JAMA Internal Medicine
Original Investigation | February 2014
Results From an Analysis of Data From a Department of Veterans Affairs Clinical Registry
Jeffrey McCombs, PhD1; Tara Matsuda, BA1,2; Ivy Tonnu-Mihara, PharmD2; Sammy Saab, MD3; Patricia Hines, BA4; Gilbert L’Italien, PhD4; Timothy Juday, PhD4; Yong Yuan, PhD4
JAMA Intern Med. 2014;174(2):204-212. doi:10.1001/jamainternmed.2013.12505.
Importance The impact of viral load suppression, genotype, race, and other factors on the risk of late-stage liver-related events in patients with hepatitis C (HCV) has been assessed previously using data from small observational cohorts or clinical trials. Data from large real-world practice samples are needed to improve risk factor estimates for late-stage liver events and death in HCV.
Objective To describe the natural history of HCV in real-world clinical practice.
Design, Setting, and Participants Observational cohort study. Patients with a detectable viral load (>25 IU/mL) and a recorded baseline genotype were selected from the Veterans Affairs (VA) HCV clinical registry (CCR), which compiles electronic medical records data from 1999 to present.
Exposures Risk factors included genotype, race, age, sex, and time to achieving an observed undetected viral load.
Main Outcomes and Measures The primary outcomes were time to death and time to a composite of liver-related clinical events. Secondary outcomes included the components of the composite clinical outcome. Outcomes were measured using a time-to-event format and were analyzed using Cox proportional hazards models.
Results A total of 28 769 of 360 857 unique HCV CCR patients met all study criteria. Only 24.3% of patients received treatment, and 16.4% of treated patients (4.0% of all patients) achieved an undetectable viral load. The unadjusted death rates were 6.8 (95% CI, 6.0-7.7) per 1000 person-years for patients who achieved viral load suppression vs 21.8 (95% CI, 21.5-22.2) deaths per 1000 person-years in patients who did not achieve this goal. Cox model results found that achieving viral suppression reduced risk of the composite clinical end point by 27% (hazard ratio [HR], 0.73 [95% CI, 0.66-0.82]) and the risk of death by 45% (HR, 0.55 [95% CI, 0.47-0.64]). Genotype 2 patients were at significantly lower risk, and genotype 3 patients were at higher risk for all study outcomes relative to genotype 1. Black patients were at lower risk for all liver events than white patients.
Conclusion and Relevance 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.