshold of 3.25 showed even smaller reductions in morbidity and mortality. When treating early, the reductions were 36% and 45%; when treating late, the reductions were 11% and 25%.

“This is the kind of information you need when you talk with your payers,” Dr. McCombs said. “If you restrict access to treatment, you are not going to be as effective.”

Treating early or late appeared to have a similar effect on viral load and the number needed to treat (NNT) increased using the FIB4 3.5 threshold. Indeed, if treatment is initiated before the FIB4 rises above 3.25, the NNT is 180 patients to prevent one death, Dr. McCombs said, but if treatment is delayed, then the NNT jumps to 325 patients.

In patients with low FIB4 a ‘watch and wait strategy’ could potentially be feasible, he acknowledged in an interview. “The bottom line is that we can’t afford to treat everybody now,” he said.

“The FIB4 is a parameter we can probably watch, but it is unknown exactly how long we can wait,” Dr. McCombs said.

The data were derived from a study that was supported by a grant from Bristol-Myers Squibb. Dr. McCombs had no disclosures.

VIENNA – Delaying hepatitis C virus (HVC) treatment can have a detrimental effect on the outcomes of some patients, according to the results of a large 10-year retrospective analysis involving more than 187,000 U.S. veterans.

Indeed, waiting until a patient with HCV infection develops advanced cirrhosis, as measured by the Fibrosis-4 (FIB4) index, can reduce the chances that treatments will be effective and significantly increases morbidity and mortality. Health economist Jeffrey McCombs, Ph.D., of the University of Southern California, Los Angeles, presented data from a 10-year retrospective analysis of the Department of Veteran’s Affairs Veterans Health Administration HCV clinical registry involving more than 187,000 U.S. veterans with detectable HCV levels.

Jezperklauzen/ThinkStock.com

The caveat is that older treatments rather than newer all-oral direct-acting agents were used in the study population at the time of data analyses.

The analysis built on three previous analyses of data from the VA System, the first of which found that viral load suppression reduced the risk of liver events by around 27% and death by 45% (JAMA Intern. Med. 2014;174: 204-12). This analysis also found that relative to patients with genotype 1 (GT1), patients with GT2 were at lower risk and patients with GT3 were at higher risk of liver events and death.

The second analysis looked at treatment timing and found that treatment effectiveness was significantly reduced if treatment was started after common laboratory tests to detect liver changes became abnormal.

The third analysis looked at using the FIB4 index to monitor the risk of long-term morbidity and mortality and found that a FIB4 in excess of 3.4 was associated with a significantly increased risk for liver events and death, whereas a FIB4 of 1.45 was associated with moderate risk.

“This brought us to the last research question, looking at the relationship between treatment efficacy and exceeding certain FIB4 levels,” Dr. McCombs said at the meeting sponsored by the European Association for the Study of the Liver. The analysis compared treating early versus treating late, based on FIB4 levels – FIB4 of 1.0, FIB4 of 1.45, and FIB4 of 3.25.

Initiating treatment early before patients’ FIB4 exceeded 1.0 was associated with a 41% reduction in morbidity and a 36% reduction in mortality. Waiting until the FIB4 exceeded 1.0 resulted in a 30% reduction in liver events and 40% in mortality.

Treating patients early before exceeding a FIB4 of 1.45 was associated with morbidity and mortality reductions of 39% and 40% and waiting until the FIB4 exceeded this threshold was associated with reductions of 27% and 39%, respectively.

Using the FIB4 threshold of 3.25 showed even smaller reductions in morbidity and mortality. When treating early, the reductions were 36% and 45%; when treating late, the reductions were 11% and 25%.

“This is the kind of information you need when you talk with your payers,” Dr. McCombs said. “If you restrict access to treatment, you are not going to be as effective.”

Treating early or late appeared to have a similar effect on viral load and the number needed to treat (NNT) increased using the FIB4 3.5 threshold. Indeed, if treatment is initiated before the FIB4 rises above 3.25, the NNT is 180 patients to prevent one death, Dr. McCombs said, but if treatment is delayed, then the NNT jumps to 325 patients.

In patients with low FIB4 a ‘watch and wait strategy’ could potentially be feasible, he acknowledged in an interview. “The bottom line is that we can’t afford to treat everybody now,” he said.

“The FIB4 is a parameter we can probably watch, but it is unknown exactly how long we can wait,” Dr. McCombs said.

The data were derived from a study that was supported by a grant from Bristol-Myers Squibb. Dr. McCombs had no disclosures.

VIENNA – Delaying hepatitis C virus (HVC) treatment can have a detrimental effect on the outcomes of some patients, according to the results of a large 10-year retrospective analysis involving more than 187,000 U.S. veterans.

Indeed, waiting until a patient with HCV infection develops advanced cirrhosis, as measured by the Fibrosis-4 (FIB4) index, can reduce the chances that treatments will be effective and significantly increases morbidity and mortality. Health economist Jeffrey McCombs, Ph.D., of the University of Southern California, Los Angeles, presented data from a 10-year retrospective analysis of the Department of Veteran’s Affairs Veterans Health Administration HCV clinical registry involving more than 187,000 U.S. veterans with detectable HCV levels.

Jezperklauzen/ThinkStock.com

The caveat is that older treatments rather than newer all-oral direct-acting agents were used in the study population at the time of data analyses.

The analysis built on three previous analyses of data from the VA System, the first of which found that viral load suppression reduced the risk of liver events by around 27% and death by 45% (JAMA Intern. Med. 2014;174: 204-12). This analysis also found that relative to patients with genotype 1 (GT1), patients with GT2 were at lower risk and patients with GT3 were at higher risk of liver events and death.

The second analysis looked at treatment timing and found that treatment effectiveness was significantly reduced if treatment was started after common laboratory tests to detect liver changes became abnormal.

The third analysis looked at using the FIB4 index to monitor the risk of long-term morbidity and mortality and found that a FIB4 in excess of 3.4 was associated with a significantly increased risk for liver events and death, whereas a FIB4 of 1.45 was associated with moderate risk.

“This brought us to the last research question, looking at the relationship between treatment efficacy and exceeding certain FIB4 levels,” Dr. McCombs said at the meeting sponsored by the European Association for the Study of the Liver. The analysis compared treating early versus treating late, based on FIB4 levels – FIB4 of 1.0, FIB4 of 1.45, and FIB4 of 3.25.

Initiating treatment early before patients’ FIB4 exceeded 1.0 was associated with a 41% reduction in morbidity and a 36% reduction in mortality. Waiting until the FIB4 exceeded 1.0 resulted in a 30% reduction in liver events and 40% in mortality.

Treating patients early before exceeding a FIB4 of 1.45 was associated with morbidity and mortality reductions of 39% and 40% and waiting until the FIB4 exceeded this threshold was associated with reductions of 27% and 39%, respectively.

Using the FIB4 threshold of 3.25 showed even smaller reductions in morbidity and mortality. When treating early, the reductions were 36% and 45%; when treating late, the reductions were 11% and 25%.

“This is the kind of information you need when you talk with your payers,” Dr. McCombs said. “If you restrict access to treatment, you are not going to be as effective.”

Treating early or late appeared to have a similar effect on viral load and the number needed to treat (NNT) increased using the FIB4 3.5 threshold. Indeed, if treatment is initiated before the FIB4 rises above 3.25, the NNT is 180 patients to prevent one death, Dr. McCombs said, but if treatment is delayed, then the NNT jumps to 325 patients.

In patients with low FIB4 a ‘watch and wait strategy’ could potentially be feasible, he acknowledged in an interview. “The bottom line is that we can’t afford to treat everybody now,” he said.

“The FIB4 is a parameter we can probably watch, but it is unknown exactly how long we can wait,” Dr. McCombs said.

The data were derived from a study that was supported by a grant from Bristol-Myers Squibb. Dr. McCombs had no disclosures.

VIENNA – Delaying hepatitis C virus (HVC) treatment can have a detrimental effect on the outcomes of some patients, according to the results of a large 10-year retrospective analysis involving more than 187,000 U.S. veterans.

Indeed, waiting until a patient with HCV infection develops advanced cirrhosis, as measured by the Fibrosis-4 (FIB4) index, can reduce the chances that treatments will be effective and significantly increases morbidity and mortality. Health economist Jeffrey McCombs, Ph.D., of the University of Southern California, Los Angeles, presented data from a 10-year retrospective analysis of the Department of Veteran’s Affairs Veterans Health Administration HCV clinical registry involving more than 187,000 U.S. veterans with detectable HCV levels.

Jezperklauzen/ThinkStock.com

The caveat is that older treatments rather than newer all-oral direct-acting agents were used in the study population at the time of data analyses.

The analysis built on three previous analyses of data from the VA System, the first of which found that viral load suppression reduced the risk of liver events by around 27% and death by 45% (JAMA Intern. Med. 2014;174: 204-12). This analysis also found that relative to patients with genotype 1 (GT1), patients with GT2 were at lower risk and patients with GT3 were at higher risk of liver events and death.

The second analysis looked at treatment timing and found that treatment effectiveness was significantly reduced if treatment was started after common laboratory tests to detect liver changes became abnormal.

The third analysis looked at using the FIB4 index to monitor the risk of long-term morbidity and mortality and found that a FIB4 in excess of 3.4 was associated with a significantly increased risk for liver events and death, whereas a FIB4 of 1.45 was associated with moderate risk.

“This brought us to the last research question, looking at the relationship between treatment efficacy and exceeding certain FIB4 levels,” Dr. McCombs said at the meeting sponsored by the European Association for the Study of the Liver. The analysis compared treating early versus treating late, based on FIB4 levels – FIB4 of 1.0, FIB4 of 1.45, and FIB4 of 3.25.

Initiating treatment early before patients’ FIB4 exceeded 1.0 was associated with a 41% reduction in morbidity and a 36% reduction in mortality. Waiting until the FIB4 exceeded 1.0 resulted in a 30% reduction in liver events and 40% in mortality.

Treating patients early before exceeding a FIB4 of 1.45 was associated with morbidity and mortality reductions of 39% and 40% and waiting until the FIB4 exceeded this threshold was associated with reductions of 27% and 39%, respectively.

Using the FIB4 threshold of 3.25 showed even smaller reductions in morbidity and mortality. When treating early, the reductions were 36% and 45%; when treating late, the reductions were 11% and 25%.

“This is the kind of information you need when you talk with your payers,” Dr. McCombs said. “If you restrict access to treatment, you are not going to be as effective.”

