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Two-drug combo effective at treating HCV genotype 1 and 3
Patients with genotype 1 or 3 hepatitis C virus infection responded well to therapy with a two-drug combination in a randomized, phase II, open-label study conducted in 58 sites in Australia, New Zealand, and the United States.
This treatment was “well tolerated and highly effective,” according to Dr. Stephen Pianko and his colleagues.
The regimen used is 400 mg of sofosbuvir combined with 100 mg of velpatasvir for 12 weeks. Patients with genotype 1 or 3 hepatitis C virus (HCV) infection responded well to therapy with 400 mg of sofosbuvir combined with 100 mg of velpatasvir for 12 weeks, in a randomized, phase II, open-label study conducted in 58 sites in Australia, New Zealand, and the United States.
This treatment program was “well tolerated and highly effective,” according to Dr. Stephen Pianko and his colleagues.
The study participants were divided into three cohorts: the first included patients with genotype 3 HCV infection without cirrhosis, the second included patients with genotype 3 HCV with compensated cirrhosis, and the third included patients with genotype 1 HCV infection that was unsuccessfully treated with a protease inhibitor with peginterferon and ribavirin (50% could have compensated cirrhosis).
All patients were treatment experienced and received 12 weeks of drug therapy that included 400 mg of sofosbuvir once daily. Patients in each cohort were randomly assigned to also being treated with 25 mg of velpatasvir once daily with or without ribavirin, or 100 mg of velpatasvir once daily with or without ribavirin.
All patients in cohort 1 who were treated with 400 mg of sofosbuvir combined with 100 mg of velpatasvir or 400 mg of sofosbuvir combined with 100 mg of velpatasvir plus ribavirin experienced a sustained virologic response at week 12 after treatment. The same was true for 100% of patients in cohort 3, who either received 400 mg of sofosbuvir combined with 25 mg velpatasvir or 400 mg of sofosbuvir combined with 100 mg of velpatasvir.
The proportion of patients in the other treatment categories who achieved sustained virologic response 12 weeks following therapy ranged from 58% to 97%.
Eighty-two percent (263 of 321) of patients experienced at least 1 adverse event. Common adverse events included headache and fatigue. "More patients in the groups receiving ribavirin had fatigue, nausea, and pruritus; decreased hemoglobin levels; and increased bilirubin." One patient had an elevated alanine aminotransferase level and y-glutamyl transferase level on treatment day 80, which resulted in treatment discontinuation. Eight study participants experienced "serious adverse events that were not considered to be related to a study drug."
“In summary, sofosbuvir plus 100 mg of velpatasvir provided high rates of [sustained virologic response at week 12 after treatment] in treatment-experienced patients with genotype 1 or 3 HCV infection, including those with compensated cirrhosis, but results will need confirmation in a phase 3 trial,” according to the researchers.
Read the full study in Annals of Internal Medicine (doi: 10.7326/M15-1014).
*This story was updated 11/11/2015.
Patients with genotype 1 or 3 hepatitis C virus infection responded well to therapy with a two-drug combination in a randomized, phase II, open-label study conducted in 58 sites in Australia, New Zealand, and the United States.
This treatment was “well tolerated and highly effective,” according to Dr. Stephen Pianko and his colleagues.
The regimen used is 400 mg of sofosbuvir combined with 100 mg of velpatasvir for 12 weeks. Patients with genotype 1 or 3 hepatitis C virus (HCV) infection responded well to therapy with 400 mg of sofosbuvir combined with 100 mg of velpatasvir for 12 weeks, in a randomized, phase II, open-label study conducted in 58 sites in Australia, New Zealand, and the United States.
This treatment program was “well tolerated and highly effective,” according to Dr. Stephen Pianko and his colleagues.
The study participants were divided into three cohorts: the first included patients with genotype 3 HCV infection without cirrhosis, the second included patients with genotype 3 HCV with compensated cirrhosis, and the third included patients with genotype 1 HCV infection that was unsuccessfully treated with a protease inhibitor with peginterferon and ribavirin (50% could have compensated cirrhosis).
All patients were treatment experienced and received 12 weeks of drug therapy that included 400 mg of sofosbuvir once daily. Patients in each cohort were randomly assigned to also being treated with 25 mg of velpatasvir once daily with or without ribavirin, or 100 mg of velpatasvir once daily with or without ribavirin.
All patients in cohort 1 who were treated with 400 mg of sofosbuvir combined with 100 mg of velpatasvir or 400 mg of sofosbuvir combined with 100 mg of velpatasvir plus ribavirin experienced a sustained virologic response at week 12 after treatment. The same was true for 100% of patients in cohort 3, who either received 400 mg of sofosbuvir combined with 25 mg velpatasvir or 400 mg of sofosbuvir combined with 100 mg of velpatasvir.
The proportion of patients in the other treatment categories who achieved sustained virologic response 12 weeks following therapy ranged from 58% to 97%.
Eighty-two percent (263 of 321) of patients experienced at least 1 adverse event. Common adverse events included headache and fatigue. "More patients in the groups receiving ribavirin had fatigue, nausea, and pruritus; decreased hemoglobin levels; and increased bilirubin." One patient had an elevated alanine aminotransferase level and y-glutamyl transferase level on treatment day 80, which resulted in treatment discontinuation. Eight study participants experienced "serious adverse events that were not considered to be related to a study drug."
“In summary, sofosbuvir plus 100 mg of velpatasvir provided high rates of [sustained virologic response at week 12 after treatment] in treatment-experienced patients with genotype 1 or 3 HCV infection, including those with compensated cirrhosis, but results will need confirmation in a phase 3 trial,” according to the researchers.
Read the full study in Annals of Internal Medicine (doi: 10.7326/M15-1014).
*This story was updated 11/11/2015.
Patients with genotype 1 or 3 hepatitis C virus infection responded well to therapy with a two-drug combination in a randomized, phase II, open-label study conducted in 58 sites in Australia, New Zealand, and the United States.
This treatment was “well tolerated and highly effective,” according to Dr. Stephen Pianko and his colleagues.
The regimen used is 400 mg of sofosbuvir combined with 100 mg of velpatasvir for 12 weeks. Patients with genotype 1 or 3 hepatitis C virus (HCV) infection responded well to therapy with 400 mg of sofosbuvir combined with 100 mg of velpatasvir for 12 weeks, in a randomized, phase II, open-label study conducted in 58 sites in Australia, New Zealand, and the United States.
This treatment program was “well tolerated and highly effective,” according to Dr. Stephen Pianko and his colleagues.
The study participants were divided into three cohorts: the first included patients with genotype 3 HCV infection without cirrhosis, the second included patients with genotype 3 HCV with compensated cirrhosis, and the third included patients with genotype 1 HCV infection that was unsuccessfully treated with a protease inhibitor with peginterferon and ribavirin (50% could have compensated cirrhosis).
All patients were treatment experienced and received 12 weeks of drug therapy that included 400 mg of sofosbuvir once daily. Patients in each cohort were randomly assigned to also being treated with 25 mg of velpatasvir once daily with or without ribavirin, or 100 mg of velpatasvir once daily with or without ribavirin.
All patients in cohort 1 who were treated with 400 mg of sofosbuvir combined with 100 mg of velpatasvir or 400 mg of sofosbuvir combined with 100 mg of velpatasvir plus ribavirin experienced a sustained virologic response at week 12 after treatment. The same was true for 100% of patients in cohort 3, who either received 400 mg of sofosbuvir combined with 25 mg velpatasvir or 400 mg of sofosbuvir combined with 100 mg of velpatasvir.
The proportion of patients in the other treatment categories who achieved sustained virologic response 12 weeks following therapy ranged from 58% to 97%.
Eighty-two percent (263 of 321) of patients experienced at least 1 adverse event. Common adverse events included headache and fatigue. "More patients in the groups receiving ribavirin had fatigue, nausea, and pruritus; decreased hemoglobin levels; and increased bilirubin." One patient had an elevated alanine aminotransferase level and y-glutamyl transferase level on treatment day 80, which resulted in treatment discontinuation. Eight study participants experienced "serious adverse events that were not considered to be related to a study drug."
“In summary, sofosbuvir plus 100 mg of velpatasvir provided high rates of [sustained virologic response at week 12 after treatment] in treatment-experienced patients with genotype 1 or 3 HCV infection, including those with compensated cirrhosis, but results will need confirmation in a phase 3 trial,” according to the researchers.
Read the full study in Annals of Internal Medicine (doi: 10.7326/M15-1014).
*This story was updated 11/11/2015.
AASLD: HCV cure associated with reduction in all-cause mortality
SAN FRANCISCO – Sustained virologic response (SVR) in patients with hepatitis C virus (HCV) infection is associated with large reductions in all-cause mortality and appears to eliminate liver-related mortality in those patients who achieve SVR before developing cirrhosis, according to a real-world study presented at the annual meeting of the American Association for the Study of Liver Disease (AASLD).
“This study strongly supports treatment and cure of HCV to reduce deaths in this patient population,” reported Dr. Lisa M. Nyberg, a specialist in hepatology at Kaiser Permanente, San Diego.
In this study, 24,968 patients diagnosed with HCV in the Kaiser Permanente health care system from January 2002 until the end of 2013 were evaluated retrospectively. The overall mortality over the course of follow-up was 18.5%, but the proportion of patients who died was higher in the group with cirrhosis (33.2%) versus those without cirrhosis (7.8%).
Of the 5,203 treated for HCV, 45.1% achieved SVR. The mortality rates were 18.9% in the absence of SVR versus 5.4% in those who achieved SVR. SVR was associated with reductions in all-cause mortality in those with cirrhosis (8.11% vs. 23.3%; P less than .0001) as well as those without cirrhosis (2.1% vs. 5.3%; P less than .0001).
When liver-related mortality was evaluated, SVR was again associated with large reductions in those with cirrhosis (24.7% vs. 41.9%; P less than .0001) as well as in those without cirrhosis (0% vs. 12%; P = .0178). Indeed, this latter finding indicates that SVR essentially eliminates risk of liver-related death in the absence of cirrhosis.
“The data suggest that treatment of HCV should be initiated at all stages of disease with the intention to cure HCV when possible before progression to cirrhosis,” said Dr. Nyberg, indicating that these findings are relevant to the debate about when to consider curative therapies.
However, Dr. Nyberg suggested that the significant reductions in death by any cause even in patients without cirrhosis suggest that HCV should be considered a systemic illness. She suggested that it is important to recognize that the benefit of eradication extends beyond complications in the liver.
The vast majority of SVRs were achieved in this study with interferon-based regimens, which typically have limited efficacy in many HCV subpopulations, such as those defined by viral genotype. During the discussion that followed presentation of these data, this was a criticism directed at the overall conclusion that SVR can be isolated as a factor in improved outcomes.
“Patients [who achieve SVR on interferon-based therapies] may be very different people to start with,” cautioned Dr. Hans L. Tillmann, professor of medicine, East Carolina University, Greenville, N.C. He pointed out that factors that influence the likelihood of achieving SVR on an interferon-based therapy might be associated with risk factors for mortality over time. With direct-acting antivirals, which have the potential to provide SVR in the vast majority of patients, “you may not be able to reproduce these outcomes.”
While acknowledging the relevance of this criticism, Dr. Nyberg reported that further study is ongoing, including efforts to consider severity of liver disease to evaluate the effect of SVR on the natural history of long-term liver complications following HCV infection.
SAN FRANCISCO – Sustained virologic response (SVR) in patients with hepatitis C virus (HCV) infection is associated with large reductions in all-cause mortality and appears to eliminate liver-related mortality in those patients who achieve SVR before developing cirrhosis, according to a real-world study presented at the annual meeting of the American Association for the Study of Liver Disease (AASLD).
“This study strongly supports treatment and cure of HCV to reduce deaths in this patient population,” reported Dr. Lisa M. Nyberg, a specialist in hepatology at Kaiser Permanente, San Diego.
In this study, 24,968 patients diagnosed with HCV in the Kaiser Permanente health care system from January 2002 until the end of 2013 were evaluated retrospectively. The overall mortality over the course of follow-up was 18.5%, but the proportion of patients who died was higher in the group with cirrhosis (33.2%) versus those without cirrhosis (7.8%).
Of the 5,203 treated for HCV, 45.1% achieved SVR. The mortality rates were 18.9% in the absence of SVR versus 5.4% in those who achieved SVR. SVR was associated with reductions in all-cause mortality in those with cirrhosis (8.11% vs. 23.3%; P less than .0001) as well as those without cirrhosis (2.1% vs. 5.3%; P less than .0001).
When liver-related mortality was evaluated, SVR was again associated with large reductions in those with cirrhosis (24.7% vs. 41.9%; P less than .0001) as well as in those without cirrhosis (0% vs. 12%; P = .0178). Indeed, this latter finding indicates that SVR essentially eliminates risk of liver-related death in the absence of cirrhosis.
“The data suggest that treatment of HCV should be initiated at all stages of disease with the intention to cure HCV when possible before progression to cirrhosis,” said Dr. Nyberg, indicating that these findings are relevant to the debate about when to consider curative therapies.
