Direct-Acting Antiviral Therapy Improves Survival in Chronic Hepatitis C

Direct-acting antiviral (DAA) therapy for patients with chronic hepatitis C (CHC) virus infection is associated with a lower risk for mortality and liver and nonliver outcomes, according to study results published in JAMA Internal Medicine.

Researchers conducted a retrospective cohort study that comprised adult patients aged 18 years or older with HC virus infection using data from the Optum Clinformatics Data Mart database from January 1, 2010, to March 31, 2021. Eligible patients had CHC and confirmation of at least 1 inpatient or 2 outpatient International Classification of Diseases, Ninth Revision and Tenth Revision, Clinical Modification diagnosis codes for HC virus infection.

The primary endpoints were incidence of liver-related outcomes, including hepatocellular carcinoma (HCC) and liver decompensation, and mortality. Statistical analyses were conducted from January 2021 to September 2022.

A total of 245,596 patients with HC virus infection (mean [SD] age, 58.7 [12.6] years; 41.0% women; 57.0% White) were included, of whom 40,654 (16.6%) had received at least 1 prescriptions for DAA medication, and 204,942 (83.4%) patients had not. Patients treated with DAA were more likely to be men (61.6% vs 58.4%; P <.001) and have a significantly higher mean Charlson comorbidity index (CCI) score compared with patients not treated with DAA (4.0 vs 3.3; P <.001).

Baseline HCC incidence rates (per 1000 patient-years) in patients without cirrhosis were low and not significantly different in DAA-treated participants compared with untreated individuals (3.8 [95% CI, 3.3-4.3] vs 4.0 [95% CI, 3.8-4.2]; P =.42), although the HCC incidence in those with cirrhosis at baseline was significantly lower (20.1 [95% CI, 18.4-21.9] vs 41.8 [95% CI, 40.3-43.3]; P <.001). Patients treated with DAA had a significantly lower incidence of liver decompensation compared with those who did not receive DAA (28.2 [95% CI, 27.0-29.4] vs 40.8 [95% CI, 40.1-41.5]; P < .001).

The crude incidence of nonliver cancers for DAA-treated and untreated patients was comparable (22.5 [95% CI, 21.6-23.5] vs 23.0 [95% CI, 22.6-23.5]; P =.07). Patients treated with DAA had a significantly higher crude incidence of cardiovascular disease (CVD) than patients not treated with DAA (128.0 [95% CI, 123.5-132.6] vs 118.7 [95% CI, 116.8-120.7]; P =.007).

The overall mortality rate per 1000 person-years was 2 times higher for untreated patients compared with the DAA-treated patients (64.7 vs 36.5; P <.001). The mortality rate was 3 times lower in participants treated with DAAs vs untreated patients (42.7 vs 121.2; P <.001) among those with baseline compensated cirrhosis.

Using multivariable Cox proportional hazards analysis, DAA treatment was independently associated with a 27% reduced risk for HCC (adjusted hazard ratio [aHR], 0.73; 95% CI, 0.68-0.77; P < .001) after adjusting for age, sex, race and ethnicity, alcohol use, and cirrhosis. Treatment with DAA was independently associated with a 64% decreased risk for liver decompensation after adjusting for age, sex, race and ethnicity, alcohol use, cirrhosis, and HCC (aHR, 0.36; 95% CI, 0.35-0.38; P <.001).

For nonliver outcomes after adjustment for age, sex, and race and ethnicity, DAA treatment was associated with a 26% reduced risk for diabetes (aHR, 0.74; 95% CI, 0.70-0.77; P <.001), a 19% decreased risk for chronic kidney disease (aHR, 0.81; 95% CI, 0.78-0.85; P <.001), and a 10% lower risk for CVD (aHR, 0.90; 95% CI, 0.86-0.94; P <.001).

Limitations of the study include the fact that the population included only patients diagnosed with HCV and covered by private insurance. Large claim databases can include miscoding and misclassification, and not all participants with a DAA prescription may have adhered to or completed the course or attained sustained virologic response.

The study authors conclude, “Our findings advocate for continued efforts to promote hepatitis C screening and early diagnosis and treatment—prior to the onset of CHC complications—to prevent liver and nonliver morbidity and mortality.”

Disclosure: Some of the study authors declared affiliations with biotech, pharmaceutical, and/or device companies. Please see the original reference for a full list of authors’ disclosures.

This article originally appeared on Gastroenterology Advisor