Treating early or late appeared to have a similar effect on viral load and the number needed to treat (NNT) increased using the FIB4 3.5 threshold. Indeed, if treatment is initiated before the FIB4 rises above 3.25, the NNT is 180 patients to prevent one death, Dr. McCombs said, but if treatment is delayed, then the NNT jumps to 325 patients.

In patients with low FIB4 a ‘watch and wait strategy’ could potentially be feasible, he acknowledged in an interview. “The bottom line is that we can’t afford to treat everybody now,” he said.

“The FIB4 is a parameter we can probably watch, but it is unknown exactly how long we can wait,” Dr. McCombs said.

The data were derived from a study that was supported by a grant from Bristol-Myers Squibb. Dr. McCombs had no disclosures.

VIENNA – Delaying hepatitis C virus (HVC) treatment can have a detrimental effect on the outcomes of some patients, according to the results of a large 10-year retrospective analysis involving more than 187,000 U.S. veterans.

Indeed, waiting until a patient with HCV infection develops advanced cirrhosis, as measured by the Fibrosis-4 (FIB4) index, can reduce the chances that treatments will be effective and significantly increases morbidity and mortality. Health economist Jeffrey McCombs, Ph.D., of the University of Southern California, Los Angeles, presented data from a 10-year retrospective analysis of the Department of Veteran’s Affairs Veterans Health Administration HCV clinical registry involving more than 187,000 U.S. veterans with detectable HCV levels.

Jezperklauzen/ThinkStock.com

The caveat is that older treatments rather than newer all-oral direct-acting agents were used in the study population at the time of data analyses.

The analysis built on three previous analyses of data from the VA System, the first of which found that viral load suppression reduced the risk of liver events by around 27% and death by 45% (JAMA Intern. Med. 2014;174: 204-12). This analysis also found that relative to patients with genotype 1 (GT1), patients with GT2 were at lower risk and patients with GT3 were at higher risk of liver events and death.

The second analysis looked at treatment timing and found that treatment effectiveness was significantly reduced if treatment was started after common laboratory tests to detect liver changes became abnormal.

The third analysis looked at using the FIB4 index to monitor the risk of long-term morbidity and mortality and found that a FIB4 in excess of 3.4 was associated with a significantly increased risk for liver events and death, whereas a FIB4 of 1.45 was associated with moderate risk.

“This brought us to the last research question, looking at the relationship between treatment efficacy and exceeding certain FIB4 levels,” Dr. McCombs said at the meeting sponsored by the European Association for the Study of the Liver. The analysis compared treating early versus treating late, based on FIB4 levels – FIB4 of 1.0, FIB4 of 1.45, and FIB4 of 3.25.

Initiating treatment early before patients’ FIB4 exceeded 1.0 was associated with a 41% reduction in morbidity and a 36% reduction in mortality. Waiting until the FIB4 exceeded 1.0 resulted in a 30% reduction in liver events and 40% in mortality.

Treating patients early before exceeding a FIB4 of 1.45 was associated with morbidity and mortality reductions of 39% and 40% and waiting until the FIB4 exceeded this threshold was associated with reductions of 27% and 39%, respectively.

Using the FIB4 threshold of 3.25 showed even smaller reductions in morbidity and mortality. When treating early, the reductions were 36% and 45%; when treating late, the reductions were 11% and 25%.

“This is the kind of information you need when you talk with your payers,” Dr. McCombs said. “If you restrict access to treatment, you are not going to be as effective.”

Treating early or late appeared to have a similar effect on viral load and the number needed to treat (NNT) increased using the FIB4 3.5 threshold. Indeed, if treatment is initiated before the FIB4 rises above 3.25, the NNT is 180 patients to prevent one death, Dr. McCombs said, but if treatment is delayed, then the NNT jumps to 325 patients.

In patients with low FIB4 a ‘watch and wait strategy’ could potentially be feasible, he acknowledged in an interview. “The bottom line is that we can’t afford to treat everybody now,” he said.

“The FIB4 is a parameter we can probably watch, but it is unknown exactly how long we can wait,” Dr. McCombs said.

The data were derived from a study that was supported by a grant from Bristol-Myers Squibb. Dr. McCombs had no disclosures.

VIENNA – More than 75% of patients with decompensated cirrhosis due to chronic hepatitis C virus (HCV) infection achieved a sustained virologic response at 12 weeks (SVR12) with all-oral HCV therapy in a routine clinical practice setting.

SVR12 was achieved in 74%-81% of patients treated with various regimens containing the direct antiviral agents sofosbuvir (Sovaldi) and simeprevir (Olysio), with or without ribavirin, based on interim data from the ongoing HCV-Target study. “All-oral DAA therapy has been readily used to treat HCV cirrhosis with MELD (Model for End-Stage Liver Disease) score greater than or equal to 10,” study investigator Dr. Rajender Reddy reported at the meeting sponsored by the European Association for the Study of the Liver.

Sara Freeman/Frontline Medical News

“There is limited experience with all-oral DAA [direct antiviral agent] therapy in patients who have advanced HCV liver disease,” said Dr. Reddy, who is director of hepatology and medical director of liver transplantation at the Hospital of the University of Pennsylvania in Philadelphia. “HCV therapy in decompensated cirrhosis in the era of interferon-based therapy has been associated with suboptimal response and poor tolerability.”

Alternatively, these early findings from HCV-Target suggest that all-oral DAA therapy is not only effective in patients with advanced liver disease, but also that such treatment is well tolerated, he said.

HCV-Target is a longitudinal, observational study involving an international consortium of academic and community medical centers in the U.S., Canada, and Europe. HCV treatment is administered according to the local standard of care and the regimen selected by the patient’s health care provider.

As of October 2014, 2,204 patients were enrolled and 253 had a baseline MELD score of 10 or higher; 216 had completed treatment and had 12 weeks’ follow-up data available for analysis. Of these, 76 received a combination of sofosbuvir and ribavirin, 108 had been treated with sofosbuvir and simeprevir, and 32 had received all three drugs.

The mean age of patients was 59 years, but ranged from 38 to 80 years. The majority (59%) of patients had failed prior treatment, and around 73% had a history of prior hepatic decompensation, suggesting advancement of their liver disease.

“Sustained virologic response varied by genotype and regimen,” Dr. Reddy observed. SVR12 rates ranged from 52% to 74% in patients with genotype 1 (GT1). Most (63%) of these patients had received a combination of sofosbuvir and simeprevir, which yielded the highest SVR12 rates (72% in treatment-experienced and 78% in previously untreated GT1 patients).

SVR12 was 81% in patients with GT2, the majority (97%) had been treated with sofosbuvir plus ribavirin, with just 3% receiving all three drugs in combination.

SVR12 was the lowest, at 39%, in patients with GT3, all of whom had received sofosbuvir plus ribavirin.

Relapse rates were highest in GT3 patients, at 46% versus 26% in GT1 and 7% in GT2 patients.

SVR12 rates were also evaluated in relation to the MELD score. Of interest, said Dr. Reddy, was that patients with a MELD score of 10-15 (n=187) and those with a MELD score of 16-21 (n=21) had comparable SVR12 rates that ranged from 55% to 73%, with the lowest response rates being seen in patients treated with sofosbuvir plus ribavirin. Although there were only eight patients with a MELD score greater than 21, SVR12 was 100%.

Multivariate analysis to look at predictors of response was performed exclusively in GT1 patients and showed that being GT1a and having elevated bilirubin levels were negative predictors of response, with respective odds ratios of 0.39 (P = .069) and 0.46 (P = .002). Higher albumin levels, however, were associated with better outcomes (OR = 2.52, P = .026).

In terms of safety, 86% of 234 patients experienced any adverse event. Dr. Reddy highlighted anemia, which was more common (seen in about 30% of patients) with the ribavirin regimens, and photosensitivity, which was only seen in patients treated with simeprevir.

There were 44 serious adverse events; 16 were due to hepatic decompensation, 10 resulted from infections, 3 were deaths (one of which was due to liver failure), and 12 were liver transplants.

“Long-term follow-up is needed to assess the impact of SVR on the reversibility of liver disease,” he said.

The study is sponsored by the University of Florida and the University of Carolina at Chapel Hill and funded in part by AbbVie, Gilead, Janssen, Kadmon, Merck, Bristol-Myers Squibb, and GlaxoSmithKline. Dr. Reddy has acted as an ad-hoc advisory board member for and received research support from Gilead, Bristol-Myers Squibb, Merck, AbbVie, and Janssen.

VIENNA – More than 75% of patients with decompensated cirrhosis due to chronic hepatitis C virus (HCV) infection achieved a sustained virologic response at 12 weeks (SVR12) with all-oral HCV therapy in a routine clinical practice setting.

SVR12 was achieved in 74%-81% of patients treated with various regimens containing the direct antiviral agents sofosbuvir (Sovaldi) and simeprevir (Olysio), with or without ribavirin, based on interim data from the ongoing HCV-Target study. “All-oral DAA therapy has been readily used to treat HCV cirrhosis with MELD (Model for End-Stage Liver Disease) score greater than or equal to 10,” study investigator Dr. Rajender Reddy reported at the meeting sponsored by the European Association for the Study of the Liver.

Sara Freeman/Frontline Medical News

“There is limited experience with all-oral DAA [direct antiviral agent] therapy in patients who have advanced HCV liver disease,” said Dr. Reddy, who is director of hepatology and medical director of liver transplantation at the Hospital of the University of Pennsylvania in Philadelphia. “HCV therapy in decompensated cirrhosis in the era of interferon-based therapy has been associated with suboptimal response and poor tolerability.”

Alternatively, these early findings from HCV-Target suggest that all-oral DAA therapy is not only effective in patients with advanced liver disease, but also that such treatment is well tolerated, he said.

HCV-Target is a longitudinal, observational study involving an international consortium of academic and community medical centers in the U.S., Canada, and Europe. HCV treatment is administered according to the local standard of care and the regimen selected by the patient’s health care provider.

As of October 2014, 2,204 patients were enrolled and 253 had a baseline MELD score of 10 or higher; 216 had completed treatment and had 12 weeks’ follow-up data available for analysis. Of these, 76 received a combination of sofosbuvir and ribavirin, 108 had been treated with sofosbuvir and simeprevir, and 32 had received all three drugs.