However, Dr. Nyberg suggested that the significant reductions in death by any cause even in patients without cirrhosis suggest that HCV should be considered a systemic illness. She suggested that it is important to recognize that the benefit of eradication extends beyond complications in the liver.
The vast majority of SVRs were achieved in this study with interferon-based regimens, which typically have limited efficacy in many HCV subpopulations, such as those defined by viral genotype. During the discussion that followed presentation of these data, this was a criticism directed at the overall conclusion that SVR can be isolated as a factor in improved outcomes.
“Patients [who achieve SVR on interferon-based therapies] may be very different people to start with,” cautioned Dr. Hans L. Tillmann, professor of medicine, East Carolina University, Greenville, N.C. He pointed out that factors that influence the likelihood of achieving SVR on an interferon-based therapy might be associated with risk factors for mortality over time. With direct-acting antivirals, which have the potential to provide SVR in the vast majority of patients, “you may not be able to reproduce these outcomes.”
While acknowledging the relevance of this criticism, Dr. Nyberg reported that further study is ongoing, including efforts to consider severity of liver disease to evaluate the effect of SVR on the natural history of long-term liver complications following HCV infection.
SAN FRANCISCO – Sustained virologic response (SVR) in patients with hepatitis C virus (HCV) infection is associated with large reductions in all-cause mortality and appears to eliminate liver-related mortality in those patients who achieve SVR before developing cirrhosis, according to a real-world study presented at the annual meeting of the American Association for the Study of Liver Disease (AASLD).
“This study strongly supports treatment and cure of HCV to reduce deaths in this patient population,” reported Dr. Lisa M. Nyberg, a specialist in hepatology at Kaiser Permanente, San Diego.
In this study, 24,968 patients diagnosed with HCV in the Kaiser Permanente health care system from January 2002 until the end of 2013 were evaluated retrospectively. The overall mortality over the course of follow-up was 18.5%, but the proportion of patients who died was higher in the group with cirrhosis (33.2%) versus those without cirrhosis (7.8%).
Of the 5,203 treated for HCV, 45.1% achieved SVR. The mortality rates were 18.9% in the absence of SVR versus 5.4% in those who achieved SVR. SVR was associated with reductions in all-cause mortality in those with cirrhosis (8.11% vs. 23.3%; P less than .0001) as well as those without cirrhosis (2.1% vs. 5.3%; P less than .0001).
When liver-related mortality was evaluated, SVR was again associated with large reductions in those with cirrhosis (24.7% vs. 41.9%; P less than .0001) as well as in those without cirrhosis (0% vs. 12%; P = .0178). Indeed, this latter finding indicates that SVR essentially eliminates risk of liver-related death in the absence of cirrhosis.
“The data suggest that treatment of HCV should be initiated at all stages of disease with the intention to cure HCV when possible before progression to cirrhosis,” said Dr. Nyberg, indicating that these findings are relevant to the debate about when to consider curative therapies.
However, Dr. Nyberg suggested that the significant reductions in death by any cause even in patients without cirrhosis suggest that HCV should be considered a systemic illness. She suggested that it is important to recognize that the benefit of eradication extends beyond complications in the liver.
The vast majority of SVRs were achieved in this study with interferon-based regimens, which typically have limited efficacy in many HCV subpopulations, such as those defined by viral genotype. During the discussion that followed presentation of these data, this was a criticism directed at the overall conclusion that SVR can be isolated as a factor in improved outcomes.
“Patients [who achieve SVR on interferon-based therapies] may be very different people to start with,” cautioned Dr. Hans L. Tillmann, professor of medicine, East Carolina University, Greenville, N.C. He pointed out that factors that influence the likelihood of achieving SVR on an interferon-based therapy might be associated with risk factors for mortality over time. With direct-acting antivirals, which have the potential to provide SVR in the vast majority of patients, “you may not be able to reproduce these outcomes.”
While acknowledging the relevance of this criticism, Dr. Nyberg reported that further study is ongoing, including efforts to consider severity of liver disease to evaluate the effect of SVR on the natural history of long-term liver complications following HCV infection.
AT THE LIVER MEETING 2015
Key clinical point: Achieving an SVR is associated with a large reduction in liver-related and all-cause mortality over long-term follow-up.
Major finding: In follow-up, all-cause mortality was more than threefold lower (5.4% vs. 18.9%) in those who achieved SVR relative to those who did not.
Data source: Retrospective cohort study performed with large database.
Disclosures: Dr. Nyberg has reported financial relationships with AbbVie, Merck, and Gilead, which was the sponsor of this study.
Elevated liver cancer risk after HCV cure may justify surveillance
SAN FRANCISCO – The risk of hepatocellular carcinoma remains sufficiently high in some subgroups who have achieved sustained virologic response to treatment to justify continued cancer surveillance, according to findings from a large cohort study presented at the annual meeting of the American Association for the Study of Liver Diseases.
The risk of hepatocellular carcinoma (HCC) after sustained virologic response (SVR) was relatively elevated in those who were infected with genotype 3 of the hepatitis C virus (HCV), those with diabetes, and those older than 65 years. But those who had cirrhosis at the time of SVR appear to have the highest risk and need for continued surveillance, reported Dr. Hashem B. El-Serag, chief of the gastroenterology and hepatology section at Baylor College of Medicine, Houston.
In this study, data from the national Veterans Affairs (VA) health system were available for 10,730 patients who achieved SVR. When compared to 11,290 patients who did not achieve SVR, the risk of HCC was reduced by two thirds (hazard ratio, 0.358), but Dr. El-Serag labeled this finding “old news.” Instead, his focus was on the 100 cases of HCC identified after SVR over the course of 30,000 patient-years of follow-up.
While the annualized overall incidence of HCC after SVR was 0.32%, incidence rates ranged greatly by subgroup. For those with genotype 3 HCV at the time of SVR, the incidence was 0.558 cancers/year (versus 0.334 for genotype 1). A similar increase in HCC was observed in patients with diabetes (0.558/year). The rate climbed to 0.953/year for those who were age 65 years or older at the time of SVR.
The incidence of HCC was 1.54%/year in those with cirrhosis at the time of SVR, which was the highest rate among subgroups evaluated. This figure is notable because guidelines suggest that surveillance for HCC is justified for patients with an estimated annual risk of 1.5% per year, according to Dr. El-Serag.
“The presence of cirrhosis at SVR carried a 4.45 increase in the adjusted hazard ratio for HCC when compared to the absence of cirrhosis [P less than .0001],” he reported. Being 65 and older was associated with a nearly fivefold increase in hazard ratio of HCC compared with younger patients (HR 4.69; P = .0003), while the presence of diabetes was associated with a nearly twofold risk (HR 2.07; P = .0001).
It is notable that no concentration of cases of HCC was observed over the course of follow-up. Rather, there was a relatively equal distribution over time.
In addition to the known limitations of cohort studies, Dr. El-Serag cautioned that almost all SVRs in this database were achieved with interferon-based therapies. This is important, because the risk for HCC may differ when SVR is achieved with the newer direct-acting antivirals (DAAs). Another limitation is that most patients in the VA database are male.
However, the data strongly suggest that HCC risk after SVR differs markedly among subpopulations of HCV patients. While these findings have implications for considering continued surveillance of HCC, they also may be meaningful for timing of HCV therapy.
“It is obvious that if you treat and cure [patients early in the course of their disease and while they are young], your risk of HCC is much lower than if you treat late and old,” said Dr. El-Serag.
This is the first study to evaluate risk of HCC after SVR in a large and diverse population, according to Dr. El-Serag. The moderator of the oral session in which the report was presented, Dr. Joseph K. Lim, director of the viral hepatitis program at Yale University, New Haven, Conn., characterized the findings as “incredibly important.” Despite the frequency with which SVR is now being achieved with DAAs, these data confirm that some groups of patients may remain at substantial risk of HCV complications even after successful therapy.
Dr. El-Serag reeported that he has a financial relationship with Gilead.
SAN FRANCISCO – The risk of hepatocellular carcinoma remains sufficiently high in some subgroups who have achieved sustained virologic response to treatment to justify continued cancer surveillance, according to findings from a large cohort study presented at the annual meeting of the American Association for the Study of Liver Diseases.
The risk of hepatocellular carcinoma (HCC) after sustained virologic response (SVR) was relatively elevated in those who were infected with genotype 3 of the hepatitis C virus (HCV), those with diabetes, and those older than 65 years. But those who had cirrhosis at the time of SVR appear to have the highest risk and need for continued surveillance, reported Dr. Hashem B. El-Serag, chief of the gastroenterology and hepatology section at Baylor College of Medicine, Houston.
In this study, data from the national Veterans Affairs (VA) health system were available for 10,730 patients who achieved SVR. When compared to 11,290 patients who did not achieve SVR, the risk of HCC was reduced by two thirds (hazard ratio, 0.358), but Dr. El-Serag labeled this finding “old news.” Instead, his focus was on the 100 cases of HCC identified after SVR over the course of 30,000 patient-years of follow-up.
While the annualized overall incidence of HCC after SVR was 0.32%, incidence rates ranged greatly by subgroup. For those with genotype 3 HCV at the time of SVR, the incidence was 0.558 cancers/year (versus 0.334 for genotype 1). A similar increase in HCC was observed in patients with diabetes (0.558/year). The rate climbed to 0.953/year for those who were age 65 years or older at the time of SVR.
The incidence of HCC was 1.54%/year in those with cirrhosis at the time of SVR, which was the highest rate among subgroups evaluated. This figure is notable because guidelines suggest that surveillance for HCC is justified for patients with an estimated annual risk of 1.5% per year, according to Dr. El-Serag.
“The presence of cirrhosis at SVR carried a 4.45 increase in the adjusted hazard ratio for HCC when compared to the absence of cirrhosis [P less than .0001],” he reported. Being 65 and older was associated with a nearly fivefold increase in hazard ratio of HCC compared with younger patients (HR 4.69; P = .0003), while the presence of diabetes was associated with a nearly twofold risk (HR 2.07; P = .0001).
It is notable that no concentration of cases of HCC was observed over the course of follow-up. Rather, there was a relatively equal distribution over time.
In addition to the known limitations of cohort studies, Dr. El-Serag cautioned that almost all SVRs in this database were achieved with interferon-based therapies. This is important, because the risk for HCC may differ when SVR is achieved with the newer direct-acting antivirals (DAAs). Another limitation is that most patients in the VA database are male.
However, the data strongly suggest that HCC risk after SVR differs markedly among subpopulations of HCV patients. While these findings have implications for considering continued surveillance of HCC, they also may be meaningful for timing of HCV therapy.
“It is obvious that if you treat and cure [patients early in the course of their disease and while they are young], your risk of HCC is much lower than if you treat late and old,” said Dr. El-Serag.
This is the first study to evaluate risk of HCC after SVR in a large and diverse population, according to Dr. El-Serag. The moderator of the oral session in which the report was presented, Dr. Joseph K. Lim, director of the viral hepatitis program at Yale University, New Haven, Conn., characterized the findings as “incredibly important.” Despite the frequency with which SVR is now being achieved with DAAs, these data confirm that some groups of patients may remain at substantial risk of HCV complications even after successful therapy.
Dr. El-Serag reeported that he has a financial relationship with Gilead.
SAN FRANCISCO – The risk of hepatocellular carcinoma remains sufficiently high in some subgroups who have achieved sustained virologic response to treatment to justify continued cancer surveillance, according to findings from a large cohort study presented at the annual meeting of the American Association for the Study of Liver Diseases.
The risk of hepatocellular carcinoma (HCC) after sustained virologic response (SVR) was relatively elevated in those who were infected with genotype 3 of the hepatitis C virus (HCV), those with diabetes, and those older than 65 years. But those who had cirrhosis at the time of SVR appear to have the highest risk and need for continued surveillance, reported Dr. Hashem B. El-Serag, chief of the gastroenterology and hepatology section at Baylor College of Medicine, Houston.
In this study, data from the national Veterans Affairs (VA) health system were available for 10,730 patients who achieved SVR. When compared to 11,290 patients who did not achieve SVR, the risk of HCC was reduced by two thirds (hazard ratio, 0.358), but Dr. El-Serag labeled this finding “old news.” Instead, his focus was on the 100 cases of HCC identified after SVR over the course of 30,000 patient-years of follow-up.
While the annualized overall incidence of HCC after SVR was 0.32%, incidence rates ranged greatly by subgroup. For those with genotype 3 HCV at the time of SVR, the incidence was 0.558 cancers/year (versus 0.334 for genotype 1). A similar increase in HCC was observed in patients with diabetes (0.558/year). The rate climbed to 0.953/year for those who were age 65 years or older at the time of SVR.
The incidence of HCC was 1.54%/year in those with cirrhosis at the time of SVR, which was the highest rate among subgroups evaluated. This figure is notable because guidelines suggest that surveillance for HCC is justified for patients with an estimated annual risk of 1.5% per year, according to Dr. El-Serag.
