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Cumulative effects of hypertriglyceridemia in HIV-infected patients switching from NNRTIs to PI-based antiretroviral therapy
Author(s) -
Yu Zhang,
Jiang Xiao,
Wen Zhang,
Ning Han,
Di Yang,
Wei Liu,
Hui Zeng,
Junyan Han,
Hongxin Zhao
Publication year - 2022
Publication title -
the journal of infection in developing countries
Language(s) - English
Resource type - Journals
eISSN - 2036-6590
pISSN - 1972-2680
DOI - 10.3855/jidc.12519
Subject(s) - hypertriglyceridemia , pi , gastroenterology , medicine , triglyceride , human immunodeficiency virus (hiv) , monocyte , immunology , endocrinology , biology , cholesterol , biochemistry
The objective of this study was to investigate changes in serum lipids among HIV-infected patients switching from non-nucleoside-reverse transcriptase inhibitors (NNRTI) to protease inhibitor (PI)-based highly active antiretroviral therapy (HAART), and to determine if changes of lipid profiles impacted the monocyte subsets recovery. Methodology: Fifty-seven subjects who switched from NNRTIs to PI-based HAART (NNRTIs to PI group) and fifty-five subjects who initially started with PI-based HAART (initial PI group) were recruited. According to their baseline triglyceride (TG) levels, the NNRTIs to PI and initial PI groups were further divided into non-hypertriglyceridemia and hypertriglyceridemia subgroups, respectively. The effects of PI-based HAART on lipid profiles and monocyte subsets were analyzed. Results: At 48 weeks, the TG changes in the NNRTIs to PI group was higher than that of the initial PI group. The increases of serum TG levels in the initial PI non-hypertriglyceridemia group was greater than that of the NNRTIs to PI non-hypertriglyceridemia group. For the hypertriglyceridemia group at baseline, significant increment in TG levels were observed in the NNRTIs to PI hypertriglyceridemia group. The percentages of circulating CD14highCD16+ and CD14lowCD16+ subsets were elevated in the two groups. At 48 weeks, the proportion of CD14highCD16+ monocytes declined gradually, and the proportion of CD14lowCD16+ monocytes decreased independently of the TG level. Conclusions: For non-hypertriglyceridemia individuals at baseline, PI-based regimens increased the TG level in the initial PI group. For the NNRTIs to PI hypertriglyceridemia group, PI-based regimens reinforced HAART-related hypertriglyceridemia.

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