The mean age of patients was 59 years, but ranged from 38 to 80 years. The majority (59%) of patients had failed prior treatment, and around 73% had a history of prior hepatic decompensation, suggesting advancement of their liver disease.

“Sustained virologic response varied by genotype and regimen,” Dr. Reddy observed. SVR12 rates ranged from 52% to 74% in patients with genotype 1 (GT1). Most (63%) of these patients had received a combination of sofosbuvir and simeprevir, which yielded the highest SVR12 rates (72% in treatment-experienced and 78% in previously untreated GT1 patients).

SVR12 was 81% in patients with GT2, the majority (97%) had been treated with sofosbuvir plus ribavirin, with just 3% receiving all three drugs in combination.

SVR12 was the lowest, at 39%, in patients with GT3, all of whom had received sofosbuvir plus ribavirin.

Relapse rates were highest in GT3 patients, at 46% versus 26% in GT1 and 7% in GT2 patients.

SVR12 rates were also evaluated in relation to the MELD score. Of interest, said Dr. Reddy, was that patients with a MELD score of 10-15 (n=187) and those with a MELD score of 16-21 (n=21) had comparable SVR12 rates that ranged from 55% to 73%, with the lowest response rates being seen in patients treated with sofosbuvir plus ribavirin. Although there were only eight patients with a MELD score greater than 21, SVR12 was 100%.

Multivariate analysis to look at predictors of response was performed exclusively in GT1 patients and showed that being GT1a and having elevated bilirubin levels were negative predictors of response, with respective odds ratios of 0.39 (P = .069) and 0.46 (P = .002). Higher albumin levels, however, were associated with better outcomes (OR = 2.52, P = .026).

In terms of safety, 86% of 234 patients experienced any adverse event. Dr. Reddy highlighted anemia, which was more common (seen in about 30% of patients) with the ribavirin regimens, and photosensitivity, which was only seen in patients treated with simeprevir.

There were 44 serious adverse events; 16 were due to hepatic decompensation, 10 resulted from infections, 3 were deaths (one of which was due to liver failure), and 12 were liver transplants.

“Long-term follow-up is needed to assess the impact of SVR on the reversibility of liver disease,” he said.

The study is sponsored by the University of Florida and the University of Carolina at Chapel Hill and funded in part by AbbVie, Gilead, Janssen, Kadmon, Merck, Bristol-Myers Squibb, and GlaxoSmithKline. Dr. Reddy has acted as an ad-hoc advisory board member for and received research support from Gilead, Bristol-Myers Squibb, Merck, AbbVie, and Janssen.

VIENNA – More than 75% of patients with decompensated cirrhosis due to chronic hepatitis C virus (HCV) infection achieved a sustained virologic response at 12 weeks (SVR12) with all-oral HCV therapy in a routine clinical practice setting.

SVR12 was achieved in 74%-81% of patients treated with various regimens containing the direct antiviral agents sofosbuvir (Sovaldi) and simeprevir (Olysio), with or without ribavirin, based on interim data from the ongoing HCV-Target study. “All-oral DAA therapy has been readily used to treat HCV cirrhosis with MELD (Model for End-Stage Liver Disease) score greater than or equal to 10,” study investigator Dr. Rajender Reddy reported at the meeting sponsored by the European Association for the Study of the Liver.

Sara Freeman/Frontline Medical News

“There is limited experience with all-oral DAA [direct antiviral agent] therapy in patients who have advanced HCV liver disease,” said Dr. Reddy, who is director of hepatology and medical director of liver transplantation at the Hospital of the University of Pennsylvania in Philadelphia. “HCV therapy in decompensated cirrhosis in the era of interferon-based therapy has been associated with suboptimal response and poor tolerability.”

Alternatively, these early findings from HCV-Target suggest that all-oral DAA therapy is not only effective in patients with advanced liver disease, but also that such treatment is well tolerated, he said.

HCV-Target is a longitudinal, observational study involving an international consortium of academic and community medical centers in the U.S., Canada, and Europe. HCV treatment is administered according to the local standard of care and the regimen selected by the patient’s health care provider.

As of October 2014, 2,204 patients were enrolled and 253 had a baseline MELD score of 10 or higher; 216 had completed treatment and had 12 weeks’ follow-up data available for analysis. Of these, 76 received a combination of sofosbuvir and ribavirin, 108 had been treated with sofosbuvir and simeprevir, and 32 had received all three drugs.

The mean age of patients was 59 years, but ranged from 38 to 80 years. The majority (59%) of patients had failed prior treatment, and around 73% had a history of prior hepatic decompensation, suggesting advancement of their liver disease.

“Sustained virologic response varied by genotype and regimen,” Dr. Reddy observed. SVR12 rates ranged from 52% to 74% in patients with genotype 1 (GT1). Most (63%) of these patients had received a combination of sofosbuvir and simeprevir, which yielded the highest SVR12 rates (72% in treatment-experienced and 78% in previously untreated GT1 patients).

SVR12 was 81% in patients with GT2, the majority (97%) had been treated with sofosbuvir plus ribavirin, with just 3% receiving all three drugs in combination.

SVR12 was the lowest, at 39%, in patients with GT3, all of whom had received sofosbuvir plus ribavirin.

Relapse rates were highest in GT3 patients, at 46% versus 26% in GT1 and 7% in GT2 patients.

SVR12 rates were also evaluated in relation to the MELD score. Of interest, said Dr. Reddy, was that patients with a MELD score of 10-15 (n=187) and those with a MELD score of 16-21 (n=21) had comparable SVR12 rates that ranged from 55% to 73%, with the lowest response rates being seen in patients treated with sofosbuvir plus ribavirin. Although there were only eight patients with a MELD score greater than 21, SVR12 was 100%.

Multivariate analysis to look at predictors of response was performed exclusively in GT1 patients and showed that being GT1a and having elevated bilirubin levels were negative predictors of response, with respective odds ratios of 0.39 (P = .069) and 0.46 (P = .002). Higher albumin levels, however, were associated with better outcomes (OR = 2.52, P = .026).

In terms of safety, 86% of 234 patients experienced any adverse event. Dr. Reddy highlighted anemia, which was more common (seen in about 30% of patients) with the ribavirin regimens, and photosensitivity, which was only seen in patients treated with simeprevir.

There were 44 serious adverse events; 16 were due to hepatic decompensation, 10 resulted from infections, 3 were deaths (one of which was due to liver failure), and 12 were liver transplants.

“Long-term follow-up is needed to assess the impact of SVR on the reversibility of liver disease,” he said.

The study is sponsored by the University of Florida and the University of Carolina at Chapel Hill and funded in part by AbbVie, Gilead, Janssen, Kadmon, Merck, Bristol-Myers Squibb, and GlaxoSmithKline. Dr. Reddy has acted as an ad-hoc advisory board member for and received research support from Gilead, Bristol-Myers Squibb, Merck, AbbVie, and Janssen.

VIENNA – The early results of a prospective, multicenter study show a high rate of hepatic focal lesions, further supporting liver cancer screening in patients with alcoholic liver disease, according to researchers.

The first results from the National Cohort of Uncomplicated Alcoholic Cirrhosis (CIRRAL) show that the cumulative incidence of hepatic focal lesions was 10.7% at 1 year and 18.1% at 2 years. The incidence of hepatocellular carcinoma (HCC) was about 1.6% at 1 year and 4.5% at 2 years.

Courtesy of ILC 2015

“Primary liver cancer has a high incidence in Europe and in France,” said Dr. Nathalie Ganne of Assistance Publique des Hôpitaux de Paris–Hôpital Jean-Verdier, Bondy, France. “However, the natural history of HCC in alcoholic cirrhosis is not well known,” she said at the meeting sponsored by the European Association for the Study of the Liver.

EASL clinical guidelines recommend screening for hepatocellular carcinoma (HCC) in cirrhotic patients and the association’s general recommendations for screening for complications should be applied to those with alcoholic cirrhosis. However, Dr. Ganne pointed out, there were conflicting data on the value of HCC surveillance in patients with alcoholic liver disease.

On the one hand, data from a large retrospective Danish Registry study involving more than 8,400 patients suggested the risk of HCC was low, at around 0.25%-0.5% per year, so screening was unlikely to save many lives or to be cost-effective (Ann. Intern. Med. 2012;156:841-7). On the other hand, prospective data from a Spanish cohort of 450 patients suggested that there was a relatively high HCC risk, at 2.5% per year, and screening could have a greater impact on mortality (Clin. Gastroenterol. Hepatol. 2013;11:95-101).

To address the controversy and better understand alcoholic liver cirrhosis, the CIRRAL cohort was established with the aim to prospectively describe the natural history of the disease, including documenting the incidence of HCC and other complications, and identifying risk factors or predictors for HCC.

The study population comprised 599 patients with histologically proven, alcohol-related cirrhosis recruited over a 4-year period at 24 centers in France and 2 centers in Belgium. For inclusion, patients needed to have a history of chronic alcohol abuse and compensated liver disease (Child-Pugh A), to be hepatitis B and hepatitis C negative, and to have no prior history of liver cancer. Patients were screened for HCC, liver biopsy samples were obtained, and ethanol breath tests were undertaken at enrollment and annually thereafter.

Most patients were male; the median age was 58.6 years. Almost 70% of patients were abstinent from alcohol, with a median time of 28.4 months since alcohol was consumed. About 17% still had mild alcohol consumption, defined as having one to six alcoholic drinks per week.

Most patients had a history of smoking, with 35% being former and 36% being current smokers. Most patients (78%) were regular coffee drinkers, at an average of two cups per day; almost 40% drank three or more cups per day.

At baseline, 24 (4%) of 548 evaluable patients had a liver nodule, of which 13 were benign hemangiomas or biliary cysts and 11 were undetermined or regenerative nodules. After a median follow-up of 17 months, 13 of these patients still had a liver nodule present, of which two were confirmed as HCC. In the group of 524 patients without a liver nodule at baseline, 60 patients had a liver nodule at follow-up, of which 16 were confirmed as HCC.

“As expected, patients with baseline nodules were more at risk of focal lesions or proven HCC at follow-up,” Dr. Ganne said. The cumulative incidences of hepatic focal lesions and HCC at 2 years’ follow-up were 13.4% and 3.7% in those without and 76.8% and 13.3% in those with liver nodules at baseline.

Because of the short duration of current follow-up, no predictive factors were found, but there was a nonsignificant trend that linked HCC to a long duration of cirrhosis and the persistence of alcohol consumption.

