Liver Deaths Cut Once HCV Viral Load Suppressed
Published: Nov 5, 2013 | Updated: Nov 6, 2013
Coverage of Hepatitis C Virus is supported in part by an independent educational grant from AbbVie Pharmaceuticals.
By Cole Petrochko, Staff Writer, MedPage Today
Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and Dorothy Caputo, MA, BSN, RN, Nurse Planner
Patients who achieved an undetectable viral load of hepatitis C virus (HCV) had decreased hepatic morbidity and mortality long-term, researchers found.
Compared with those who did not achieve viral load suppression, virally suppressed HCV patients in a veterans population had an unadjusted death rate of 6.8 per 1,000 person-years (95% CI 6-7.7) versus 21.8 per 1,000 person years (95% CI 21.5-22.2), according to Jeffrey McCombs, PhD, of the University of Southern California in Los Angeles, and colleagues.
Viral suppression was associated with a 45% lower risk of death (hazard ratio 0.55, 95% CI 0.47-0.64) and a 27% reduced composite risk of newly diagnosed cirrhosis, hepatocellular cancer, and liver-related hospitalization (HR 0.73, 95% CI 0.66-0.82), they wrote online in JAMA Internal Medicine. The data also were presented at the meeting of the American Association for the Study of Liver Diseases.
Roughly half of HCV patients only get tested for the disease after signs or symptoms show, rather than because of risk, an August 2013 study by the CDC found. In addition, half of U.S. HCV patients follow up on an initial test to confirm findings, according to another CDC study.
The authors conducted an observational cohort study of 28,769 HCV patients to analyze the history of HCV in real-world clinical practice through comparing patient groups with and without detectable viral load.
Study endpoints included time to death and time to the composite liver-related clinical events, as well as individual outcomes in the composite endpoint.
Data were collected through the Veterans Affairs clinical case registry system for patients with HCV, and included information from the month before and after enrollment in the database on demographics, monthly-updated diagnostic profiles, hospital admission for any or liver-related diagnoses, prescription drug use for HCV and others, and event dates for viral load suppression to the study endpoints.
Outcomes were controlled for genotype, race, age, sex, and "other factors."
Follow-up occurred for a mean 6.1 years, mostly among white (51.4%) and black men (31.3%). Mean patient age was 52 years and roughly 80% of those enrolled had genotype 1 HCV. They produced 734,829 person-years of data.
"Higher unadjusted composite event rates were found in treated patients than in untreated patients and in those who achieved viral suppression than in those who did not," they wrote.
Patients with HCV genotype 3 were at significantly higher risk for a composite of clinical outcomes versus those with genotype 1 disease (HR 1.11, 95% CI 1.07-1.16), as well as for death (HR 1.17, 95% CI 1.11-1.24). Those who had prior hospital admission were also significantly at risk for composite clinical outcomes (HR 1.60, 95% CI 1.56-1.65) and death (HR 1.73, 95% CI 1.66-1.79).
On the other hand, patients with genotype 2 disease had significantly reduced odds of clinical event (HR 0.77, 95% CI 0.74-0.80) and death (HR 0.80, 95% CI 0.76-0.84) outcomes.
Male sex was associated with increased risk of clinical events and death, while each additional year increased risk of death by 6%.
The authors cautioned that very few patients achieve undetectable viral load without treatment, but cautioned that effectiveness of therapy is tarnished by adverse events and other factors, adding that "only one in four patients with HCV and a detectable viral load were willing to initiate treatment" in their study.
They also cautioned that their study results may not be generalizable to the larger population. They did not measure sustained viral response or the effects of treatment on clinical endpoints and death. Care delivered outside of the VA system was not recorded.
The group concluded that "achieving an undetectable viral load was associated with decreased hepatic morbidity and mortality. It remains to be determined whether newer treatment regimens can offer higher response rates with fewer adverse effects in real-world settings."
Primary source: JAMA Internal Medicine
Patients who achieved an undetectable viral load of hepatitis C virus (HCV) had decreased hepatic morbidity and mortality long-term, researchers found.
Compared with those who did not achieve viral load suppression, virally suppressed HCV patients in a veterans population had an unadjusted death rate of 6.8 per 1,000 person-years (95% CI 6-7.7) versus 21.8 per 1,000 person years (95% CI 21.5-22.2), according to Jeffrey McCombs, PhD, of the University of Southern California in Los Angeles, and colleagues.
Viral suppression was associated with a 45% lower risk of death (hazard ratio 0.55, 95% CI 0.47-0.64) and a 27% reduced composite risk of newly diagnosed cirrhosis, hepatocellular cancer, and liver-related hospitalization (HR 0.73, 95% CI 0.66-0.82), they wrote online in JAMA Internal Medicine. The data also were presented at the meeting of the American Association for the Study of Liver Diseases.
Roughly half of HCV patients only get tested for the disease after signs or symptoms show, rather than because of risk, an August 2013 study by the CDC found. In addition, half of U.S. HCV patients follow up on an initial test to confirm findings, according to another CDC study.
The authors conducted an observational cohort study of 28,769 HCV patients to analyze the history of HCV in real-world clinical practice through comparing patient groups with and without detectable viral load.
Study endpoints included time to death and time to the composite liver-related clinical events, as well as individual outcomes in the composite endpoint.
Data were collected through the Veterans Affairs clinical case registry system for patients with HCV, and included information from the month before and after enrollment in the database on demographics, monthly-updated diagnostic profiles, hospital admission for any or liver-related diagnoses, prescription drug use for HCV and others, and event dates for viral load suppression to the study endpoints.
Outcomes were controlled for genotype, race, age, sex, and "other factors."
Follow-up occurred for a mean 6.1 years, mostly among white (51.4%) and black men (31.3%). Mean patient age was 52 years and roughly 80% of those enrolled had genotype 1 HCV. They produced 734,829 person-years of data.
"Higher unadjusted composite event rates were found in treated patients than in untreated patients and in those who achieved viral suppression than in those who did not," they wrote.
Patients with HCV genotype 3 were at significantly higher risk for a composite of clinical outcomes versus those with genotype 1 disease (HR 1.11, 95% CI 1.07-1.16), as well as for death (HR 1.17, 95% CI 1.11-1.24). Those who had prior hospital admission were also significantly at risk for composite clinical outcomes (HR 1.60, 95% CI 1.56-1.65) and death (HR 1.73, 95% CI 1.66-1.79).
On the other hand, patients with genotype 2 disease had significantly reduced odds of clinical event (HR 0.77, 95% CI 0.74-0.80) and death (HR 0.80, 95% CI 0.76-0.84) outcomes.
Male sex was associated with increased risk of clinical events and death, while each additional year increased risk of death by 6%.
The authors cautioned that very few patients achieve undetectable viral load without treatment, but cautioned that effectiveness of therapy is tarnished by adverse events and other factors, adding that "only one in four patients with HCV and a detectable viral load were willing to initiate treatment" in their study.
They also cautioned that their study results may not be generalizable to the larger population. They did not measure sustained viral response or the effects of treatment on clinical endpoints and death. Care delivered outside of the VA system was not recorded.
The group concluded that "achieving an undetectable viral load was associated with decreased hepatic morbidity and mortality. It remains to be determined whether newer treatment regimens can offer higher response rates with fewer adverse effects in real-world settings."
Primary source: JAMA Internal Medicine
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