Cancer risk in HIV patients with incomplete viral suppression after initiation of antiretroviral therapy

AIDS Research (CFAR) Network of Integrated Clinical Systems (CNICS)

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8 Scopus citations

Abstract

Background Cancer causes significant morbidity and mortality among HIV patients in the US due to extended life expectancy with access to effective antiretroviral therapy. Low, detectable HIV RNA has been studied as a risk factor for adverse health outcomes, but its clinical impact on cancer risk remains unclear. The objective of this study was to determine whether HIV RNA <1,000 copies/mL six months after starting therapy was associated with 10-year first cancer risk. Methods We followed 7,515 HIV therapy initiators from a US-based multicenter clinical cohort from 1998 to 2014. We used nonparametric multiple imputation to account for viral loads that fell below assay detection limits, and categorized viral loads six months after therapy initiation into four groups: <20, 20–199, 200–999, and >999 copies/mL. We calculated estimates of the cumulative incidence of cancer diagnosis, accounting for death as a competing event. Inverse probability of exposure and censoring weights were used to control for confounding and differential loss to follow up, respectively. Results Crude 10-year first cancer risk in the study sample was 7.03% (95% CI: 6.08%, 7.98%), with the highest risk observed among patients with viral loads between 200 and 999 copies/mL six months after ART initiation (10.7%). After controlling for baseline confounders, 10-year first cancer risk was 6.90% (95% CI: 5.69%, 8.12%), and was similar across viral load categories. Conclusion Overall risk of first cancer was not associated with incomplete viral suppression; however, cancer remains a significant threat to HIV patients after treatment initiation. As more HIV patients gain access to treatment in the current “treat all” era, occurrences of incomplete viral suppression will be observed more frequently in clinical practice, which supports continued study of the role of low-level HIV RNA on cancer development.

Original languageEnglish (US)
Article numbere0197665
JournalPloS one
Volume13
Issue number6
DOIs
StatePublished - Jun 2018

Funding

This work was supported by National Institutes of Health grants T32 AI007001, R01 AI100654, U01 AI069918, and R01 AG053100. CNICS is an NIH-funded program (R24 AI067039) made possible by the National Institute of Allergy and Infectious Diseases (NIAID) and the National Heart, Lung, and Blood Institute (NHLBI). The CFAR sites involved in CNICS include Univ of Alabama at Birmingham (P30 AI027767), Univ of Washington (P30 AI027757), Univ of California San Diego (P30 AI036214), Univ of California San Francisco (P30 AI027763), Case Western Reserve Univ (P30 AI036219), Johns Hopkins Univ (P30 AI094189, U01 DA036935), Fenway Health/ Harvard (P30 AI060354), and Univ of North Carolina Chapel Hill (P30 AI50410). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

ASJC Scopus subject areas

  • General

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