Looking at the characteristics and treatment of the 18 cases of HCC, the researchers noted that 17 met noninvasive criteria. Eight were uninodular, nine were multinodular, and one was infiltrative. Fifteen (55%) met Milan criteria for liver transplantation. Seven cases (38%) received curative treatment involving percutaneous ablation.

Dr. Ganne reported that the overall and event-free survival rates at 2 years were 92.1% and 80.2%. The high rate of hepatic focal lesions found suggests that about 10% of patients per year will need a recall diagnosis procedure, she said.

Also, as the incidence of HCC was greater than 1.5% during the first year and probably an additional 3% per year thereafter, judging by the second year cumulative incidence rate, surveillance for HCC in patients with alcoholic liver cirrhosis “might be cost effective,” she concluded.

The CIRRAL cohort is an ongoing study that will form the backbone for additional studies into HCC in alcoholic liver disease, Dr. Ganne observed. Biological samples are being stored and a prospective database has been set up to include details of all assessments performed. Three nested studies are underway: one is looking at genetics using biobanked material (PANGEN), another is using the database to understand the role of the intestinal microbiota (MACHA), and another is looking at the potential role of nutrition (ALICIR).

The French National Cancer Institute, the French Association for Cancer Research, and the French National Agency for Research on AIDS and Viral Hepatitis funded the study. Dr. Ganne has no conflicts of interest.

VIENNA – The early results of a prospective, multicenter study show a high rate of hepatic focal lesions, further supporting liver cancer screening in patients with alcoholic liver disease, according to researchers.

The first results from the National Cohort of Uncomplicated Alcoholic Cirrhosis (CIRRAL) show that the cumulative incidence of hepatic focal lesions was 10.7% at 1 year and 18.1% at 2 years. The incidence of hepatocellular carcinoma (HCC) was about 1.6% at 1 year and 4.5% at 2 years.

Courtesy of ILC 2015

“Primary liver cancer has a high incidence in Europe and in France,” said Dr. Nathalie Ganne of Assistance Publique des Hôpitaux de Paris–Hôpital Jean-Verdier, Bondy, France. “However, the natural history of HCC in alcoholic cirrhosis is not well known,” she said at the meeting sponsored by the European Association for the Study of the Liver.

EASL clinical guidelines recommend screening for hepatocellular carcinoma (HCC) in cirrhotic patients and the association’s general recommendations for screening for complications should be applied to those with alcoholic cirrhosis. However, Dr. Ganne pointed out, there were conflicting data on the value of HCC surveillance in patients with alcoholic liver disease.

On the one hand, data from a large retrospective Danish Registry study involving more than 8,400 patients suggested the risk of HCC was low, at around 0.25%-0.5% per year, so screening was unlikely to save many lives or to be cost-effective (Ann. Intern. Med. 2012;156:841-7). On the other hand, prospective data from a Spanish cohort of 450 patients suggested that there was a relatively high HCC risk, at 2.5% per year, and screening could have a greater impact on mortality (Clin. Gastroenterol. Hepatol. 2013;11:95-101).

To address the controversy and better understand alcoholic liver cirrhosis, the CIRRAL cohort was established with the aim to prospectively describe the natural history of the disease, including documenting the incidence of HCC and other complications, and identifying risk factors or predictors for HCC.

The study population comprised 599 patients with histologically proven, alcohol-related cirrhosis recruited over a 4-year period at 24 centers in France and 2 centers in Belgium. For inclusion, patients needed to have a history of chronic alcohol abuse and compensated liver disease (Child-Pugh A), to be hepatitis B and hepatitis C negative, and to have no prior history of liver cancer. Patients were screened for HCC, liver biopsy samples were obtained, and ethanol breath tests were undertaken at enrollment and annually thereafter.

Most patients were male; the median age was 58.6 years. Almost 70% of patients were abstinent from alcohol, with a median time of 28.4 months since alcohol was consumed. About 17% still had mild alcohol consumption, defined as having one to six alcoholic drinks per week.

Most patients had a history of smoking, with 35% being former and 36% being current smokers. Most patients (78%) were regular coffee drinkers, at an average of two cups per day; almost 40% drank three or more cups per day.

At baseline, 24 (4%) of 548 evaluable patients had a liver nodule, of which 13 were benign hemangiomas or biliary cysts and 11 were undetermined or regenerative nodules. After a median follow-up of 17 months, 13 of these patients still had a liver nodule present, of which two were confirmed as HCC. In the group of 524 patients without a liver nodule at baseline, 60 patients had a liver nodule at follow-up, of which 16 were confirmed as HCC.

“As expected, patients with baseline nodules were more at risk of focal lesions or proven HCC at follow-up,” Dr. Ganne said. The cumulative incidences of hepatic focal lesions and HCC at 2 years’ follow-up were 13.4% and 3.7% in those without and 76.8% and 13.3% in those with liver nodules at baseline.

Because of the short duration of current follow-up, no predictive factors were found, but there was a nonsignificant trend that linked HCC to a long duration of cirrhosis and the persistence of alcohol consumption.

Looking at the characteristics and treatment of the 18 cases of HCC, the researchers noted that 17 met noninvasive criteria. Eight were uninodular, nine were multinodular, and one was infiltrative. Fifteen (55%) met Milan criteria for liver transplantation. Seven cases (38%) received curative treatment involving percutaneous ablation.

Dr. Ganne reported that the overall and event-free survival rates at 2 years were 92.1% and 80.2%. The high rate of hepatic focal lesions found suggests that about 10% of patients per year will need a recall diagnosis procedure, she said.

Also, as the incidence of HCC was greater than 1.5% during the first year and probably an additional 3% per year thereafter, judging by the second year cumulative incidence rate, surveillance for HCC in patients with alcoholic liver cirrhosis “might be cost effective,” she concluded.

The CIRRAL cohort is an ongoing study that will form the backbone for additional studies into HCC in alcoholic liver disease, Dr. Ganne observed. Biological samples are being stored and a prospective database has been set up to include details of all assessments performed. Three nested studies are underway: one is looking at genetics using biobanked material (PANGEN), another is using the database to understand the role of the intestinal microbiota (MACHA), and another is looking at the potential role of nutrition (ALICIR).

The French National Cancer Institute, the French Association for Cancer Research, and the French National Agency for Research on AIDS and Viral Hepatitis funded the study. Dr. Ganne has no conflicts of interest.

VIENNA – The early results of a prospective, multicenter study show a high rate of hepatic focal lesions, further supporting liver cancer screening in patients with alcoholic liver disease, according to researchers.

The first results from the National Cohort of Uncomplicated Alcoholic Cirrhosis (CIRRAL) show that the cumulative incidence of hepatic focal lesions was 10.7% at 1 year and 18.1% at 2 years. The incidence of hepatocellular carcinoma (HCC) was about 1.6% at 1 year and 4.5% at 2 years.

Courtesy of ILC 2015

“Primary liver cancer has a high incidence in Europe and in France,” said Dr. Nathalie Ganne of Assistance Publique des Hôpitaux de Paris–Hôpital Jean-Verdier, Bondy, France. “However, the natural history of HCC in alcoholic cirrhosis is not well known,” she said at the meeting sponsored by the European Association for the Study of the Liver.

EASL clinical guidelines recommend screening for hepatocellular carcinoma (HCC) in cirrhotic patients and the association’s general recommendations for screening for complications should be applied to those with alcoholic cirrhosis. However, Dr. Ganne pointed out, there were conflicting data on the value of HCC surveillance in patients with alcoholic liver disease.

On the one hand, data from a large retrospective Danish Registry study involving more than 8,400 patients suggested the risk of HCC was low, at around 0.25%-0.5% per year, so screening was unlikely to save many lives or to be cost-effective (Ann. Intern. Med. 2012;156:841-7). On the other hand, prospective data from a Spanish cohort of 450 patients suggested that there was a relatively high HCC risk, at 2.5% per year, and screening could have a greater impact on mortality (Clin. Gastroenterol. Hepatol. 2013;11:95-101).

To address the controversy and better understand alcoholic liver cirrhosis, the CIRRAL cohort was established with the aim to prospectively describe the natural history of the disease, including documenting the incidence of HCC and other complications, and identifying risk factors or predictors for HCC.

The study population comprised 599 patients with histologically proven, alcohol-related cirrhosis recruited over a 4-year period at 24 centers in France and 2 centers in Belgium. For inclusion, patients needed to have a history of chronic alcohol abuse and compensated liver disease (Child-Pugh A), to be hepatitis B and hepatitis C negative, and to have no prior history of liver cancer. Patients were screened for HCC, liver biopsy samples were obtained, and ethanol breath tests were undertaken at enrollment and annually thereafter.

Most patients were male; the median age was 58.6 years. Almost 70% of patients were abstinent from alcohol, with a median time of 28.4 months since alcohol was consumed. About 17% still had mild alcohol consumption, defined as having one to six alcoholic drinks per week.

Most patients had a history of smoking, with 35% being former and 36% being current smokers. Most patients (78%) were regular coffee drinkers, at an average of two cups per day; almost 40% drank three or more cups per day.

At baseline, 24 (4%) of 548 evaluable patients had a liver nodule, of which 13 were benign hemangiomas or biliary cysts and 11 were undetermined or regenerative nodules. After a median follow-up of 17 months, 13 of these patients still had a liver nodule present, of which two were confirmed as HCC. In the group of 524 patients without a liver nodule at baseline, 60 patients had a liver nodule at follow-up, of which 16 were confirmed as HCC.

“As expected, patients with baseline nodules were more at risk of focal lesions or proven HCC at follow-up,” Dr. Ganne said. The cumulative incidences of hepatic focal lesions and HCC at 2 years’ follow-up were 13.4% and 3.7% in those without and 76.8% and 13.3% in those with liver nodules at baseline.

Because of the short duration of current follow-up, no predictive factors were found, but there was a nonsignificant trend that linked HCC to a long duration of cirrhosis and the persistence of alcohol consumption.

Looking at the characteristics and treatment of the 18 cases of HCC, the researchers noted that 17 met noninvasive criteria. Eight were uninodular, nine were multinodular, and one was infiltrative. Fifteen (55%) met Milan criteria for liver transplantation. Seven cases (38%) received curative treatment involving percutaneous ablation.

Dr. Ganne reported that the overall and event-free survival rates at 2 years were 92.1% and 80.2%. The high rate of hepatic focal lesions found suggests that about 10% of patients per year will need a recall diagnosis procedure, she said.