“The presence of cirrhosis at SVR carried a 4.45 increase in the adjusted hazard ratio for HCC when compared to the absence of cirrhosis [P less than .0001],” he reported. Being 65 and older was associated with a nearly fivefold increase in hazard ratio of HCC compared with younger patients (HR 4.69; P = .0003), while the presence of diabetes was associated with a nearly twofold risk (HR 2.07; P = .0001).
It is notable that no concentration of cases of HCC was observed over the course of follow-up. Rather, there was a relatively equal distribution over time.
In addition to the known limitations of cohort studies, Dr. El-Serag cautioned that almost all SVRs in this database were achieved with interferon-based therapies. This is important, because the risk for HCC may differ when SVR is achieved with the newer direct-acting antivirals (DAAs). Another limitation is that most patients in the VA database are male.
However, the data strongly suggest that HCC risk after SVR differs markedly among subpopulations of HCV patients. While these findings have implications for considering continued surveillance of HCC, they also may be meaningful for timing of HCV therapy.
“It is obvious that if you treat and cure [patients early in the course of their disease and while they are young], your risk of HCC is much lower than if you treat late and old,” said Dr. El-Serag.
This is the first study to evaluate risk of HCC after SVR in a large and diverse population, according to Dr. El-Serag. The moderator of the oral session in which the report was presented, Dr. Joseph K. Lim, director of the viral hepatitis program at Yale University, New Haven, Conn., characterized the findings as “incredibly important.” Despite the frequency with which SVR is now being achieved with DAAs, these data confirm that some groups of patients may remain at substantial risk of HCV complications even after successful therapy.
Dr. El-Serag reeported that he has a financial relationship with Gilead.
AT THE LIVER MEETING 2015
Key clinical point: Elevated rates of hepatocellular carcinoma (HCC) remain elevated in patients with hepatitis C virus infection who achieved a sustained virologic response.
Major finding: In a VA database, the overall risk of HCC after SVR was 0.3% per year but was higher among the elderly, those with diabetes, and those with cirrhosis.
Data source: Retrospective cohort study performed with a large database.
Disclosures: Dr. El-Serag has a financial relationship with Gilead.
Gastrointestinal and liver diseases remain substantial public health burden
Diseases such as Clostridium difficile infection, inflammatory bowel disease, and liver cancer continue to cost billions and cause many thousands of deaths in the United States every year, investigators reported in the December issue of Gastroenterology.
“Gastrointestinal and liver diseases are a source of substantial burden and cost,” said Dr. Anne Peery and her associates at the University of North Carolina School of Medicine and the Gillings School of Public Health, both in Chapel Hill. The Affordable Care Act has extended health insurance to more than 16 million Americans, which is “expected to change the landscape of care for GI illnesses” and intensifies the need for their comprehensive study, the researchers added.
They analyzed health care visits, costs, and deaths from GI, pancreatic, and hepatic diseases for 2007 through 2012 by using surveillance data from the Centers for Disease Control and Prevention, the Agency for Healthcare Research and Quality, and the National Cancer Institute. Chronic hepatitis C virus infection was a leading disease burden, they found. Associated emergency department visits rose by 176% between 2006 and 2012, hospital admissions increased by 225% between 2003 and 2012, and in-hospital mortality approached 6%. These trends reflect the aging of baby boomers, who make up three-quarters of infected patients, the investigators noted. As a result, rates of new liver cancers also are rising, and end-stage liver disease is expected to keep increasing until 2030, they added (Gastroenterology. 2015 Aug 20. doi: 10.1053/j.gastro.2015.08.045). Aging boomers are increasingly seeking care for other age-related GI disorders, the investigators reported. Outpatient visits for hemorrhoids are rising, as are emergency department visits for constipation and lower-GI bleeding, and hospitalizations for acute diverticulitis and C. difficile infection. Gastrointestinal hemorrhage was the most common diagnosis at hospitalization, accounting for more than 500,000 discharges and costing almost $5 billion dollars in 2012 alone, the researchers said.
Despite better treatments, hospital admissions for Crohn’s disease and ulcerative colitis also rose from less than 60,000 in 1993 to about 100,000 in 2012, said Dr. Peery and her associates. “This is congruent with earlier trends using the National Hospital Discharge Survey. Emergency department visits [for inflammatory bowel disease] are also rising,” they added.
In contrast, cases and deaths from colorectal cancer continue to drop, partly because of intensified screening efforts, the investigators said. They called the trend “encouraging,” but noted that CRC still tops cancers of the pancreas, liver, and intrahepatic bile ducts as the leading GI cause of mortality in the United States. In 2012, more than 51,000 Americans died from CRC, and screening efforts captured only 58% of those between 50 and 75 years old. Boosting that percentage to 80% by 2018 http://nccrt.org/tools/80-percent-by-2018/ could prevent 280,000 CRC cases and 200,000 deaths within 20 years, Dr. Peery and her associates noted.
The National Institutes of Health helped fund the work. The investigators reported having no conflicts of interest.
Source: American Gastroenterological Association
In the excellent study by Peery and colleagues, statistics on health care utilization in the ambulatory and hospital settings, incidence and mortality from GI cancers, and mortality associated with other GI illnesses from 2007 to 2012 was collected using data from multiple complementary databases. This is the ideal methodology for this type of study because it quantifies utilization data from several complementary national databases. Of course, these data may be limited by systematic errors in ICD coding and costs are estimated using Medicare’s cost-to-charge ratio. Nevertheless, these data provide the best “snap shot” of trends in the burden of gastrointestinal and liver illness as of 2012.
What are the key points? First, the increase in the burden of GI and liver illness probably reflects the aging of the “baby boomer” population. Furthermore, since the Affordable Care Act is expanding access to health care, the burden on gastroenterologists is also likely to expand. Second, although we’re doing a good job with CRC screening, there is also room for improvement. While the incidence of CRC continues to decrease, only 58% of adults aged 50-75 years old had CRC screening in 2010. Third, HCV-associated hospitalizations have doubled from 2003 to 2012. Since HCV-associated cirrhosis is likely to increase until 2030, insurers and public health officials will have to carefully weigh the initial high cost of using new and highly effective regimens of direct-acting antiviral agents versus the downstream costs of managing these individuals after developing decompensated cirrhosis.
Dr. Philip S. Schoenfeld is professor of medicine and director, training program in GI epidemiology, division of gastroenterology, University of Michigan, Ann Arbor. He has no conflicts of interest.
In the excellent study by Peery and colleagues, statistics on health care utilization in the ambulatory and hospital settings, incidence and mortality from GI cancers, and mortality associated with other GI illnesses from 2007 to 2012 was collected using data from multiple complementary databases. This is the ideal methodology for this type of study because it quantifies utilization data from several complementary national databases. Of course, these data may be limited by systematic errors in ICD coding and costs are estimated using Medicare’s cost-to-charge ratio. Nevertheless, these data provide the best “snap shot” of trends in the burden of gastrointestinal and liver illness as of 2012.
What are the key points? First, the increase in the burden of GI and liver illness probably reflects the aging of the “baby boomer” population. Furthermore, since the Affordable Care Act is expanding access to health care, the burden on gastroenterologists is also likely to expand. Second, although we’re doing a good job with CRC screening, there is also room for improvement. While the incidence of CRC continues to decrease, only 58% of adults aged 50-75 years old had CRC screening in 2010. Third, HCV-associated hospitalizations have doubled from 2003 to 2012. Since HCV-associated cirrhosis is likely to increase until 2030, insurers and public health officials will have to carefully weigh the initial high cost of using new and highly effective regimens of direct-acting antiviral agents versus the downstream costs of managing these individuals after developing decompensated cirrhosis.
Dr. Philip S. Schoenfeld is professor of medicine and director, training program in GI epidemiology, division of gastroenterology, University of Michigan, Ann Arbor. He has no conflicts of interest.
In the excellent study by Peery and colleagues, statistics on health care utilization in the ambulatory and hospital settings, incidence and mortality from GI cancers, and mortality associated with other GI illnesses from 2007 to 2012 was collected using data from multiple complementary databases. This is the ideal methodology for this type of study because it quantifies utilization data from several complementary national databases. Of course, these data may be limited by systematic errors in ICD coding and costs are estimated using Medicare’s cost-to-charge ratio. Nevertheless, these data provide the best “snap shot” of trends in the burden of gastrointestinal and liver illness as of 2012.
What are the key points? First, the increase in the burden of GI and liver illness probably reflects the aging of the “baby boomer” population. Furthermore, since the Affordable Care Act is expanding access to health care, the burden on gastroenterologists is also likely to expand. Second, although we’re doing a good job with CRC screening, there is also room for improvement. While the incidence of CRC continues to decrease, only 58% of adults aged 50-75 years old had CRC screening in 2010. Third, HCV-associated hospitalizations have doubled from 2003 to 2012. Since HCV-associated cirrhosis is likely to increase until 2030, insurers and public health officials will have to carefully weigh the initial high cost of using new and highly effective regimens of direct-acting antiviral agents versus the downstream costs of managing these individuals after developing decompensated cirrhosis.
Dr. Philip S. Schoenfeld is professor of medicine and director, training program in GI epidemiology, division of gastroenterology, University of Michigan, Ann Arbor. He has no conflicts of interest.
Diseases such as Clostridium difficile infection, inflammatory bowel disease, and liver cancer continue to cost billions and cause many thousands of deaths in the United States every year, investigators reported in the December issue of Gastroenterology.
“Gastrointestinal and liver diseases are a source of substantial burden and cost,” said Dr. Anne Peery and her associates at the University of North Carolina School of Medicine and the Gillings School of Public Health, both in Chapel Hill. The Affordable Care Act has extended health insurance to more than 16 million Americans, which is “expected to change the landscape of care for GI illnesses” and intensifies the need for their comprehensive study, the researchers added.
They analyzed health care visits, costs, and deaths from GI, pancreatic, and hepatic diseases for 2007 through 2012 by using surveillance data from the Centers for Disease Control and Prevention, the Agency for Healthcare Research and Quality, and the National Cancer Institute. Chronic hepatitis C virus infection was a leading disease burden, they found. Associated emergency department visits rose by 176% between 2006 and 2012, hospital admissions increased by 225% between 2003 and 2012, and in-hospital mortality approached 6%. These trends reflect the aging of baby boomers, who make up three-quarters of infected patients, the investigators noted. As a result, rates of new liver cancers also are rising, and end-stage liver disease is expected to keep increasing until 2030, they added (Gastroenterology. 2015 Aug 20. doi: 10.1053/j.gastro.2015.08.045). Aging boomers are increasingly seeking care for other age-related GI disorders, the investigators reported. Outpatient visits for hemorrhoids are rising, as are emergency department visits for constipation and lower-GI bleeding, and hospitalizations for acute diverticulitis and C. difficile infection. Gastrointestinal hemorrhage was the most common diagnosis at hospitalization, accounting for more than 500,000 discharges and costing almost $5 billion dollars in 2012 alone, the researchers said.
Despite better treatments, hospital admissions for Crohn’s disease and ulcerative colitis also rose from less than 60,000 in 1993 to about 100,000 in 2012, said Dr. Peery and her associates. “This is congruent with earlier trends using the National Hospital Discharge Survey. Emergency department visits [for inflammatory bowel disease] are also rising,” they added.
In contrast, cases and deaths from colorectal cancer continue to drop, partly because of intensified screening efforts, the investigators said. They called the trend “encouraging,” but noted that CRC still tops cancers of the pancreas, liver, and intrahepatic bile ducts as the leading GI cause of mortality in the United States. In 2012, more than 51,000 Americans died from CRC, and screening efforts captured only 58% of those between 50 and 75 years old. Boosting that percentage to 80% by 2018 http://nccrt.org/tools/80-percent-by-2018/ could prevent 280,000 CRC cases and 200,000 deaths within 20 years, Dr. Peery and her associates noted.
The National Institutes of Health helped fund the work. The investigators reported having no conflicts of interest.
Source: American Gastroenterological Association
Diseases such as Clostridium difficile infection, inflammatory bowel disease, and liver cancer continue to cost billions and cause many thousands of deaths in the United States every year, investigators reported in the December issue of Gastroenterology.
“Gastrointestinal and liver diseases are a source of substantial burden and cost,” said Dr. Anne Peery and her associates at the University of North Carolina School of Medicine and the Gillings School of Public Health, both in Chapel Hill. The Affordable Care Act has extended health insurance to more than 16 million Americans, which is “expected to change the landscape of care for GI illnesses” and intensifies the need for their comprehensive study, the researchers added.
