A research team led by the Yale School of Public Health has found that for people living with HIV/AIDS, both recent immunosuppression (a low recent CD4 T-cell count [white blood cells that fight infection]) and prolonged HIV viremia (the presence of HIV in the blood) play important and independent roles in the development of non-Hodgkin lymphoma. Furthermore, the team observed differences across non-Hodgkin lymphoma subtypes.
The study is believed to be the largest to comprehensively evaluate a variety of measures of T-cell count and viral load to determine the key predictors of risk for non-Hodgkin lymphoma, both overall and by its subtypes. Since the early days of the AIDS epidemic, HIV infection has been strongly associated with the development of two types of cancer: non-Hodgkin lymphoma and Kaposi sarcoma.
The study, published in The Lancet HIV journal, examined people living with HIV from 1996 to 2014 from the United States and Canada, comprising more than 100,000 individuals, of which 712 patients were diagnosed with non-Hodgkin lymphoma. Using models, researchers solidified earlier evidence suggesting that recent T-cell count and cumulative viral load both play important and independent roles in the development of non-Hodgkin lymphoma, and generated new evidence regarding their roles in the development of non-Hodgkin lymphoma subtypes.
“Our finding that prolonged HIV viremia is an independent risk factor for non-Hodgkin lymphoma reinforces the importance of early diagnosis of HIV infection followed by prompt initiation of antiretroviral therapy (ART),” said Raul U. Hernandez-Ramirez, Ph.D., an associate research scientist in biostatistics at the Center for Methods in Implementation and Prevention Science at the Yale School of Public Health. “Curtailing chronic HIV viremia and restoring immune function with early and sustained ART is crucial for preventing non-Hodgkin lymphoma.”
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