Also, as the incidence of HCC was greater than 1.5% during the first year and probably an additional 3% per year thereafter, judging by the second year cumulative incidence rate, surveillance for HCC in patients with alcoholic liver cirrhosis “might be cost effective,” she concluded.

The CIRRAL cohort is an ongoing study that will form the backbone for additional studies into HCC in alcoholic liver disease, Dr. Ganne observed. Biological samples are being stored and a prospective database has been set up to include details of all assessments performed. Three nested studies are underway: one is looking at genetics using biobanked material (PANGEN), another is using the database to understand the role of the intestinal microbiota (MACHA), and another is looking at the potential role of nutrition (ALICIR).

The French National Cancer Institute, the French Association for Cancer Research, and the French National Agency for Research on AIDS and Viral Hepatitis funded the study. Dr. Ganne has no conflicts of interest.

VIENNA – Major cardiovascular (CV) events are significantly increased in hospital patients who are infected with the hepatitis C virus (HCV) versus those who are not, according to data presented at the meeting sponsored by the European Association for the Study of the Liver.

A retrospective analysis of more than 200,000 inpatients with and without HCV infection at discharge showed that those with HCV were 29% more likely to have had an acute MI, 98% more likely to have had a cerebral vascular accident (CVA), and 88% times more likely to have coronary artery disease (CAD). There was also an 8% increased risk for heart failure (HF).

“HCV infection is strongly linked to an increase in cardiovascular outcome, length of hospital stay, and cost of care,” Dr. Firew Wubiee and Dr. Charles Howell of Howard University, Washington, D.C., reported in an ePoster at the meeting.

For their retrospective analysis, data were obtained from the 2011 Nationwide Inpatient Sample, which is a large all-payer inpatient care database in the United States that contains information on more than 7 million hospital stays.

ICD-9 codes were used to identify all inpatient cases with and without HCV infection at discharge and those with major CV events, excluding those with liver cirrhosis, hepatocellular carcinoma, and cases of liver transplantation. Dr. Wubiee and Dr. Howell found that inpatients with HCV infection were significantly (P < .001) younger than were those without HCV (mean age 52.8 vs. 57.9 years). They were significantly more likely (P < .001) to be male (62.2% vs. 40%), have a smoking history (45.5% vs. 22.7%), be from ethnic or racial minorities (26.4% vs. 5.1%), and have a household income of less than $39,000 (41% vs. 29.1%).

While inpatients with HCV were also significantly (P < .001) more likely than were those without HCV to have diabetes mellitus (2.1% vs. 1.8%), they were significantly less likely (P < .001) to have other known CV risk factors such as obesity (8.7% vs. 11.8%), dyslipidemia (13.2% vs. 28.1%), and hypertension (49.7% vs. 51%).

Odds ratios for CV outcomes were adjusted for multiple confounding factors, including age, race, obesity, diabetes, dyslipidemia, smoking, alcohol use, hypertension, and hepatitis B infection. The adjusted odds ratios for major CV outcomes were 2.29 for AMI, 1.98 for CVA, 1.88 for CAD, and 1.08 for HF (all P < .001).

The duration of in-hospital treatment was longer for patients with HCV than for those without, with adjusted differences of 1.3 days for AMI (P < .001), 2.02 days for CVA (P < .003), 0.52 days for CAD (P < .001), and 0.37 days for HF (P < .001).

The adjusted cost of inpatient care was also higher for HCV-infected versus noninfected individuals with a mean cost difference of $10,126 for AMI, (P < .001), $10,105 for CVA (P < .002), $2,703 for CAD (P < .001), and $1,895 for HF (P < .001).

“We hypothesized that the inflammation and insulin resistance related to HCV increases the prevalence of cardiovascular diseases compared to patients without HCV,” Dr. Wubiee and Dr. Howell observed.

“The results are consistent with mounting evidence for [a] biological and epidemiological association between HCV infection and cardiovascular morbidity,” they said and suggested “HCV needs to be considered a cardiovascular risk factor.”

VIENNA – Major cardiovascular (CV) events are significantly increased in hospital patients who are infected with the hepatitis C virus (HCV) versus those who are not, according to data presented at the meeting sponsored by the European Association for the Study of the Liver.

A retrospective analysis of more than 200,000 inpatients with and without HCV infection at discharge showed that those with HCV were 29% more likely to have had an acute MI, 98% more likely to have had a cerebral vascular accident (CVA), and 88% times more likely to have coronary artery disease (CAD). There was also an 8% increased risk for heart failure (HF).

“HCV infection is strongly linked to an increase in cardiovascular outcome, length of hospital stay, and cost of care,” Dr. Firew Wubiee and Dr. Charles Howell of Howard University, Washington, D.C., reported in an ePoster at the meeting.

For their retrospective analysis, data were obtained from the 2011 Nationwide Inpatient Sample, which is a large all-payer inpatient care database in the United States that contains information on more than 7 million hospital stays.

ICD-9 codes were used to identify all inpatient cases with and without HCV infection at discharge and those with major CV events, excluding those with liver cirrhosis, hepatocellular carcinoma, and cases of liver transplantation. Dr. Wubiee and Dr. Howell found that inpatients with HCV infection were significantly (P < .001) younger than were those without HCV (mean age 52.8 vs. 57.9 years). They were significantly more likely (P < .001) to be male (62.2% vs. 40%), have a smoking history (45.5% vs. 22.7%), be from ethnic or racial minorities (26.4% vs. 5.1%), and have a household income of less than $39,000 (41% vs. 29.1%).

While inpatients with HCV were also significantly (P < .001) more likely than were those without HCV to have diabetes mellitus (2.1% vs. 1.8%), they were significantly less likely (P < .001) to have other known CV risk factors such as obesity (8.7% vs. 11.8%), dyslipidemia (13.2% vs. 28.1%), and hypertension (49.7% vs. 51%).

Odds ratios for CV outcomes were adjusted for multiple confounding factors, including age, race, obesity, diabetes, dyslipidemia, smoking, alcohol use, hypertension, and hepatitis B infection. The adjusted odds ratios for major CV outcomes were 2.29 for AMI, 1.98 for CVA, 1.88 for CAD, and 1.08 for HF (all P < .001).

The duration of in-hospital treatment was longer for patients with HCV than for those without, with adjusted differences of 1.3 days for AMI (P < .001), 2.02 days for CVA (P < .003), 0.52 days for CAD (P < .001), and 0.37 days for HF (P < .001).

The adjusted cost of inpatient care was also higher for HCV-infected versus noninfected individuals with a mean cost difference of $10,126 for AMI, (P < .001), $10,105 for CVA (P < .002), $2,703 for CAD (P < .001), and $1,895 for HF (P < .001).

“We hypothesized that the inflammation and insulin resistance related to HCV increases the prevalence of cardiovascular diseases compared to patients without HCV,” Dr. Wubiee and Dr. Howell observed.

“The results are consistent with mounting evidence for [a] biological and epidemiological association between HCV infection and cardiovascular morbidity,” they said and suggested “HCV needs to be considered a cardiovascular risk factor.”

VIENNA – Major cardiovascular (CV) events are significantly increased in hospital patients who are infected with the hepatitis C virus (HCV) versus those who are not, according to data presented at the meeting sponsored by the European Association for the Study of the Liver.

A retrospective analysis of more than 200,000 inpatients with and without HCV infection at discharge showed that those with HCV were 29% more likely to have had an acute MI, 98% more likely to have had a cerebral vascular accident (CVA), and 88% times more likely to have coronary artery disease (CAD). There was also an 8% increased risk for heart failure (HF).

“HCV infection is strongly linked to an increase in cardiovascular outcome, length of hospital stay, and cost of care,” Dr. Firew Wubiee and Dr. Charles Howell of Howard University, Washington, D.C., reported in an ePoster at the meeting.

For their retrospective analysis, data were obtained from the 2011 Nationwide Inpatient Sample, which is a large all-payer inpatient care database in the United States that contains information on more than 7 million hospital stays.

ICD-9 codes were used to identify all inpatient cases with and without HCV infection at discharge and those with major CV events, excluding those with liver cirrhosis, hepatocellular carcinoma, and cases of liver transplantation. Dr. Wubiee and Dr. Howell found that inpatients with HCV infection were significantly (P < .001) younger than were those without HCV (mean age 52.8 vs. 57.9 years). They were significantly more likely (P < .001) to be male (62.2% vs. 40%), have a smoking history (45.5% vs. 22.7%), be from ethnic or racial minorities (26.4% vs. 5.1%), and have a household income of less than $39,000 (41% vs. 29.1%).

While inpatients with HCV were also significantly (P < .001) more likely than were those without HCV to have diabetes mellitus (2.1% vs. 1.8%), they were significantly less likely (P < .001) to have other known CV risk factors such as obesity (8.7% vs. 11.8%), dyslipidemia (13.2% vs. 28.1%), and hypertension (49.7% vs. 51%).

Odds ratios for CV outcomes were adjusted for multiple confounding factors, including age, race, obesity, diabetes, dyslipidemia, smoking, alcohol use, hypertension, and hepatitis B infection. The adjusted odds ratios for major CV outcomes were 2.29 for AMI, 1.98 for CVA, 1.88 for CAD, and 1.08 for HF (all P < .001).

The duration of in-hospital treatment was longer for patients with HCV than for those without, with adjusted differences of 1.3 days for AMI (P < .001), 2.02 days for CVA (P < .003), 0.52 days for CAD (P < .001), and 0.37 days for HF (P < .001).

The adjusted cost of inpatient care was also higher for HCV-infected versus noninfected individuals with a mean cost difference of $10,126 for AMI, (P < .001), $10,105 for CVA (P < .002), $2,703 for CAD (P < .001), and $1,895 for HF (P < .001).

“We hypothesized that the inflammation and insulin resistance related to HCV increases the prevalence of cardiovascular diseases compared to patients without HCV,” Dr. Wubiee and Dr. Howell observed.

“The results are consistent with mounting evidence for [a] biological and epidemiological association between HCV infection and cardiovascular morbidity,” they said and suggested “HCV needs to be considered a cardiovascular risk factor.”

VIENNA – Major cardiovascular (CV) events are significantly increased in hospital patients who are infected with the hepatitis C virus (HCV) versus those who are not, according to data presented at the meeting sponsored by the European Association for the Study of the Liver.