They analyzed health care visits, costs, and deaths from GI, pancreatic, and hepatic diseases for 2007 through 2012 by using surveillance data from the Centers for Disease Control and Prevention, the Agency for Healthcare Research and Quality, and the National Cancer Institute. Chronic hepatitis C virus infection was a leading disease burden, they found. Associated emergency department visits rose by 176% between 2006 and 2012, hospital admissions increased by 225% between 2003 and 2012, and in-hospital mortality approached 6%. These trends reflect the aging of baby boomers, who make up three-quarters of infected patients, the investigators noted. As a result, rates of new liver cancers also are rising, and end-stage liver disease is expected to keep increasing until 2030, they added (Gastroenterology. 2015 Aug 20. doi: 10.1053/j.gastro.2015.08.045). Aging boomers are increasingly seeking care for other age-related GI disorders, the investigators reported. Outpatient visits for hemorrhoids are rising, as are emergency department visits for constipation and lower-GI bleeding, and hospitalizations for acute diverticulitis and C. difficile infection. Gastrointestinal hemorrhage was the most common diagnosis at hospitalization, accounting for more than 500,000 discharges and costing almost $5 billion dollars in 2012 alone, the researchers said.
Despite better treatments, hospital admissions for Crohn’s disease and ulcerative colitis also rose from less than 60,000 in 1993 to about 100,000 in 2012, said Dr. Peery and her associates. “This is congruent with earlier trends using the National Hospital Discharge Survey. Emergency department visits [for inflammatory bowel disease] are also rising,” they added.
In contrast, cases and deaths from colorectal cancer continue to drop, partly because of intensified screening efforts, the investigators said. They called the trend “encouraging,” but noted that CRC still tops cancers of the pancreas, liver, and intrahepatic bile ducts as the leading GI cause of mortality in the United States. In 2012, more than 51,000 Americans died from CRC, and screening efforts captured only 58% of those between 50 and 75 years old. Boosting that percentage to 80% by 2018 http://nccrt.org/tools/80-percent-by-2018/ could prevent 280,000 CRC cases and 200,000 deaths within 20 years, Dr. Peery and her associates noted.
The National Institutes of Health helped fund the work. The investigators reported having no conflicts of interest.
Source: American Gastroenterological Association
FROM GASTROENTEROLOGY
Key clinical point: Gastrointestinal and liver diseases remain a major cause of health care utilization and associated costs in the United States.
Major finding: Hospital admissions and associated costs for Clostridium difficile infection, inflammatory bowel disease, and liver disease all rose substantially between 1993 and 2012.
Data source: Analysis of surveillance data from the Centers for Disease Control and Prevention, Agency for Healthcare Research and Quality, and National Cancer Institute.
Disclosures: The National Institutes of Health helped fund the work. The investigators reported having no conflicts of interest.
IDWeek: Despite better drugs, HCV deaths keep rising
SAN DIEGO – Despite better therapies, deaths from hepatitis C virus (HCV) infection continue to rise, indicating poor penetrance of medications and care to patients who need them, Dr. Scott Holmberg said at an annual scientific meeting on infectious diseases.
“Deaths in chronic HCV–infected persons, even when grossly under-enumerated on death certificates, far outstrip deaths from 60 other infectious conditions reportable to CDC,” said Dr. Holmberg of the Centers for Disease Control and Prevention Division of Viral Hepatitis in Atlanta.
Drugs for chronic HCV infection have vastly improved in the past several years, yielding far better rates of sustained viral response (SVR) and high chances of cure after 8-24 weeks of treatment. To see if better antiviral therapies have affected HCV mortality rates, Dr. Holmberg and his associates studied ICD-9 data from Multiple Cause of Death records for all U.S. death certificates between 2003 and 2013. They divided deaths that were linked to HCV or 60 other nationally notifiable infectious diseases by U.S. Census numbers for the same year. They also examined data from the Chronic Hepatitis Cohort Study (Clin Infect Dis. 2014;58:1055-61), which includes patients presumed to have adequate access to HCV treatment.
Chronic HCV-related deaths climbed from about 12,000 annually in 2003 to more than 19,000 in 2013, said Dr. Holmberg. In contrast, deaths from the 60 other reportable infectious diseases dropped from about 25,000 annually to below 20,000 per year. Annual deaths tied to HIV infection ranked second behind HCV at about 8,800, followed by Staphylococcus aureus (including MRSA), hepatitis B virus, tuberculosis, and pneumococcal disease. “This does not include 4,444 adult influenza deaths, but does include 165 childhood influenza deaths in 2013,” Dr. Holmberg noted.
The analysis of the Chronic Hepatitis Cohort Study revealed a doubling in mortality from chronic HCV infection among patients who should have had adequate access to treatment, according to Dr. Holmberg. For every 100 person-years of observation, about 2.5 people died from consequences of chronic HCV infection in 2007, compared with about 5.5 in 2013, he said. “Hidden mortality from HCV is considerable,” he added. “Only 19% of HCV patients who died had their infection noted anywhere on their death certificates, despite the fact that more than 75% had premortem evidence of liver disease.”
Uptake of sofosbuvir-based regimens more than quintupled in the second quarter of 2015, compared with a year earlier, according to data from Gilead Sciences presented by Dr. Holmberg. But high drug costs have spurred state Medicaid programs and private payers to stipulate many preapproval requirements, he noted. Patients must be drug and alcohol free for at least 6 months, and in many states, must provide evidence of liver scarring from a recent biopsy or FibroScan, which is not always easy to access. “This is often a barrier,” Dr. Holmberg said. “For those in more rural areas, finding a specialist, as required by many state Medicaid offices, can be very difficult.”
And there are even more obstacles. Many clinicians still see HCV as a “benign condition,” and patients often have other urgent health, social, or financial problems, Dr. Holmberg said. The public, for its part, may not prioritize infectious diseases. “These patients lack a strong advocacy group,” he added. “Most are former injection drug users, and the public is often reluctant to help them.”
So what are the measurable results of these barriers? Among about 3.2 million individuals in the United States with chronic HCV infection, only half were ever tested for HCV, 38% received some sort of care related to their infection, 11% were treated, and 6% achieved SVR, Dr. Holmberg and his associates noted in a perspective piece (N Engl J Med. 2013;368:1859-861).
At the same time, the United States faces an emerging epidemic of new HCV infections in nonurban areas among young persons who inject drugs (MMWR. 64;453-8). “This is really a tale of two epidemics,” he added. “Control of the chronic and the acute outbreaks will require a multipronged approach, with interventions along a testing to cure continuum of care.”
Dr. Holmberg and his associates reported their findings at the combined annual meetings of the Infectious Diseases Society of America, the Society for Healthcare Epidemiology of America, the HIV Medicine Association, and the Pediatric Infectious Diseases Society. The researchers reported no funding sources and had no financial disclosures.
SAN DIEGO – Despite better therapies, deaths from hepatitis C virus (HCV) infection continue to rise, indicating poor penetrance of medications and care to patients who need them, Dr. Scott Holmberg said at an annual scientific meeting on infectious diseases.
“Deaths in chronic HCV–infected persons, even when grossly under-enumerated on death certificates, far outstrip deaths from 60 other infectious conditions reportable to CDC,” said Dr. Holmberg of the Centers for Disease Control and Prevention Division of Viral Hepatitis in Atlanta.
Drugs for chronic HCV infection have vastly improved in the past several years, yielding far better rates of sustained viral response (SVR) and high chances of cure after 8-24 weeks of treatment. To see if better antiviral therapies have affected HCV mortality rates, Dr. Holmberg and his associates studied ICD-9 data from Multiple Cause of Death records for all U.S. death certificates between 2003 and 2013. They divided deaths that were linked to HCV or 60 other nationally notifiable infectious diseases by U.S. Census numbers for the same year. They also examined data from the Chronic Hepatitis Cohort Study (Clin Infect Dis. 2014;58:1055-61), which includes patients presumed to have adequate access to HCV treatment.
Chronic HCV-related deaths climbed from about 12,000 annually in 2003 to more than 19,000 in 2013, said Dr. Holmberg. In contrast, deaths from the 60 other reportable infectious diseases dropped from about 25,000 annually to below 20,000 per year. Annual deaths tied to HIV infection ranked second behind HCV at about 8,800, followed by Staphylococcus aureus (including MRSA), hepatitis B virus, tuberculosis, and pneumococcal disease. “This does not include 4,444 adult influenza deaths, but does include 165 childhood influenza deaths in 2013,” Dr. Holmberg noted.
The analysis of the Chronic Hepatitis Cohort Study revealed a doubling in mortality from chronic HCV infection among patients who should have had adequate access to treatment, according to Dr. Holmberg. For every 100 person-years of observation, about 2.5 people died from consequences of chronic HCV infection in 2007, compared with about 5.5 in 2013, he said. “Hidden mortality from HCV is considerable,” he added. “Only 19% of HCV patients who died had their infection noted anywhere on their death certificates, despite the fact that more than 75% had premortem evidence of liver disease.”
Uptake of sofosbuvir-based regimens more than quintupled in the second quarter of 2015, compared with a year earlier, according to data from Gilead Sciences presented by Dr. Holmberg. But high drug costs have spurred state Medicaid programs and private payers to stipulate many preapproval requirements, he noted. Patients must be drug and alcohol free for at least 6 months, and in many states, must provide evidence of liver scarring from a recent biopsy or FibroScan, which is not always easy to access. “This is often a barrier,” Dr. Holmberg said. “For those in more rural areas, finding a specialist, as required by many state Medicaid offices, can be very difficult.”
And there are even more obstacles. Many clinicians still see HCV as a “benign condition,” and patients often have other urgent health, social, or financial problems, Dr. Holmberg said. The public, for its part, may not prioritize infectious diseases. “These patients lack a strong advocacy group,” he added. “Most are former injection drug users, and the public is often reluctant to help them.”
So what are the measurable results of these barriers? Among about 3.2 million individuals in the United States with chronic HCV infection, only half were ever tested for HCV, 38% received some sort of care related to their infection, 11% were treated, and 6% achieved SVR, Dr. Holmberg and his associates noted in a perspective piece (N Engl J Med. 2013;368:1859-861).
At the same time, the United States faces an emerging epidemic of new HCV infections in nonurban areas among young persons who inject drugs (MMWR. 64;453-8). “This is really a tale of two epidemics,” he added. “Control of the chronic and the acute outbreaks will require a multipronged approach, with interventions along a testing to cure continuum of care.”
Dr. Holmberg and his associates reported their findings at the combined annual meetings of the Infectious Diseases Society of America, the Society for Healthcare Epidemiology of America, the HIV Medicine Association, and the Pediatric Infectious Diseases Society. The researchers reported no funding sources and had no financial disclosures.
SAN DIEGO – Despite better therapies, deaths from hepatitis C virus (HCV) infection continue to rise, indicating poor penetrance of medications and care to patients who need them, Dr. Scott Holmberg said at an annual scientific meeting on infectious diseases.
“Deaths in chronic HCV–infected persons, even when grossly under-enumerated on death certificates, far outstrip deaths from 60 other infectious conditions reportable to CDC,” said Dr. Holmberg of the Centers for Disease Control and Prevention Division of Viral Hepatitis in Atlanta.
Drugs for chronic HCV infection have vastly improved in the past several years, yielding far better rates of sustained viral response (SVR) and high chances of cure after 8-24 weeks of treatment. To see if better antiviral therapies have affected HCV mortality rates, Dr. Holmberg and his associates studied ICD-9 data from Multiple Cause of Death records for all U.S. death certificates between 2003 and 2013. They divided deaths that were linked to HCV or 60 other nationally notifiable infectious diseases by U.S. Census numbers for the same year. They also examined data from the Chronic Hepatitis Cohort Study (Clin Infect Dis. 2014;58:1055-61), which includes patients presumed to have adequate access to HCV treatment.
Chronic HCV-related deaths climbed from about 12,000 annually in 2003 to more than 19,000 in 2013, said Dr. Holmberg. In contrast, deaths from the 60 other reportable infectious diseases dropped from about 25,000 annually to below 20,000 per year. Annual deaths tied to HIV infection ranked second behind HCV at about 8,800, followed by Staphylococcus aureus (including MRSA), hepatitis B virus, tuberculosis, and pneumococcal disease. “This does not include 4,444 adult influenza deaths, but does include 165 childhood influenza deaths in 2013,” Dr. Holmberg noted.
The analysis of the Chronic Hepatitis Cohort Study revealed a doubling in mortality from chronic HCV infection among patients who should have had adequate access to treatment, according to Dr. Holmberg. For every 100 person-years of observation, about 2.5 people died from consequences of chronic HCV infection in 2007, compared with about 5.5 in 2013, he said. “Hidden mortality from HCV is considerable,” he added. “Only 19% of HCV patients who died had their infection noted anywhere on their death certificates, despite the fact that more than 75% had premortem evidence of liver disease.”
Uptake of sofosbuvir-based regimens more than quintupled in the second quarter of 2015, compared with a year earlier, according to data from Gilead Sciences presented by Dr. Holmberg. But high drug costs have spurred state Medicaid programs and private payers to stipulate many preapproval requirements, he noted. Patients must be drug and alcohol free for at least 6 months, and in many states, must provide evidence of liver scarring from a recent biopsy or FibroScan, which is not always easy to access. “This is often a barrier,” Dr. Holmberg said. “For those in more rural areas, finding a specialist, as required by many state Medicaid offices, can be very difficult.”
