HIV

Study Examines Link Between HIV and Risk for Lung Cancer

A recent study suggests that dysfunctional immune activation and chronic inflammation in individuals with HIV contributes to the development of lung cancer.

The researchers included 21,666 participants with HIV from the Veterans Aging Cohort study, and followed them for 3 years between January 1, 1998 and December 31, 2012. Incidences of cancer were identified using data from the cancer registry.
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They used Cox regression models to investigate the relationship between the risk of lung cancer and different time-updated lagged and cumulative exposures of CD4 cell count, CD8 cell count, CD4/CD8 ratio, HIV RNA, and bacterial pneumonia. In addition, researchers adjusted for age, race or ethnicity, smoking, hepatitis C virus infection, alcohol use disorders, drug use disorders, and history of chronic obstructive pulmonary disease and occupational lung disease.

Overall, 277 cases of lung cancer were diagnosed.

“In separate models for each time-updated 12 month lagged, 24 month simple moving average cumulative exposure, increased risk of lung cancer was associated with low CD4 cell count (p trend=0·001), low CD4/CD8 ratio (p trend=0·0001), high HIV RNA concentration (p=0·004), and more cumulative bacterial pneumonia episodes (12 month lag only; p trend=0·0004),” the researchers wrote.

In mutually adjusted models, the CD4/CD8 ratio and cumulative bacterial pneumonia episodes remained significant factors for the increased risk of lung cancer in HIV patients.

The study suggested that dysfunctional immune activation and chronic inflammation were associated with the development of lung cancer in HIV-infected individuals.

“These findings could be used to target lung-cancer prevention measures to high-risk group,” the researchers concluded.

—Melissa Weiss

Reference:

Sigel K, Wisnivesky J, Crothers K, et al. Immunological and infectious risk factors for lung cancer in US veterans with HIV: a longitudinal cohort study [published online December 1, 2016]. The Lancet. doi: http://dx.doi.org/10.1016/S2352-3018(16)30215-6.