A retrospective analysis of more than 200,000 inpatients with and without HCV infection at discharge showed that those with HCV were 29% more likely to have had an acute MI, 98% more likely to have had a cerebral vascular accident (CVA), and 88% times more likely to have coronary artery disease (CAD). There was also an 8% increased risk for heart failure (HF).

“HCV infection is strongly linked to an increase in cardiovascular outcome, length of hospital stay, and cost of care,” Dr. Firew Wubiee and Dr. Charles Howell of Howard University, Washington, D.C., reported in an ePoster at the meeting.

For their retrospective analysis, data were obtained from the 2011 Nationwide Inpatient Sample, which is a large all-payer inpatient care database in the United States that contains information on more than 7 million hospital stays.

ICD-9 codes were used to identify all inpatient cases with and without HCV infection at discharge and those with major CV events, excluding those with liver cirrhosis, hepatocellular carcinoma, and cases of liver transplantation. Dr. Wubiee and Dr. Howell found that inpatients with HCV infection were significantly (P < .001) younger than were those without HCV (mean age 52.8 vs. 57.9 years). They were significantly more likely (P < .001) to be male (62.2% vs. 40%), have a smoking history (45.5% vs. 22.7%), be from ethnic or racial minorities (26.4% vs. 5.1%), and have a household income of less than $39,000 (41% vs. 29.1%).

While inpatients with HCV were also significantly (P < .001) more likely than were those without HCV to have diabetes mellitus (2.1% vs. 1.8%), they were significantly less likely (P < .001) to have other known CV risk factors such as obesity (8.7% vs. 11.8%), dyslipidemia (13.2% vs. 28.1%), and hypertension (49.7% vs. 51%).

Odds ratios for CV outcomes were adjusted for multiple confounding factors, including age, race, obesity, diabetes, dyslipidemia, smoking, alcohol use, hypertension, and hepatitis B infection. The adjusted odds ratios for major CV outcomes were 2.29 for AMI, 1.98 for CVA, 1.88 for CAD, and 1.08 for HF (all P < .001).

The duration of in-hospital treatment was longer for patients with HCV than for those without, with adjusted differences of 1.3 days for AMI (P < .001), 2.02 days for CVA (P < .003), 0.52 days for CAD (P < .001), and 0.37 days for HF (P < .001).

The adjusted cost of inpatient care was also higher for HCV-infected versus noninfected individuals with a mean cost difference of $10,126 for AMI, (P < .001), $10,105 for CVA (P < .002), $2,703 for CAD (P < .001), and $1,895 for HF (P < .001).

“We hypothesized that the inflammation and insulin resistance related to HCV increases the prevalence of cardiovascular diseases compared to patients without HCV,” Dr. Wubiee and Dr. Howell observed.

“The results are consistent with mounting evidence for [a] biological and epidemiological association between HCV infection and cardiovascular morbidity,” they said and suggested “HCV needs to be considered a cardiovascular risk factor.”

VIENNA – Major cardiovascular (CV) events are significantly increased in hospital patients who are infected with the hepatitis C virus (HCV) versus those who are not, according to data presented at the meeting sponsored by the European Association for the Study of the Liver.

A retrospective analysis of more than 200,000 inpatients with and without HCV infection at discharge showed that those with HCV were 29% more likely to have had an acute MI, 98% more likely to have had a cerebral vascular accident (CVA), and 88% times more likely to have coronary artery disease (CAD). There was also an 8% increased risk for heart failure (HF).

“HCV infection is strongly linked to an increase in cardiovascular outcome, length of hospital stay, and cost of care,” Dr. Firew Wubiee and Dr. Charles Howell of Howard University, Washington, D.C., reported in an ePoster at the meeting.

For their retrospective analysis, data were obtained from the 2011 Nationwide Inpatient Sample, which is a large all-payer inpatient care database in the United States that contains information on more than 7 million hospital stays.

ICD-9 codes were used to identify all inpatient cases with and without HCV infection at discharge and those with major CV events, excluding those with liver cirrhosis, hepatocellular carcinoma, and cases of liver transplantation. Dr. Wubiee and Dr. Howell found that inpatients with HCV infection were significantly (P < .001) younger than were those without HCV (mean age 52.8 vs. 57.9 years). They were significantly more likely (P < .001) to be male (62.2% vs. 40%), have a smoking history (45.5% vs. 22.7%), be from ethnic or racial minorities (26.4% vs. 5.1%), and have a household income of less than $39,000 (41% vs. 29.1%).

While inpatients with HCV were also significantly (P < .001) more likely than were those without HCV to have diabetes mellitus (2.1% vs. 1.8%), they were significantly less likely (P < .001) to have other known CV risk factors such as obesity (8.7% vs. 11.8%), dyslipidemia (13.2% vs. 28.1%), and hypertension (49.7% vs. 51%).

Odds ratios for CV outcomes were adjusted for multiple confounding factors, including age, race, obesity, diabetes, dyslipidemia, smoking, alcohol use, hypertension, and hepatitis B infection. The adjusted odds ratios for major CV outcomes were 2.29 for AMI, 1.98 for CVA, 1.88 for CAD, and 1.08 for HF (all P < .001).

The duration of in-hospital treatment was longer for patients with HCV than for those without, with adjusted differences of 1.3 days for AMI (P < .001), 2.02 days for CVA (P < .003), 0.52 days for CAD (P < .001), and 0.37 days for HF (P < .001).

The adjusted cost of inpatient care was also higher for HCV-infected versus noninfected individuals with a mean cost difference of $10,126 for AMI, (P < .001), $10,105 for CVA (P < .002), $2,703 for CAD (P < .001), and $1,895 for HF (P < .001).

“We hypothesized that the inflammation and insulin resistance related to HCV increases the prevalence of cardiovascular diseases compared to patients without HCV,” Dr. Wubiee and Dr. Howell observed.

“The results are consistent with mounting evidence for [a] biological and epidemiological association between HCV infection and cardiovascular morbidity,” they said and suggested “HCV needs to be considered a cardiovascular risk factor.”

VIENNA – Major cardiovascular (CV) events are significantly increased in hospital patients who are infected with the hepatitis C virus (HCV) versus those who are not, according to data presented at the meeting sponsored by the European Association for the Study of the Liver.

A retrospective analysis of more than 200,000 inpatients with and without HCV infection at discharge showed that those with HCV were 29% more likely to have had an acute MI, 98% more likely to have had a cerebral vascular accident (CVA), and 88% times more likely to have coronary artery disease (CAD). There was also an 8% increased risk for heart failure (HF).

“HCV infection is strongly linked to an increase in cardiovascular outcome, length of hospital stay, and cost of care,” Dr. Firew Wubiee and Dr. Charles Howell of Howard University, Washington, D.C., reported in an ePoster at the meeting.

For their retrospective analysis, data were obtained from the 2011 Nationwide Inpatient Sample, which is a large all-payer inpatient care database in the United States that contains information on more than 7 million hospital stays.

ICD-9 codes were used to identify all inpatient cases with and without HCV infection at discharge and those with major CV events, excluding those with liver cirrhosis, hepatocellular carcinoma, and cases of liver transplantation. Dr. Wubiee and Dr. Howell found that inpatients with HCV infection were significantly (P < .001) younger than were those without HCV (mean age 52.8 vs. 57.9 years). They were significantly more likely (P < .001) to be male (62.2% vs. 40%), have a smoking history (45.5% vs. 22.7%), be from ethnic or racial minorities (26.4% vs. 5.1%), and have a household income of less than $39,000 (41% vs. 29.1%).

While inpatients with HCV were also significantly (P < .001) more likely than were those without HCV to have diabetes mellitus (2.1% vs. 1.8%), they were significantly less likely (P < .001) to have other known CV risk factors such as obesity (8.7% vs. 11.8%), dyslipidemia (13.2% vs. 28.1%), and hypertension (49.7% vs. 51%).

Odds ratios for CV outcomes were adjusted for multiple confounding factors, including age, race, obesity, diabetes, dyslipidemia, smoking, alcohol use, hypertension, and hepatitis B infection. The adjusted odds ratios for major CV outcomes were 2.29 for AMI, 1.98 for CVA, 1.88 for CAD, and 1.08 for HF (all P < .001).

The duration of in-hospital treatment was longer for patients with HCV than for those without, with adjusted differences of 1.3 days for AMI (P < .001), 2.02 days for CVA (P < .003), 0.52 days for CAD (P < .001), and 0.37 days for HF (P < .001).

The adjusted cost of inpatient care was also higher for HCV-infected versus noninfected individuals with a mean cost difference of $10,126 for AMI, (P < .001), $10,105 for CVA (P < .002), $2,703 for CAD (P < .001), and $1,895 for HF (P < .001).

“We hypothesized that the inflammation and insulin resistance related to HCV increases the prevalence of cardiovascular diseases compared to patients without HCV,” Dr. Wubiee and Dr. Howell observed.

“The results are consistent with mounting evidence for [a] biological and epidemiological association between HCV infection and cardiovascular morbidity,” they said and suggested “HCV needs to be considered a cardiovascular risk factor.”

VIENNA – As the severity of nonalcoholic fatty liver disease (NAFLD) increases, so does the risk for death and cardiovascular disease, according to data from a large population study reported at the meeting sponsored by the European Association for the Study of the Liver.

There was a 50% increase in the adjusted all-cause morality rate when comparing patients who developed nonalcoholic steatohepatitis (NASH) with those who had NAFLD (hazard ratio of 1.5).

The risk of death was also five times as high when comparing patients with NASH-related cirrhosis to those with NAFLD, with an adjusted HR of 5.1.

Heart failure (HF), atrial fibrillation (AF), type 2 diabetes mellitus, and chronic kidney disease (CKD) rates were also increased in patients with NAFLD, compared with those in the healthy population.*

“Nonalcoholic fatty liver disease has got a strong association with cardiovascular disease; it may be an independent risk factor for cardiovascular disease, but that is still open to debate,” said study investigator Dr. Jake Mann, who is an academic clinical fellow in pediatrics at the University of Cambridge (England).

“What isn’t quite so clear is whether or not there is progressively increasing risk of cardiovascular comorbidities as you move from NAFLD to NASH to NASH cirrhosis,” he added at the meeting, which was sponsored by the European Association for the Study of the Liver (EASL).