And there are even more obstacles. Many clinicians still see HCV as a “benign condition,” and patients often have other urgent health, social, or financial problems, Dr. Holmberg said. The public, for its part, may not prioritize infectious diseases. “These patients lack a strong advocacy group,” he added. “Most are former injection drug users, and the public is often reluctant to help them.”
So what are the measurable results of these barriers? Among about 3.2 million individuals in the United States with chronic HCV infection, only half were ever tested for HCV, 38% received some sort of care related to their infection, 11% were treated, and 6% achieved SVR, Dr. Holmberg and his associates noted in a perspective piece (N Engl J Med. 2013;368:1859-861).
At the same time, the United States faces an emerging epidemic of new HCV infections in nonurban areas among young persons who inject drugs (MMWR. 64;453-8). “This is really a tale of two epidemics,” he added. “Control of the chronic and the acute outbreaks will require a multipronged approach, with interventions along a testing to cure continuum of care.”
Dr. Holmberg and his associates reported their findings at the combined annual meetings of the Infectious Diseases Society of America, the Society for Healthcare Epidemiology of America, the HIV Medicine Association, and the Pediatric Infectious Diseases Society. The researchers reported no funding sources and had no financial disclosures.
AT IDWEEK 2015
Key clinical point: Mortality from chronic hepatitis C virus infection continues to rise, despite significant improvements in antiviral therapies.
Major finding: Even with substantial underreporting, in 2013, deaths tied to chronic HCV infection exceeded mortality from 60 other reportable infectious diseases.
Data source: Analysis of 10 years of national death certificate data and 7 years of data from the Chronic Hepatitis Cohort Study.
Disclosures: The researchers reported no funding sources and made no financial disclosures.
High ALT/AST ratio linked to fatty liver risk in HCV
Individuals infected with the hepatitis C virus who have a higher ratio of alanine aminotransferase to aspartate aminotransferase may be at greater risk of developing nonalcoholic fatty liver disease and hepatosteatosis, new data suggest.
A community-based observational study in 1,354 Taiwanese individuals seropositive for hepatitis C virus – including 433 with nonalcoholic fatty liver disease – found a high alanine aminotransferase to aspartate aminotransferase ratio was significantly and independently associated with nonalcoholic fatty liver disease (OR, 1.90; 95% CI, 1.37 to 2.65; P less than .001) and high-degree nonalcoholic fatty liver disease (OR, 2.44; 95% CI, 1.58 to 3.77; P less than .001).
This effect was observed even after researchers accounted for potential confounders: age, body mass index, metabolic syndrome, cholesterol level, hepatitis B virus infection, and smoking.
The study found the ALT/AST ratio was significantly higher among patients with nonalcoholic fatty liver disease (1.2 ± 0.4 vs. 1.1 ± 0.4; P less than .001) – defined as hepatic steatosis by echogenic imaging – according to a paper published online Sept. 14 in BMJ Open.
Nonalcoholic fatty liver disease is a particular issue because not only can it progress to severe liver disease but it is also associated with a lower likelihood of achieving a sustained virologic response to antiviral therapy. In addition, the majority of cases of nonalcoholic fatty liver disease are silent and are discovered incidentally, the authors wrote.
“This is the first study to reveal a strong relationship between the ALT/AST ratio and NAFLD in patients with HCV, and the ALT/AST ratio was also an independent risk factor apart from the conventional risk factors for hepatosteatosis including the MetS [metabolic syndrome], LDL, TC, waist/hip ratio, and body mass index,” wrote Dr. Ming-Shyan Lin of Chang Gung Memorial Hospital, Taiwan, and coauthors.
While the AST/ALT ratio is a marker of liver cirrhosis and advanced liver disease, the ALT/AST ratio is also a marker for insulin resistance and metabolic syndrome.
Researchers also noted that individuals with hepatitis C infection and nonalcoholic fatty liver disease had a significantly higher incidence of metabolic syndrome, significantly higher fasting glucose, uric acid, and triglycerides, and a lower HDL than did those with low-degree nonalcoholic fatty liver disease.
“The prevalence of hepatosteatosis in chronic hepatitis C infection has been reported in up to 31%-72%, which is significantly higher than that in participants with other chronic liver disease such as hepatitis B or autoimmune hepatitis, suggesting a direct effect of HCV replication in the development of excess fat accumulation in the liver,” the authors wrote.
In this cohort, the prevalence of nonalcoholic fatty liver disease was 31.9%, and 19.6% of participants had moderate to severe hepatosteatosis (BMJ Open 2015, Sep 14. doi:10.1136/bmjopen-2015-008797).
Given the silent nature of nonalcoholic fatty liver disease, the authors suggested that the findings could help clinicians identify individuals with hepatosteatosis and implement interventions such as weight loss to reduce their risk of further progression.
No conflicts of interest were declared.
Individuals infected with the hepatitis C virus who have a higher ratio of alanine aminotransferase to aspartate aminotransferase may be at greater risk of developing nonalcoholic fatty liver disease and hepatosteatosis, new data suggest.
A community-based observational study in 1,354 Taiwanese individuals seropositive for hepatitis C virus – including 433 with nonalcoholic fatty liver disease – found a high alanine aminotransferase to aspartate aminotransferase ratio was significantly and independently associated with nonalcoholic fatty liver disease (OR, 1.90; 95% CI, 1.37 to 2.65; P less than .001) and high-degree nonalcoholic fatty liver disease (OR, 2.44; 95% CI, 1.58 to 3.77; P less than .001).
This effect was observed even after researchers accounted for potential confounders: age, body mass index, metabolic syndrome, cholesterol level, hepatitis B virus infection, and smoking.
The study found the ALT/AST ratio was significantly higher among patients with nonalcoholic fatty liver disease (1.2 ± 0.4 vs. 1.1 ± 0.4; P less than .001) – defined as hepatic steatosis by echogenic imaging – according to a paper published online Sept. 14 in BMJ Open.
Nonalcoholic fatty liver disease is a particular issue because not only can it progress to severe liver disease but it is also associated with a lower likelihood of achieving a sustained virologic response to antiviral therapy. In addition, the majority of cases of nonalcoholic fatty liver disease are silent and are discovered incidentally, the authors wrote.
“This is the first study to reveal a strong relationship between the ALT/AST ratio and NAFLD in patients with HCV, and the ALT/AST ratio was also an independent risk factor apart from the conventional risk factors for hepatosteatosis including the MetS [metabolic syndrome], LDL, TC, waist/hip ratio, and body mass index,” wrote Dr. Ming-Shyan Lin of Chang Gung Memorial Hospital, Taiwan, and coauthors.
While the AST/ALT ratio is a marker of liver cirrhosis and advanced liver disease, the ALT/AST ratio is also a marker for insulin resistance and metabolic syndrome.
Researchers also noted that individuals with hepatitis C infection and nonalcoholic fatty liver disease had a significantly higher incidence of metabolic syndrome, significantly higher fasting glucose, uric acid, and triglycerides, and a lower HDL than did those with low-degree nonalcoholic fatty liver disease.
“The prevalence of hepatosteatosis in chronic hepatitis C infection has been reported in up to 31%-72%, which is significantly higher than that in participants with other chronic liver disease such as hepatitis B or autoimmune hepatitis, suggesting a direct effect of HCV replication in the development of excess fat accumulation in the liver,” the authors wrote.
In this cohort, the prevalence of nonalcoholic fatty liver disease was 31.9%, and 19.6% of participants had moderate to severe hepatosteatosis (BMJ Open 2015, Sep 14. doi:10.1136/bmjopen-2015-008797).
Given the silent nature of nonalcoholic fatty liver disease, the authors suggested that the findings could help clinicians identify individuals with hepatosteatosis and implement interventions such as weight loss to reduce their risk of further progression.
No conflicts of interest were declared.
Individuals infected with the hepatitis C virus who have a higher ratio of alanine aminotransferase to aspartate aminotransferase may be at greater risk of developing nonalcoholic fatty liver disease and hepatosteatosis, new data suggest.
A community-based observational study in 1,354 Taiwanese individuals seropositive for hepatitis C virus – including 433 with nonalcoholic fatty liver disease – found a high alanine aminotransferase to aspartate aminotransferase ratio was significantly and independently associated with nonalcoholic fatty liver disease (OR, 1.90; 95% CI, 1.37 to 2.65; P less than .001) and high-degree nonalcoholic fatty liver disease (OR, 2.44; 95% CI, 1.58 to 3.77; P less than .001).
This effect was observed even after researchers accounted for potential confounders: age, body mass index, metabolic syndrome, cholesterol level, hepatitis B virus infection, and smoking.
The study found the ALT/AST ratio was significantly higher among patients with nonalcoholic fatty liver disease (1.2 ± 0.4 vs. 1.1 ± 0.4; P less than .001) – defined as hepatic steatosis by echogenic imaging – according to a paper published online Sept. 14 in BMJ Open.
Nonalcoholic fatty liver disease is a particular issue because not only can it progress to severe liver disease but it is also associated with a lower likelihood of achieving a sustained virologic response to antiviral therapy. In addition, the majority of cases of nonalcoholic fatty liver disease are silent and are discovered incidentally, the authors wrote.
“This is the first study to reveal a strong relationship between the ALT/AST ratio and NAFLD in patients with HCV, and the ALT/AST ratio was also an independent risk factor apart from the conventional risk factors for hepatosteatosis including the MetS [metabolic syndrome], LDL, TC, waist/hip ratio, and body mass index,” wrote Dr. Ming-Shyan Lin of Chang Gung Memorial Hospital, Taiwan, and coauthors.
While the AST/ALT ratio is a marker of liver cirrhosis and advanced liver disease, the ALT/AST ratio is also a marker for insulin resistance and metabolic syndrome.
Researchers also noted that individuals with hepatitis C infection and nonalcoholic fatty liver disease had a significantly higher incidence of metabolic syndrome, significantly higher fasting glucose, uric acid, and triglycerides, and a lower HDL than did those with low-degree nonalcoholic fatty liver disease.
“The prevalence of hepatosteatosis in chronic hepatitis C infection has been reported in up to 31%-72%, which is significantly higher than that in participants with other chronic liver disease such as hepatitis B or autoimmune hepatitis, suggesting a direct effect of HCV replication in the development of excess fat accumulation in the liver,” the authors wrote.
In this cohort, the prevalence of nonalcoholic fatty liver disease was 31.9%, and 19.6% of participants had moderate to severe hepatosteatosis (BMJ Open 2015, Sep 14. doi:10.1136/bmjopen-2015-008797).
Given the silent nature of nonalcoholic fatty liver disease, the authors suggested that the findings could help clinicians identify individuals with hepatosteatosis and implement interventions such as weight loss to reduce their risk of further progression.
No conflicts of interest were declared.
FROM BMJ OPEN
Key clinical point: A higher ratio of alanine aminotransferase to aspartate aminotransferase in individuals seropositive for hepatitis C virus may be associated with nonalcoholic fatty liver disease.
Major finding: A high ALT/AST ratio was significantly and independently associated with nonalcoholic fatty liver disease.
Data source: A community-based observational study in 1354 Taiwanese individuals seropositive for hepatitis C virus.
Disclosures: No conflicts of interest were declared.
Nonalcoholic hepatic steatosis a key indicator for liver transplant
Chronic nonmalignant liver disease is on the rise in the United States in part because of increasing incidence of nonalcoholic fatty liver disease, according to a report published online in Clinical Gastroenterology and Hepatology.
Nearly 2 million deaths each year in the United States are linked to chronic liver disease and recently, the overall mortality rate has been increasing, wrote Dr. Prowpanga Udompap and colleagues in the division of gastroenterology and hepatology at Stanford (Calif.) University.
Chronic liver disease can be caused by a number of factors, such as hepatitis B and hepatitis C infection, alcohol consumption, diabetes, and metabolic syndrome. “In general, HBV infection tends to have a large burden in resource-limited countries and nonalcoholic fatty liver disease (NAFLD) in more established economies, whereas HCV infection and alcohol use are prevalent throughout,” the researchers wrote.
In the United States, chronic liver disease and cirrhosis are the 12th leading cause of death, claiming more than 36,000 lives in 2013 – representing 1.4% of all deaths that year – and the prevalence of cirrhosis is estimated to be approximately 0.27% (Clin Gastroenterol Hepatol. 2015, Aug 17. doi: 10.1016/j.cgh.2015.08.015).
The mortality rate from chronic liver disease and cirrhosis has increased from 9.4 deaths per 100,000 in 1999 to 11.5 in 2013, but the increase is particularly evident in individuals aged 55-64 years, which the authors attributed to aging of the HCV birth cohort.
“Projection studies have estimated that although the incidence of new HCV infection in the United States decreased over time, the number of individuals living with advanced fibrosis and cirrhosis will rise as the birth cohort of baby boomers with HCV infection grows older and their duration of infection reaches long enough time for their liver fibrosis to have progressed to cirrhosis,” the authors wrote.