To investigate this further, Dr. Mann and collaborators therefore obtained data collected on more than 929,465 patients with NAFLD-related diseases included in the U.K. ACALM (Algorithm for Comorbidities, Associations, Length of stay, and Mortality) study database. ICD-10 codes were used to identify patients with NAFLD, NASH, cryptogenic (NASH)-cirrhosis, and cardiovascular morbidities.

During the 14-year follow-up period, 1,294 patients were diagnosed with NAFLD, 122 with NASH, and 1,285 with cirrhosis. Around 57% of patients in each group were male, with the mean age rising from 50.6 years in the NAFLD patients to 51.6% in the NASH patients to 59.2% in the patients with cirrhosis. Most (76%-80%) patients were white, with around 10%-12% being of Asian ethnicity.

HF was more prevalent in patients with NASH (9% vs. 3.8%, P < .01) and cirrhosis (6.6% vs. 3.8%; P < .001) than in those with NAFLD. The prevalence of AF was increased progressing from NAFLD to NASH (4.9% vs. 8.2%) and NAFLD to cirrhosis (4.9% vs. 8.3%; P < .0001). Rates for diabetes were 20.9%, 24.6%, and 31.2% and for CKD were 2.1%, 4.9%, and 6.9% progressing from NAFLD to NASH to cirrhosis.

Hyperlipidemia and hypertension rates for NAFLD, NASH, and cirrhosis were 12.1%, 17.2%, and 5%, and 29.4%, 34.4%, and 27.3%, respectively.

Crude mortality rates were 11.5% for the general population and 14.5% for NAFLD, 22.1% for NASH, and 53.1% for cirrhosis. “Unfortunately we do not have disease-specific mortality data,” Dr. Mann said.

There are of course several limitations that need consideration, including assuming NASH was a biopsy-proven diagnosis. The findings are also reliant on data coding and of course it is possible that patients with NASH are included in the NAFLD group, and non-NASH cirrhosis could be included in the cryptogenic cirrhosis group.

There is also the chance of underdiagnosis and undercoding, Dr. Mann said. The overall prevalence of NAFLD-spectrum disease was 2.5%, which is perhaps somewhat lower than might be expected in a large U.K. population.

Other limiting factors were that the patients with the cryptogenic cirrhosis group were older than those in the other groups and also that these findings could be describing the natural history of the disease rather than implying causation.

Nevertheless, this is the largest study of its kind, Dr. Mann said, and shows that there is a trend towards increasing mortality and burden of CVD with increasing severity of NAFLD-spectrum disease.

“The take-home message is that clinicians should be very aware of this association, such that hepatologists should consider that patients are at very high risk of heart disease, and as they currently do, they should screen for cardiovascular disease and refer on as appropriate,” Dr. Mann said in an interview.

“Likewise, cardiologists and general practitioners should be very aware that patients with cardiac disease are at risk of NAFLD and equally would refer to GI and liver teams,” Dr. Mann said.

“These findings clearly link the severity of [nonalcoholic fatty liver disease] with the increased risk of cardiovascular disease and death,” Dr. Laurent Castera of Hôpital Beaujon in France said in a press release issued by the EASL.

Dr. Castera, who is the vice-secretary of the association added: “It is therefore imperative that we identify people in the early stages of [the disease] so they can be treated through diet and lifestyle interventions before their condition becomes potentially deadly.”

*A correction was made to this sentence on 5/22/2015.

VIENNA – As the severity of nonalcoholic fatty liver disease (NAFLD) increases, so does the risk for death and cardiovascular disease, according to data from a large population study reported at the meeting sponsored by the European Association for the Study of the Liver.

There was a 50% increase in the adjusted all-cause morality rate when comparing patients who developed nonalcoholic steatohepatitis (NASH) with those who had NAFLD (hazard ratio of 1.5).

The risk of death was also five times as high when comparing patients with NASH-related cirrhosis to those with NAFLD, with an adjusted HR of 5.1.

Heart failure (HF), atrial fibrillation (AF), type 2 diabetes mellitus, and chronic kidney disease (CKD) rates were also increased in patients with NAFLD, compared with those in the healthy population.*

“Nonalcoholic fatty liver disease has got a strong association with cardiovascular disease; it may be an independent risk factor for cardiovascular disease, but that is still open to debate,” said study investigator Dr. Jake Mann, who is an academic clinical fellow in pediatrics at the University of Cambridge (England).

“What isn’t quite so clear is whether or not there is progressively increasing risk of cardiovascular comorbidities as you move from NAFLD to NASH to NASH cirrhosis,” he added at the meeting, which was sponsored by the European Association for the Study of the Liver (EASL).

To investigate this further, Dr. Mann and collaborators therefore obtained data collected on more than 929,465 patients with NAFLD-related diseases included in the U.K. ACALM (Algorithm for Comorbidities, Associations, Length of stay, and Mortality) study database. ICD-10 codes were used to identify patients with NAFLD, NASH, cryptogenic (NASH)-cirrhosis, and cardiovascular morbidities.

During the 14-year follow-up period, 1,294 patients were diagnosed with NAFLD, 122 with NASH, and 1,285 with cirrhosis. Around 57% of patients in each group were male, with the mean age rising from 50.6 years in the NAFLD patients to 51.6% in the NASH patients to 59.2% in the patients with cirrhosis. Most (76%-80%) patients were white, with around 10%-12% being of Asian ethnicity.

HF was more prevalent in patients with NASH (9% vs. 3.8%, P < .01) and cirrhosis (6.6% vs. 3.8%; P < .001) than in those with NAFLD. The prevalence of AF was increased progressing from NAFLD to NASH (4.9% vs. 8.2%) and NAFLD to cirrhosis (4.9% vs. 8.3%; P < .0001). Rates for diabetes were 20.9%, 24.6%, and 31.2% and for CKD were 2.1%, 4.9%, and 6.9% progressing from NAFLD to NASH to cirrhosis.

Hyperlipidemia and hypertension rates for NAFLD, NASH, and cirrhosis were 12.1%, 17.2%, and 5%, and 29.4%, 34.4%, and 27.3%, respectively.

Crude mortality rates were 11.5% for the general population and 14.5% for NAFLD, 22.1% for NASH, and 53.1% for cirrhosis. “Unfortunately we do not have disease-specific mortality data,” Dr. Mann said.

There are of course several limitations that need consideration, including assuming NASH was a biopsy-proven diagnosis. The findings are also reliant on data coding and of course it is possible that patients with NASH are included in the NAFLD group, and non-NASH cirrhosis could be included in the cryptogenic cirrhosis group.

There is also the chance of underdiagnosis and undercoding, Dr. Mann said. The overall prevalence of NAFLD-spectrum disease was 2.5%, which is perhaps somewhat lower than might be expected in a large U.K. population.

Other limiting factors were that the patients with the cryptogenic cirrhosis group were older than those in the other groups and also that these findings could be describing the natural history of the disease rather than implying causation.

Nevertheless, this is the largest study of its kind, Dr. Mann said, and shows that there is a trend towards increasing mortality and burden of CVD with increasing severity of NAFLD-spectrum disease.

“The take-home message is that clinicians should be very aware of this association, such that hepatologists should consider that patients are at very high risk of heart disease, and as they currently do, they should screen for cardiovascular disease and refer on as appropriate,” Dr. Mann said in an interview.

“Likewise, cardiologists and general practitioners should be very aware that patients with cardiac disease are at risk of NAFLD and equally would refer to GI and liver teams,” Dr. Mann said.

“These findings clearly link the severity of [nonalcoholic fatty liver disease] with the increased risk of cardiovascular disease and death,” Dr. Laurent Castera of Hôpital Beaujon in France said in a press release issued by the EASL.

Dr. Castera, who is the vice-secretary of the association added: “It is therefore imperative that we identify people in the early stages of [the disease] so they can be treated through diet and lifestyle interventions before their condition becomes potentially deadly.”

*A correction was made to this sentence on 5/22/2015.

VIENNA – As the severity of nonalcoholic fatty liver disease (NAFLD) increases, so does the risk for death and cardiovascular disease, according to data from a large population study reported at the meeting sponsored by the European Association for the Study of the Liver.

There was a 50% increase in the adjusted all-cause morality rate when comparing patients who developed nonalcoholic steatohepatitis (NASH) with those who had NAFLD (hazard ratio of 1.5).

The risk of death was also five times as high when comparing patients with NASH-related cirrhosis to those with NAFLD, with an adjusted HR of 5.1.

Heart failure (HF), atrial fibrillation (AF), type 2 diabetes mellitus, and chronic kidney disease (CKD) rates were also increased in patients with NAFLD, compared with those in the healthy population.*

“Nonalcoholic fatty liver disease has got a strong association with cardiovascular disease; it may be an independent risk factor for cardiovascular disease, but that is still open to debate,” said study investigator Dr. Jake Mann, who is an academic clinical fellow in pediatrics at the University of Cambridge (England).

“What isn’t quite so clear is whether or not there is progressively increasing risk of cardiovascular comorbidities as you move from NAFLD to NASH to NASH cirrhosis,” he added at the meeting, which was sponsored by the European Association for the Study of the Liver (EASL).

To investigate this further, Dr. Mann and collaborators therefore obtained data collected on more than 929,465 patients with NAFLD-related diseases included in the U.K. ACALM (Algorithm for Comorbidities, Associations, Length of stay, and Mortality) study database. ICD-10 codes were used to identify patients with NAFLD, NASH, cryptogenic (NASH)-cirrhosis, and cardiovascular morbidities.

During the 14-year follow-up period, 1,294 patients were diagnosed with NAFLD, 122 with NASH, and 1,285 with cirrhosis. Around 57% of patients in each group were male, with the mean age rising from 50.6 years in the NAFLD patients to 51.6% in the NASH patients to 59.2% in the patients with cirrhosis. Most (76%-80%) patients were white, with around 10%-12% being of Asian ethnicity.

HF was more prevalent in patients with NASH (9% vs. 3.8%, P < .01) and cirrhosis (6.6% vs. 3.8%; P < .001) than in those with NAFLD. The prevalence of AF was increased progressing from NAFLD to NASH (4.9% vs. 8.2%) and NAFLD to cirrhosis (4.9% vs. 8.3%; P < .0001). Rates for diabetes were 20.9%, 24.6%, and 31.2% and for CKD were 2.1%, 4.9%, and 6.9% progressing from NAFLD to NASH to cirrhosis.

Hyperlipidemia and hypertension rates for NAFLD, NASH, and cirrhosis were 12.1%, 17.2%, and 5%, and 29.4%, 34.4%, and 27.3%, respectively.

Crude mortality rates were 11.5% for the general population and 14.5% for NAFLD, 22.1% for NASH, and 53.1% for cirrhosis. “Unfortunately we do not have disease-specific mortality data,” Dr. Mann said.

There are of course several limitations that need consideration, including assuming NASH was a biopsy-proven diagnosis. The findings are also reliant on data coding and of course it is possible that patients with NASH are included in the NAFLD group, and non-NASH cirrhosis could be included in the cryptogenic cirrhosis group.

There is also the chance of underdiagnosis and undercoding, Dr. Mann said. The overall prevalence of NAFLD-spectrum disease was 2.5%, which is perhaps somewhat lower than might be expected in a large U.K. population.

Other limiting factors were that the patients with the cryptogenic cirrhosis group were older than those in the other groups and also that these findings could be describing the natural history of the disease rather than implying causation.

Nevertheless, this is the largest study of its kind, Dr. Mann said, and shows that there is a trend towards increasing mortality and burden of CVD with increasing severity of NAFLD-spectrum disease.

“The take-home message is that clinicians should be very aware of this association, such that hepatologists should consider that patients are at very high risk of heart disease, and as they currently do, they should screen for cardiovascular disease and refer on as appropriate,” Dr. Mann said in an interview.

“Likewise, cardiologists and general practitioners should be very aware that patients with cardiac disease are at risk of NAFLD and equally would refer to GI and liver teams,” Dr. Mann said.

“These findings clearly link the severity of [nonalcoholic fatty liver disease] with the increased risk of cardiovascular disease and death,” Dr. Laurent Castera of Hôpital Beaujon in France said in a press release issued by the EASL.

Dr. Castera, who is the vice-secretary of the association added: “It is therefore imperative that we identify people in the early stages of [the disease] so they can be treated through diet and lifestyle interventions before their condition becomes potentially deadly.”

*A correction was made to this sentence on 5/22/2015.

VIENNA – Patients infected with hepatitis C virus who developed cirrhosis and received statin treatment had significantly lower rates of both death and cirrhosis decompensation, compared with cirrhosis patients who did not receive a statin in a confounder-adjusted analysis of data from more than 2,700 patients in a U.S. Department of Veterans Affairs database.

While this suggestive evidence is not strong enough to warrant routinely prescribing statins to cirrhosis patients, it does highlight the need to prescribe a statin to any cirrhosis patient who qualifies for the drug by standard criteria because of established cardiovascular disease or as part of primary prevention when there is elevated cardiovascular risk, Dr. Arpan Mohanty said at the meeting sponsored by the European Association for the Study of the Liver.

Conventional wisdom has often led to withholding statins from patients with liver disease out of concern for risk of statin-induced hepatotoxicity, said Dr. Mohanty, a gastroenterology researcher at Yale University in New Haven, Conn. But the new findings suggesting such overwhelming benefit from statin treatment in these patients indicates that “statin use should not be avoided” when patients with liver disease would otherwise qualify for statin treatment. “Statins should be prescribed when required for atherosclerosis,” she said, adding that in New Haven her program has run sessions to educate primary care physicians on this.

The study used data collected during 1996-2009 by the Hepatitis C Virus Clinical Case Registry of the U.S. Department of Veterans Affairs, which includes more than 340,000 veterans, of whom more than 45,000 had been diagnosed with cirrhosis. Further analysis identified 1,323 eligible veterans from this group on statin treatment, and 12,522 not on statin treatment. Propensity score matching narrowed the study group down to 685 hepatitis C virus–infected veterans with cirrhosis who were on statin treatment, and 2,062 closely matched veterans infected with HCV and with cirrhosis but not receiving statin therapy.

©Sebastian Kaulitzki/thinkstockphotos.com

The patients averaged 56 years old, 98% were men, and comorbidities were common; a third had a history of coronary artery disease, more than 80% had hypertension, more than half had diabetes, and more than half had alcohol dependency. Among patients with a serum cholesterol level greater than 200 mg/dL, 57% were not on a statin; among those with a serum low-density cholesterol level of about 160 mg/dL, 35% were not receiving a statin. “Statin use is low in patients with cirrhosis, even in those with high cardiovascular risk,” Dr. Mohanty said.

She and her associates tracked the incidence of death for a median of more than 2 years in these patients, and they followed new episodes of cirrhosis decompensation for nearly 2 years. With adjustment for age, body mass index, serum albumin, and fibrosis-4 and MELD (Model for End-Stage Liver Disease) scores, the rates of both death and cirrhosis decompensation were each a statistically significant 45% lower among the patients on statins, compared with those not on a statin, they reported.

mzoler@frontlinemedcom.com

On Twitter @mitchelzoler

VIENNA – Patients infected with hepatitis C virus who developed cirrhosis and received statin treatment had significantly lower rates of both death and cirrhosis decompensation, compared with cirrhosis patients who did not receive a statin in a confounder-adjusted analysis of data from more than 2,700 patients in a U.S. Department of Veterans Affairs database.

While this suggestive evidence is not strong enough to warrant routinely prescribing statins to cirrhosis patients, it does highlight the need to prescribe a statin to any cirrhosis patient who qualifies for the drug by standard criteria because of established cardiovascular disease or as part of primary prevention when there is elevated cardiovascular risk, Dr. Arpan Mohanty said at the meeting sponsored by the European Association for the Study of the Liver.

Conventional wisdom has often led to withholding statins from patients with liver disease out of concern for risk of statin-induced hepatotoxicity, said Dr. Mohanty, a gastroenterology researcher at Yale University in New Haven, Conn. But the new findings suggesting such overwhelming benefit from statin treatment in these patients indicates that “statin use should not be avoided” when patients with liver disease would otherwise qualify for statin treatment. “Statins should be prescribed when required for atherosclerosis,” she said, adding that in New Haven her program has run sessions to educate primary care physicians on this.

The study used data collected during 1996-2009 by the Hepatitis C Virus Clinical Case Registry of the U.S. Department of Veterans Affairs, which includes more than 340,000 veterans, of whom more than 45,000 had been diagnosed with cirrhosis. Further analysis identified 1,323 eligible veterans from this group on statin treatment, and 12,522 not on statin treatment. Propensity score matching narrowed the study group down to 685 hepatitis C virus–infected veterans with cirrhosis who were on statin treatment, and 2,062 closely matched veterans infected with HCV and with cirrhosis but not receiving statin therapy.

©Sebastian Kaulitzki/thinkstockphotos.com

The patients averaged 56 years old, 98% were men, and comorbidities were common; a third had a history of coronary artery disease, more than 80% had hypertension, more than half had diabetes, and more than half had alcohol dependency. Among patients with a serum cholesterol level greater than 200 mg/dL, 57% were not on a statin; among those with a serum low-density cholesterol level of about 160 mg/dL, 35% were not receiving a statin. “Statin use is low in patients with cirrhosis, even in those with high cardiovascular risk,” Dr. Mohanty said.

She and her associates tracked the incidence of death for a median of more than 2 years in these patients, and they followed new episodes of cirrhosis decompensation for nearly 2 years. With adjustment for age, body mass index, serum albumin, and fibrosis-4 and MELD (Model for End-Stage Liver Disease) scores, the rates of both death and cirrhosis decompensation were each a statistically significant 45% lower among the patients on statins, compared with those not on a statin, they reported.

mzoler@frontlinemedcom.com

On Twitter @mitchelzoler

VIENNA – Patients infected with hepatitis C virus who developed cirrhosis and received statin treatment had significantly lower rates of both death and cirrhosis decompensation, compared with cirrhosis patients who did not receive a statin in a confounder-adjusted analysis of data from more than 2,700 patients in a U.S. Department of Veterans Affairs database.

While this suggestive evidence is not strong enough to warrant routinely prescribing statins to cirrhosis patients, it does highlight the need to prescribe a statin to any cirrhosis patient who qualifies for the drug by standard criteria because of established cardiovascular disease or as part of primary prevention when there is elevated cardiovascular risk, Dr. Arpan Mohanty said at the meeting sponsored by the European Association for the Study of the Liver.

Conventional wisdom has often led to withholding statins from patients with liver disease out of concern for risk of statin-induced hepatotoxicity, said Dr. Mohanty, a gastroenterology researcher at Yale University in New Haven, Conn. But the new findings suggesting such overwhelming benefit from statin treatment in these patients indicates that “statin use should not be avoided” when patients with liver disease would otherwise qualify for statin treatment. “Statins should be prescribed when required for atherosclerosis,” she said, adding that in New Haven her program has run sessions to educate primary care physicians on this.

The study used data collected during 1996-2009 by the Hepatitis C Virus Clinical Case Registry of the U.S. Department of Veterans Affairs, which includes more than 340,000 veterans, of whom more than 45,000 had been diagnosed with cirrhosis. Further analysis identified 1,323 eligible veterans from this group on statin treatment, and 12,522 not on statin treatment. Propensity score matching narrowed the study group down to 685 hepatitis C virus–infected veterans with cirrhosis who were on statin treatment, and 2,062 closely matched veterans infected with HCV and with cirrhosis but not receiving statin therapy.

©Sebastian Kaulitzki/thinkstockphotos.com

The patients averaged 56 years old, 98% were men, and comorbidities were common; a third had a history of coronary artery disease, more than 80% had hypertension, more than half had diabetes, and more than half had alcohol dependency. Among patients with a serum cholesterol level greater than 200 mg/dL, 57% were not on a statin; among those with a serum low-density cholesterol level of about 160 mg/dL, 35% were not receiving a statin. “Statin use is low in patients with cirrhosis, even in those with high cardiovascular risk,” Dr. Mohanty said.

She and her associates tracked the incidence of death for a median of more than 2 years in these patients, and they followed new episodes of cirrhosis decompensation for nearly 2 years. With adjustment for age, body mass index, serum albumin, and fibrosis-4 and MELD (Model for End-Stage Liver Disease) scores, the rates of both death and cirrhosis decompensation were each a statistically significant 45% lower among the patients on statins, compared with those not on a statin, they reported.

mzoler@frontlinemedcom.com

On Twitter @mitchelzoler

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.

Courtesy ILC 2015

“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.

Courtesy ILC 2015

“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.

Courtesy ILC 2015

“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.

Courtesy ILC 2015

“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.

Courtesy ILC 2015

“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.

Courtesy ILC 2015

“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.