While estimates for the prevalence of nonalcoholic fatty liver disease in the United States vary significantly because of differences in test sensitivities, a study based on NHANES data suggested the incidence of ultrasound-diagnosed nonalcoholic hepatic steatosis (NASH) could be as high as 34%.
Patients with NASH have a higher risk of progression to cirrhosis than do patients with nonalcoholic fatty liver disease; one study found an incidence of 3.1% for incident cirrhosis over a 7.6-year follow-up of patients with NASH.
“NASH is quickly becoming a major etiology in liver transplantation in the United States, and it may soon become the most common indication,” the authors wrote.
Alcoholic liver disease is another global health problem, and in 2013, 7% of American adults were estimated to have an alcohol use disorder.
Given 30%-45% of individuals with chronic alcohol use disorder will develop alcoholic hepatitis at some stage, alcoholic liver disease is the second most common indication for liver transplantation in the United States and even this is likely an underestimation of the true burden of alcohol liver disease, the authors wrote.
Other less common contributors to the burden of chronic liver disease in this country include chronic hepatitis B infection, metabolic liver diseases such as hereditary hemochromatosis, and rarer autoimmune and cholestatic liver diseases such primary biliary cirrhosis and autoimmune hepatitis.
No conflicts of interest were disclosed.
Chronic nonmalignant liver disease is on the rise in the United States in part because of increasing incidence of nonalcoholic fatty liver disease, according to a report published online in Clinical Gastroenterology and Hepatology.
Nearly 2 million deaths each year in the United States are linked to chronic liver disease and recently, the overall mortality rate has been increasing, wrote Dr. Prowpanga Udompap and colleagues in the division of gastroenterology and hepatology at Stanford (Calif.) University.
Chronic liver disease can be caused by a number of factors, such as hepatitis B and hepatitis C infection, alcohol consumption, diabetes, and metabolic syndrome. “In general, HBV infection tends to have a large burden in resource-limited countries and nonalcoholic fatty liver disease (NAFLD) in more established economies, whereas HCV infection and alcohol use are prevalent throughout,” the researchers wrote.
In the United States, chronic liver disease and cirrhosis are the 12th leading cause of death, claiming more than 36,000 lives in 2013 – representing 1.4% of all deaths that year – and the prevalence of cirrhosis is estimated to be approximately 0.27% (Clin Gastroenterol Hepatol. 2015, Aug 17. doi: 10.1016/j.cgh.2015.08.015).
The mortality rate from chronic liver disease and cirrhosis has increased from 9.4 deaths per 100,000 in 1999 to 11.5 in 2013, but the increase is particularly evident in individuals aged 55-64 years, which the authors attributed to aging of the HCV birth cohort.
“Projection studies have estimated that although the incidence of new HCV infection in the United States decreased over time, the number of individuals living with advanced fibrosis and cirrhosis will rise as the birth cohort of baby boomers with HCV infection grows older and their duration of infection reaches long enough time for their liver fibrosis to have progressed to cirrhosis,” the authors wrote.
While estimates for the prevalence of nonalcoholic fatty liver disease in the United States vary significantly because of differences in test sensitivities, a study based on NHANES data suggested the incidence of ultrasound-diagnosed nonalcoholic hepatic steatosis (NASH) could be as high as 34%.
Patients with NASH have a higher risk of progression to cirrhosis than do patients with nonalcoholic fatty liver disease; one study found an incidence of 3.1% for incident cirrhosis over a 7.6-year follow-up of patients with NASH.
“NASH is quickly becoming a major etiology in liver transplantation in the United States, and it may soon become the most common indication,” the authors wrote.
Alcoholic liver disease is another global health problem, and in 2013, 7% of American adults were estimated to have an alcohol use disorder.
Given 30%-45% of individuals with chronic alcohol use disorder will develop alcoholic hepatitis at some stage, alcoholic liver disease is the second most common indication for liver transplantation in the United States and even this is likely an underestimation of the true burden of alcohol liver disease, the authors wrote.
Other less common contributors to the burden of chronic liver disease in this country include chronic hepatitis B infection, metabolic liver diseases such as hereditary hemochromatosis, and rarer autoimmune and cholestatic liver diseases such primary biliary cirrhosis and autoimmune hepatitis.
No conflicts of interest were disclosed.
Chronic nonmalignant liver disease is on the rise in the United States in part because of increasing incidence of nonalcoholic fatty liver disease, according to a report published online in Clinical Gastroenterology and Hepatology.
Nearly 2 million deaths each year in the United States are linked to chronic liver disease and recently, the overall mortality rate has been increasing, wrote Dr. Prowpanga Udompap and colleagues in the division of gastroenterology and hepatology at Stanford (Calif.) University.
Chronic liver disease can be caused by a number of factors, such as hepatitis B and hepatitis C infection, alcohol consumption, diabetes, and metabolic syndrome. “In general, HBV infection tends to have a large burden in resource-limited countries and nonalcoholic fatty liver disease (NAFLD) in more established economies, whereas HCV infection and alcohol use are prevalent throughout,” the researchers wrote.
In the United States, chronic liver disease and cirrhosis are the 12th leading cause of death, claiming more than 36,000 lives in 2013 – representing 1.4% of all deaths that year – and the prevalence of cirrhosis is estimated to be approximately 0.27% (Clin Gastroenterol Hepatol. 2015, Aug 17. doi: 10.1016/j.cgh.2015.08.015).
The mortality rate from chronic liver disease and cirrhosis has increased from 9.4 deaths per 100,000 in 1999 to 11.5 in 2013, but the increase is particularly evident in individuals aged 55-64 years, which the authors attributed to aging of the HCV birth cohort.
“Projection studies have estimated that although the incidence of new HCV infection in the United States decreased over time, the number of individuals living with advanced fibrosis and cirrhosis will rise as the birth cohort of baby boomers with HCV infection grows older and their duration of infection reaches long enough time for their liver fibrosis to have progressed to cirrhosis,” the authors wrote.
While estimates for the prevalence of nonalcoholic fatty liver disease in the United States vary significantly because of differences in test sensitivities, a study based on NHANES data suggested the incidence of ultrasound-diagnosed nonalcoholic hepatic steatosis (NASH) could be as high as 34%.
Patients with NASH have a higher risk of progression to cirrhosis than do patients with nonalcoholic fatty liver disease; one study found an incidence of 3.1% for incident cirrhosis over a 7.6-year follow-up of patients with NASH.
“NASH is quickly becoming a major etiology in liver transplantation in the United States, and it may soon become the most common indication,” the authors wrote.
Alcoholic liver disease is another global health problem, and in 2013, 7% of American adults were estimated to have an alcohol use disorder.
Given 30%-45% of individuals with chronic alcohol use disorder will develop alcoholic hepatitis at some stage, alcoholic liver disease is the second most common indication for liver transplantation in the United States and even this is likely an underestimation of the true burden of alcohol liver disease, the authors wrote.
Other less common contributors to the burden of chronic liver disease in this country include chronic hepatitis B infection, metabolic liver diseases such as hereditary hemochromatosis, and rarer autoimmune and cholestatic liver diseases such primary biliary cirrhosis and autoimmune hepatitis.
No conflicts of interest were disclosed.
FROM CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
Key clinical point: Chronic nonmalignant liver disease is on the rise in the United States, in part because of increasing incidence of nonalcoholic fatty liver disease and its progression to hepatic steatosis.
Major finding: The mortality rate from chronic liver disease and cirrhosis has increased from 9.4 deaths per 100,000 in 1999 to 11.5 in 2013.
Data source: Review of available information on chronic liver disease in the United States.
Disclosures: No conflicts of interest were declared.
Sofosbuvir reduces liver fibrosis in chronic hepatitis C
Antiviral treatment with sofosbuvir reduced liver fibrosis, as measured by three independent noninvasive predictors for liver fibrosis, and liver stiffness, in patients with chronic hepatitis C (CHC), according to new research published in the Digestive and Liver Disease (doi:10.1016/j.dld.2015.09.015).
“Despite the relatively small sample size, the effects on fibrosis parameters are impressive, implying clinically significant fibrosis regression and potential reduction of cirrhosis-associated mortality in successfully treated patients with CHC,” wrote Dr. Sebastian Bernuth of Cirrhosis Center Mainz (CCM), Johannes Gutenberg University Mainz, Germany, and colleagues.
CHC is a major cause of liver-associated mortality, and is responsible for approximately 25% of primary hepatocellular carcinomas and 25% of liver cirrhosis. Successful antiviral therapy with a sustained virological response (SVR) can reduce liver-related morbidity and mortality, including a decreased need for transplantation.
In 2014, the first NS5B RNA-polymerase inhibitor, sofosbuvir, was approved for use in conjunction with pegylated interferon-alpha (PEG-IFN) and/or ribavirin to treat hepatitis C infection, and yielded high SVR rates of around 90% after short-term therapy in genotype 1-3-infected patients.In this study, Dr. Benuth and his colleagues evaluated early changes in dynamic fibrosis-related parameters using the enhanced liver fibrosis (ELF) panel, combined with liver stiffness measurement (LSM), along with metabolic alterations in insulin resistance, and lipid and iron metabolism during sofosbuvir-based antiviral therapy.
A total of 32 patients were included in the analysis, and all received treatment with sofosbuvir, 19 in combination with PEG-IFN, 29 in combination with ribavirin, and four in combination with simeprevir.Patients experienced a biochemical and virological response within 4 weeks of starting treatment. At 12 weeks, the SVR was 93.8% and two patients experienced a relapse.There was a significant decrease from baseline to 12-week posttreatment follow-up in ELF (10.00 vs. 9.37; P = .007), and the median of the LSM (measured by Fibroscan) significantly decreased over the whole observation period, from 8 kPa (METAVIR F2) at baseline to 6.8 kPa (METAVIR F0-1) at 12 weeks (P = .016). This suggests a significant regression of liver fibrosis at 12 weeks, compared to baseline.The liver enzymes (ALT, AST, and gamma-GT) rapidly normalized under treatment, and total bilirubin also decreased from the baseline upper normal values (0.91 mg/dL) to 0.74 mg/dL (P = .034).“In conclusion, this is the first study implying significant and clinically relevant reduction in liver fibrosis measures by three independent noninvasive predictors for liver fibrosis assessment and liver stiffness measurement under highly effective antiviral regimens with sofosbuvir,” said the authors.
The study was supported by intramural funding of the University of Mainz (Inneruniversitäre Forschungsförderung Stufe I grant) to Dr. Tim Zimmermann, who has also received consultant/lecture fees and/or travel support from Abbvie, BMS, Gilead, Janssen-Cilag, Merck, and Roche. Dr. Martin F. Sprinzl received research funding from Gilead and lecture fees from Roche. All other authors have no conflicts of interest to declare in terms of this manuscript.
AGA ResourceThrough the AGA Roadmap to the Future of Practice, AGA offers a hepatitis C clinical service line to help support high-quality patient care at http://www.gastro.org/patient-care/conditions-
diseases/hepatitis-c.
Antiviral treatment with sofosbuvir reduced liver fibrosis, as measured by three independent noninvasive predictors for liver fibrosis, and liver stiffness, in patients with chronic hepatitis C (CHC), according to new research published in the Digestive and Liver Disease (doi:10.1016/j.dld.2015.09.015).
“Despite the relatively small sample size, the effects on fibrosis parameters are impressive, implying clinically significant fibrosis regression and potential reduction of cirrhosis-associated mortality in successfully treated patients with CHC,” wrote Dr. Sebastian Bernuth of Cirrhosis Center Mainz (CCM), Johannes Gutenberg University Mainz, Germany, and colleagues.
CHC is a major cause of liver-associated mortality, and is responsible for approximately 25% of primary hepatocellular carcinomas and 25% of liver cirrhosis. Successful antiviral therapy with a sustained virological response (SVR) can reduce liver-related morbidity and mortality, including a decreased need for transplantation.
In 2014, the first NS5B RNA-polymerase inhibitor, sofosbuvir, was approved for use in conjunction with pegylated interferon-alpha (PEG-IFN) and/or ribavirin to treat hepatitis C infection, and yielded high SVR rates of around 90% after short-term therapy in genotype 1-3-infected patients.In this study, Dr. Benuth and his colleagues evaluated early changes in dynamic fibrosis-related parameters using the enhanced liver fibrosis (ELF) panel, combined with liver stiffness measurement (LSM), along with metabolic alterations in insulin resistance, and lipid and iron metabolism during sofosbuvir-based antiviral therapy.
A total of 32 patients were included in the analysis, and all received treatment with sofosbuvir, 19 in combination with PEG-IFN, 29 in combination with ribavirin, and four in combination with simeprevir.Patients experienced a biochemical and virological response within 4 weeks of starting treatment. At 12 weeks, the SVR was 93.8% and two patients experienced a relapse.There was a significant decrease from baseline to 12-week posttreatment follow-up in ELF (10.00 vs. 9.37; P = .007), and the median of the LSM (measured by Fibroscan) significantly decreased over the whole observation period, from 8 kPa (METAVIR F2) at baseline to 6.8 kPa (METAVIR F0-1) at 12 weeks (P = .016). This suggests a significant regression of liver fibrosis at 12 weeks, compared to baseline.The liver enzymes (ALT, AST, and gamma-GT) rapidly normalized under treatment, and total bilirubin also decreased from the baseline upper normal values (0.91 mg/dL) to 0.74 mg/dL (P = .034).“In conclusion, this is the first study implying significant and clinically relevant reduction in liver fibrosis measures by three independent noninvasive predictors for liver fibrosis assessment and liver stiffness measurement under highly effective antiviral regimens with sofosbuvir,” said the authors.
The study was supported by intramural funding of the University of Mainz (Inneruniversitäre Forschungsförderung Stufe I grant) to Dr. Tim Zimmermann, who has also received consultant/lecture fees and/or travel support from Abbvie, BMS, Gilead, Janssen-Cilag, Merck, and Roche. Dr. Martin F. Sprinzl received research funding from Gilead and lecture fees from Roche. All other authors have no conflicts of interest to declare in terms of this manuscript.
AGA ResourceThrough the AGA Roadmap to the Future of Practice, AGA offers a hepatitis C clinical service line to help support high-quality patient care at http://www.gastro.org/patient-care/conditions-
diseases/hepatitis-c.
Antiviral treatment with sofosbuvir reduced liver fibrosis, as measured by three independent noninvasive predictors for liver fibrosis, and liver stiffness, in patients with chronic hepatitis C (CHC), according to new research published in the Digestive and Liver Disease (doi:10.1016/j.dld.2015.09.015).
“Despite the relatively small sample size, the effects on fibrosis parameters are impressive, implying clinically significant fibrosis regression and potential reduction of cirrhosis-associated mortality in successfully treated patients with CHC,” wrote Dr. Sebastian Bernuth of Cirrhosis Center Mainz (CCM), Johannes Gutenberg University Mainz, Germany, and colleagues.
CHC is a major cause of liver-associated mortality, and is responsible for approximately 25% of primary hepatocellular carcinomas and 25% of liver cirrhosis. Successful antiviral therapy with a sustained virological response (SVR) can reduce liver-related morbidity and mortality, including a decreased need for transplantation.
In 2014, the first NS5B RNA-polymerase inhibitor, sofosbuvir, was approved for use in conjunction with pegylated interferon-alpha (PEG-IFN) and/or ribavirin to treat hepatitis C infection, and yielded high SVR rates of around 90% after short-term therapy in genotype 1-3-infected patients.In this study, Dr. Benuth and his colleagues evaluated early changes in dynamic fibrosis-related parameters using the enhanced liver fibrosis (ELF) panel, combined with liver stiffness measurement (LSM), along with metabolic alterations in insulin resistance, and lipid and iron metabolism during sofosbuvir-based antiviral therapy.
A total of 32 patients were included in the analysis, and all received treatment with sofosbuvir, 19 in combination with PEG-IFN, 29 in combination with ribavirin, and four in combination with simeprevir.Patients experienced a biochemical and virological response within 4 weeks of starting treatment. At 12 weeks, the SVR was 93.8% and two patients experienced a relapse.There was a significant decrease from baseline to 12-week posttreatment follow-up in ELF (10.00 vs. 9.37; P = .007), and the median of the LSM (measured by Fibroscan) significantly decreased over the whole observation period, from 8 kPa (METAVIR F2) at baseline to 6.8 kPa (METAVIR F0-1) at 12 weeks (P = .016). This suggests a significant regression of liver fibrosis at 12 weeks, compared to baseline.The liver enzymes (ALT, AST, and gamma-GT) rapidly normalized under treatment, and total bilirubin also decreased from the baseline upper normal values (0.91 mg/dL) to 0.74 mg/dL (P = .034).“In conclusion, this is the first study implying significant and clinically relevant reduction in liver fibrosis measures by three independent noninvasive predictors for liver fibrosis assessment and liver stiffness measurement under highly effective antiviral regimens with sofosbuvir,” said the authors.
The study was supported by intramural funding of the University of Mainz (Inneruniversitäre Forschungsförderung Stufe I grant) to Dr. Tim Zimmermann, who has also received consultant/lecture fees and/or travel support from Abbvie, BMS, Gilead, Janssen-Cilag, Merck, and Roche. Dr. Martin F. Sprinzl received research funding from Gilead and lecture fees from Roche. All other authors have no conflicts of interest to declare in terms of this manuscript.
AGA ResourceThrough the AGA Roadmap to the Future of Practice, AGA offers a hepatitis C clinical service line to help support high-quality patient care at http://www.gastro.org/patient-care/conditions-
diseases/hepatitis-c.
FROM DIGESTIVE AND LIVER DISEASE
Key clinical point: Treatment with sofosbuvir achieved clinically significant fibrosis regression and potential reduction of cirrhosis-associated mortality in patients with hepatitis C.
Major finding: There was a sustained virological response rate at 12-week follow-up (93.8%), and a significant decrease from baseline to 12-week posttreatment follow-up in enhanced liver fibrosis (ELF) scores (10.00 vs. 9.37; P = .007) and FibroScan (8.0 vs. 6.8 kPa; P = .016)
Data source: A total of 32 hepatitis C patients were treated prospectively with sofosbuvir and ELF scores and FibroScan measurements were taken at baseline, week 4, end of treatment, and 12 weeks thereafter.
Disclosures: The study was supported by intramural funding of the University of Mainz (Inneruniversitäre Forschungsförderung Stufe I grant) to Dr. Tim Zimmermann, who has also received consultant/lecture fees and/or travel support from Abbvie, BMS, Gilead, Janssen-Cilag, Merck, and Roche. Dr. Martin F. Sprinzl received research funding from Gilead and lecture fees from Roche. All other authors have no conflicts of interest to declare in terms of this manuscript.
Liver and functional GI issues
Dr. Lin Chang at the University of California, Los Angeles, discussed how to work-up and manage functional abdominal pain. She reviewed a diagnostic algorithm that is evidence based and uses characteristics of the abdominal pain, coexisting warning signs, and a diagnostic work-up. A patient must be diagnosed with functional abdominal pain only after careful medical history, physical examination, and adequate consideration of competing etiologies.
Physical examination can be helpful in differentiating abdominal wall pain from that of visceral pain (Carnett’s sign) although some patients with functional abdominal pain may exhibit positive Carnett’s sign. Managing a patient with suspected functional abdominal pain includes careful attention to warning signs for organic disease (for example, unintended weight loss, hematochezia, abnormal labs, fever, or family history of serious GI disorders), avoiding unnecessary diagnostic testing, consideration of mental health consultation and pharmacotherapy as appropriate.
Dr. Chang reviewed the role of various pharmacologic agents for irritable bowel syndrome (IBS) with diarrhea (alosetron, rifaximin, and loperamide), IBS with constipation (linaclotide, lubiprostone, and polyethylene glycol) and agents such antispasmodics, tricyclic antidepressants, and SSRIs (reviewed extensively in the AGA Technical Review and Guidelines for Pharmacotherapy for IBS published in Gastroenterology. 2014 Nov;147[5]:1149-72.e2). It is important to establish a strong patient-provider relationship and to incorporate behavioral therapies into management of patients with recurrent or chronic functional abdominal pain.
Dr. Peter Gibson at Monash University in Melbourne discussed non–celiac gluten sensitivity and low-FODMAP diet in managing food sensitivity and functional bowel disorders. He pointed out that recent dietary strategies have changed from patient-initiated, whole-food strategies to avoiding specific dietary components such as FODMAPs and gluten and wheat products. FODMAPS (fermentable oligo-, di-, and monosaccharides and polyols) are foods that are generally high in fructose, lactose, oligosaccharides (e.g., beans, onions, garlic, complex carbohydrates) and polyols (e.g., mushrooms). FODMAPs are generally osmotic and lead to fermentation and diarrhea, bloating, and flatulence. General principles in offering a low-FODMAP diet are the selection of appropriate patients; correct education about FODMAP diets, preferably by a trained dietitian; and a step-down approach in which a strict diet is slowly liberalized. Dr. Gibson pointed out that there are a subset of IBS patients who are gluten sensitive but recent data suggest that wheat protein sensitivity may not be as common as it has been suggested and, in fact, FODMAPs may indeed be the major inducers of symptoms in individuals with supposed wheat intolerance. The potential risks of dietary manipulation such as creation of a dietary cripple or induction of an eating disorder should be kept in mind.
Dr. Anna Mae Diehl at Duke University Medical Center in Durham, N.C., spoke about the diagnosis, role of the microbiome, and the treatment of nonalcoholic fatty liver disease (NAFLD). It was pointed out that most patients with NAFLD have benign progression although individuals with nonalcoholic steatohepatitis (NASH), especially those with significant fibrosis, are at risk for developing cirrhosis, liver failure, and liver cancer. Therapeutic investigations undertaken to date have not sufficiently focused on improving fibrosis although several ongoing clinical trials are directed at this goal. Gut microbiome might be a new NAFLD diagnostic/therapeutic target because several recent animal studies have shown that gut microbiome may play a role in conferring susceptibility to liver injury, fibrosis, and cancer.
Dr. Lawrence J. Brandt at Albert Einstein College of Medicine, New York, gave an update on fecal microbiota therapy (FMT). He highlighted that FMT has historic roots going back to the 4th century when Ge Hong described use of human fecal suspension to treat food poisoning or severe diarrhea. He made it clear that FMT should be offered only to those with recurrent Clostridium difficile infections (CDI), meeting selected criteria such as severe illness and prior treatment failures. The protocol for FMT in recurrent CDI includes careful selection of donor (may range from any healthy person, universal donor, or stool-bank product) and testing stool and blood of potential donors for any transmittable agents. A recent systematic review showed that the success rate for FMT in individuals with CDI is generally quite high (greater than 80%) but it may depend on the site of FMT – for example, if FMT is administered to duodenum/jejunum, the success rate is 86%, whereas if it is delivered to right colon/cecum, then the success rate can be as high as 93%. He highlighted the efficacy of FMT in severe, complicated CDI, which generally carries high morbidity and mortality. Practitioners offering FMT should carefully review the FDA guidance that was issued in March 2014. He noted that long-term consequences of FMT are not well understood and thus, risks versus benefits of FMT on a patient-by-patient basis must be carefully weighed.
Dr. Naga P. Chalasani is the David W. Crabb Professor and director of the division of gastroenterology and hepatology, Indiana University, Indianapolis. He has consulting agreements and receives research support from several pharmaceutical companies but none represent a conflict of interest for this activity.
This is a summary provided by the moderator of one of the spring postgraduate course sessions held at DDW 2015.
Dr. Lin Chang at the University of California, Los Angeles, discussed how to work-up and manage functional abdominal pain. She reviewed a diagnostic algorithm that is evidence based and uses characteristics of the abdominal pain, coexisting warning signs, and a diagnostic work-up. A patient must be diagnosed with functional abdominal pain only after careful medical history, physical examination, and adequate consideration of competing etiologies.
Physical examination can be helpful in differentiating abdominal wall pain from that of visceral pain (Carnett’s sign) although some patients with functional abdominal pain may exhibit positive Carnett’s sign. Managing a patient with suspected functional abdominal pain includes careful attention to warning signs for organic disease (for example, unintended weight loss, hematochezia, abnormal labs, fever, or family history of serious GI disorders), avoiding unnecessary diagnostic testing, consideration of mental health consultation and pharmacotherapy as appropriate.
Dr. Chang reviewed the role of various pharmacologic agents for irritable bowel syndrome (IBS) with diarrhea (alosetron, rifaximin, and loperamide), IBS with constipation (linaclotide, lubiprostone, and polyethylene glycol) and agents such antispasmodics, tricyclic antidepressants, and SSRIs (reviewed extensively in the AGA Technical Review and Guidelines for Pharmacotherapy for IBS published in Gastroenterology. 2014 Nov;147[5]:1149-72.e2). It is important to establish a strong patient-provider relationship and to incorporate behavioral therapies into management of patients with recurrent or chronic functional abdominal pain.
Dr. Peter Gibson at Monash University in Melbourne discussed non–celiac gluten sensitivity and low-FODMAP diet in managing food sensitivity and functional bowel disorders. He pointed out that recent dietary strategies have changed from patient-initiated, whole-food strategies to avoiding specific dietary components such as FODMAPs and gluten and wheat products. FODMAPS (fermentable oligo-, di-, and monosaccharides and polyols) are foods that are generally high in fructose, lactose, oligosaccharides (e.g., beans, onions, garlic, complex carbohydrates) and polyols (e.g., mushrooms). FODMAPs are generally osmotic and lead to fermentation and diarrhea, bloating, and flatulence. General principles in offering a low-FODMAP diet are the selection of appropriate patients; correct education about FODMAP diets, preferably by a trained dietitian; and a step-down approach in which a strict diet is slowly liberalized. Dr. Gibson pointed out that there are a subset of IBS patients who are gluten sensitive but recent data suggest that wheat protein sensitivity may not be as common as it has been suggested and, in fact, FODMAPs may indeed be the major inducers of symptoms in individuals with supposed wheat intolerance. The potential risks of dietary manipulation such as creation of a dietary cripple or induction of an eating disorder should be kept in mind.
Dr. Anna Mae Diehl at Duke University Medical Center in Durham, N.C., spoke about the diagnosis, role of the microbiome, and the treatment of nonalcoholic fatty liver disease (NAFLD). It was pointed out that most patients with NAFLD have benign progression although individuals with nonalcoholic steatohepatitis (NASH), especially those with significant fibrosis, are at risk for developing cirrhosis, liver failure, and liver cancer. Therapeutic investigations undertaken to date have not sufficiently focused on improving fibrosis although several ongoing clinical trials are directed at this goal. Gut microbiome might be a new NAFLD diagnostic/therapeutic target because several recent animal studies have shown that gut microbiome may play a role in conferring susceptibility to liver injury, fibrosis, and cancer.
Dr. Lawrence J. Brandt at Albert Einstein College of Medicine, New York, gave an update on fecal microbiota therapy (FMT). He highlighted that FMT has historic roots going back to the 4th century when Ge Hong described use of human fecal suspension to treat food poisoning or severe diarrhea. He made it clear that FMT should be offered only to those with recurrent Clostridium difficile infections (CDI), meeting selected criteria such as severe illness and prior treatment failures. The protocol for FMT in recurrent CDI includes careful selection of donor (may range from any healthy person, universal donor, or stool-bank product) and testing stool and blood of potential donors for any transmittable agents. A recent systematic review showed that the success rate for FMT in individuals with CDI is generally quite high (greater than 80%) but it may depend on the site of FMT – for example, if FMT is administered to duodenum/jejunum, the success rate is 86%, whereas if it is delivered to right colon/cecum, then the success rate can be as high as 93%. He highlighted the efficacy of FMT in severe, complicated CDI, which generally carries high morbidity and mortality. Practitioners offering FMT should carefully review the FDA guidance that was issued in March 2014. He noted that long-term consequences of FMT are not well understood and thus, risks versus benefits of FMT on a patient-by-patient basis must be carefully weighed.
Dr. Naga P. Chalasani is the David W. Crabb Professor and director of the division of gastroenterology and hepatology, Indiana University, Indianapolis. He has consulting agreements and receives research support from several pharmaceutical companies but none represent a conflict of interest for this activity.
This is a summary provided by the moderator of one of the spring postgraduate course sessions held at DDW 2015.
Dr. Lin Chang at the University of California, Los Angeles, discussed how to work-up and manage functional abdominal pain. She reviewed a diagnostic algorithm that is evidence based and uses characteristics of the abdominal pain, coexisting warning signs, and a diagnostic work-up. A patient must be diagnosed with functional abdominal pain only after careful medical history, physical examination, and adequate consideration of competing etiologies.
Physical examination can be helpful in differentiating abdominal wall pain from that of visceral pain (Carnett’s sign) although some patients with functional abdominal pain may exhibit positive Carnett’s sign. Managing a patient with suspected functional abdominal pain includes careful attention to warning signs for organic disease (for example, unintended weight loss, hematochezia, abnormal labs, fever, or family history of serious GI disorders), avoiding unnecessary diagnostic testing, consideration of mental health consultation and pharmacotherapy as appropriate.
Dr. Chang reviewed the role of various pharmacologic agents for irritable bowel syndrome (IBS) with diarrhea (alosetron, rifaximin, and loperamide), IBS with constipation (linaclotide, lubiprostone, and polyethylene glycol) and agents such antispasmodics, tricyclic antidepressants, and SSRIs (reviewed extensively in the AGA Technical Review and Guidelines for Pharmacotherapy for IBS published in Gastroenterology. 2014 Nov;147[5]:1149-72.e2). It is important to establish a strong patient-provider relationship and to incorporate behavioral therapies into management of patients with recurrent or chronic functional abdominal pain.
Dr. Peter Gibson at Monash University in Melbourne discussed non–celiac gluten sensitivity and low-FODMAP diet in managing food sensitivity and functional bowel disorders. He pointed out that recent dietary strategies have changed from patient-initiated, whole-food strategies to avoiding specific dietary components such as FODMAPs and gluten and wheat products. FODMAPS (fermentable oligo-, di-, and monosaccharides and polyols) are foods that are generally high in fructose, lactose, oligosaccharides (e.g., beans, onions, garlic, complex carbohydrates) and polyols (e.g., mushrooms). FODMAPs are generally osmotic and lead to fermentation and diarrhea, bloating, and flatulence. General principles in offering a low-FODMAP diet are the selection of appropriate patients; correct education about FODMAP diets, preferably by a trained dietitian; and a step-down approach in which a strict diet is slowly liberalized. Dr. Gibson pointed out that there are a subset of IBS patients who are gluten sensitive but recent data suggest that wheat protein sensitivity may not be as common as it has been suggested and, in fact, FODMAPs may indeed be the major inducers of symptoms in individuals with supposed wheat intolerance. The potential risks of dietary manipulation such as creation of a dietary cripple or induction of an eating disorder should be kept in mind.
Dr. Anna Mae Diehl at Duke University Medical Center in Durham, N.C., spoke about the diagnosis, role of the microbiome, and the treatment of nonalcoholic fatty liver disease (NAFLD). It was pointed out that most patients with NAFLD have benign progression although individuals with nonalcoholic steatohepatitis (NASH), especially those with significant fibrosis, are at risk for developing cirrhosis, liver failure, and liver cancer. Therapeutic investigations undertaken to date have not sufficiently focused on improving fibrosis although several ongoing clinical trials are directed at this goal. Gut microbiome might be a new NAFLD diagnostic/therapeutic target because several recent animal studies have shown that gut microbiome may play a role in conferring susceptibility to liver injury, fibrosis, and cancer.
Dr. Lawrence J. Brandt at Albert Einstein College of Medicine, New York, gave an update on fecal microbiota therapy (FMT). He highlighted that FMT has historic roots going back to the 4th century when Ge Hong described use of human fecal suspension to treat food poisoning or severe diarrhea. He made it clear that FMT should be offered only to those with recurrent Clostridium difficile infections (CDI), meeting selected criteria such as severe illness and prior treatment failures. The protocol for FMT in recurrent CDI includes careful selection of donor (may range from any healthy person, universal donor, or stool-bank product) and testing stool and blood of potential donors for any transmittable agents. A recent systematic review showed that the success rate for FMT in individuals with CDI is generally quite high (greater than 80%) but it may depend on the site of FMT – for example, if FMT is administered to duodenum/jejunum, the success rate is 86%, whereas if it is delivered to right colon/cecum, then the success rate can be as high as 93%. He highlighted the efficacy of FMT in severe, complicated CDI, which generally carries high morbidity and mortality. Practitioners offering FMT should carefully review the FDA guidance that was issued in March 2014. He noted that long-term consequences of FMT are not well understood and thus, risks versus benefits of FMT on a patient-by-patient basis must be carefully weighed.
Dr. Naga P. Chalasani is the David W. Crabb Professor and director of the division of gastroenterology and hepatology, Indiana University, Indianapolis. He has consulting agreements and receives research support from several pharmaceutical companies but none represent a conflict of interest for this activity.
This is a summary provided by the moderator of one of the spring postgraduate course sessions held at DDW 2015.
Integrated care overcomes HCV treatment barriers
Patients with hepatitis C and psychiatric disorders or substance abuse problems benefit significantly from an integrated care model of treatment, with a randomized controlled trial showing such an approach is linked to greater rates of antiviral therapy and treatment response.
The prospective trial of integrated care versus usual care involved 363 patients attending three hepatitis C (HCV) clinics, with the integrated care being delivered by a midlevel mental health provider within the clinic who served as the regular contact and case manager.
Patients randomized to integrated care, which included brief psychological interventions and case management, were more than twice as likely to start antiviral therapy earlier and achieve a sustained virologic response than those who received usual care, according to Dr. Samuel B. Ho of the VA San Diego Healthcare System and his coauthors.
While individuals with a history of prior psychiatric disorder or active drug use were significantly less likely to achieve sustained virologic response, the integrated-care approach had particularly positive effects on treatment initiative and response for individuals with a risk for active psychiatric disease at baseline, they said (Clin Gastroenterol Hepatol. 2015. doi: 10.1016/j.cgh.2015.02.022).
“To optimize the public health impact of antiviral treatments for HCV, the number of patients who are able to receive these treatments must be expanded,” wrote Dr. Ho and his associates, adding that “new interferon-free regimens have fewer side effects and are expected to expand treatment populations to include a broader range of patients, many with very significant psychiatric and substance abuse disorders.”
The study was supported by VA Health Services Research and Development. Three authors declared research support, grants, advisory board positions or speakers bureau roles with the pharmaceutical industry.
AGA Resource
Through the AGA Roadmap to the Future of Practice, AGA offers a Hepatitis C Clinical Service line to support high-quality patient care at www.gastro.org/patient-care/conditions-diseases/hepatitis-c.
Patients with hepatitis C and psychiatric disorders or substance abuse problems benefit significantly from an integrated care model of treatment, with a randomized controlled trial showing such an approach is linked to greater rates of antiviral therapy and treatment response.
The prospective trial of integrated care versus usual care involved 363 patients attending three hepatitis C (HCV) clinics, with the integrated care being delivered by a midlevel mental health provider within the clinic who served as the regular contact and case manager.
Patients randomized to integrated care, which included brief psychological interventions and case management, were more than twice as likely to start antiviral therapy earlier and achieve a sustained virologic response than those who received usual care, according to Dr. Samuel B. Ho of the VA San Diego Healthcare System and his coauthors.
While individuals with a history of prior psychiatric disorder or active drug use were significantly less likely to achieve sustained virologic response, the integrated-care approach had particularly positive effects on treatment initiative and response for individuals with a risk for active psychiatric disease at baseline, they said (Clin Gastroenterol Hepatol. 2015. doi: 10.1016/j.cgh.2015.02.022).
“To optimize the public health impact of antiviral treatments for HCV, the number of patients who are able to receive these treatments must be expanded,” wrote Dr. Ho and his associates, adding that “new interferon-free regimens have fewer side effects and are expected to expand treatment populations to include a broader range of patients, many with very significant psychiatric and substance abuse disorders.”
The study was supported by VA Health Services Research and Development. Three authors declared research support, grants, advisory board positions or speakers bureau roles with the pharmaceutical industry.
AGA Resource
Through the AGA Roadmap to the Future of Practice, AGA offers a Hepatitis C Clinical Service line to support high-quality patient care at www.gastro.org/patient-care/conditions-diseases/hepatitis-c.
Patients with hepatitis C and psychiatric disorders or substance abuse problems benefit significantly from an integrated care model of treatment, with a randomized controlled trial showing such an approach is linked to greater rates of antiviral therapy and treatment response.
The prospective trial of integrated care versus usual care involved 363 patients attending three hepatitis C (HCV) clinics, with the integrated care being delivered by a midlevel mental health provider within the clinic who served as the regular contact and case manager.
Patients randomized to integrated care, which included brief psychological interventions and case management, were more than twice as likely to start antiviral therapy earlier and achieve a sustained virologic response than those who received usual care, according to Dr. Samuel B. Ho of the VA San Diego Healthcare System and his coauthors.
While individuals with a history of prior psychiatric disorder or active drug use were significantly less likely to achieve sustained virologic response, the integrated-care approach had particularly positive effects on treatment initiative and response for individuals with a risk for active psychiatric disease at baseline, they said (Clin Gastroenterol Hepatol. 2015. doi: 10.1016/j.cgh.2015.02.022).
“To optimize the public health impact of antiviral treatments for HCV, the number of patients who are able to receive these treatments must be expanded,” wrote Dr. Ho and his associates, adding that “new interferon-free regimens have fewer side effects and are expected to expand treatment populations to include a broader range of patients, many with very significant psychiatric and substance abuse disorders.”
The study was supported by VA Health Services Research and Development. Three authors declared research support, grants, advisory board positions or speakers bureau roles with the pharmaceutical industry.
AGA Resource
Through the AGA Roadmap to the Future of Practice, AGA offers a Hepatitis C Clinical Service line to support high-quality patient care at www.gastro.org/patient-care/conditions-diseases/hepatitis-c.
FROM CLINICAL GASTROENTEROLOGY AND HEPATOLOGY
Key clinical point:Patients with hepatitis C and psychiatric disorders or substance abuse problems benefit significantly from an integrated care model of treatment.
Major finding: Integrated care was associated with a more than twofold increase in early initiation of antiviral therapy and sustained virologic response.
Data source: A prospective, randomized controlled trial in 363 patients with hepatitis C and psychiatric disorders or substance abuse problems.
Disclosures: The study was supported by VA Health Services Research and Development. Three authors declared research support, grants, advisory board positions, or speakers bureau roles with the pharmaceutical industry.