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    • br Acknowledgements We thank the support

    2021-09-16


    Acknowledgements We thank the support of the National Natural Science Foundation of China (NSFC) project 81501342 and support from the Disciplinary Group of Oncology and Immunology program of Xinxiang Medical University.
    Introduction First described as a new clinical entity in 1981, the Acquired Immune Deficiency Syndrome (AIDS) was later attributed to infection with the human immunodeficiency virus (HIV). Our understanding of this disease has expanded significantly over the last decades. Following its natural course, HIV infection leads to severe depletion of CD4 T FR 236924 in the gut-associated lymphoid tissue with subsequent reduced levels of circulating CD4 lymphocytes in the peripheral blood. The CD4 cell count (which normally varies between 500 and 1400 cells/μL) reflects the level of immune suppression. As the CD4 cell count falls below normal, and particularly once thresholds of 200 cells/μL or a CD4 percentage of 14% are reached, the risk of opportunistic infection rises. Hence, CD4 cell count has been regarded as the key surrogate marker for prognostic staging and therapeutic monitoring of HIV-infected individuals and has had considerable value for both clinicians and people living with HIV.6, 7 Currently, absolute CD4 cell counts are regularly used as a surrogate for the risk of developing opportunistic infections and as an endpoint in HIV randomized controlled trials. Current guidelines advocates the initiation of ART, regardless of CD4 cell count.5, 8, 9 However, viral load monitoring has become more accessible in many countries and a key instrument in monitoring therapeutic success; in this setting, the role of CD4 monitoring has been recently questioned. Current guidelines5, 9 recommend 3–6 month CD4 monitoring in HIV-infected patients, but advise to consider less frequent evaluation for clinically stable, virally suppressed patients with high CD4 cell counts. Contrary to viral load monitoring, CD4 cell count has a low sensitivity and specificity to detect virological failure or the emergence of drug resistance during antiretroviral therapy.10, 11 Recent studies (including a meta-analysis) have debated whether there is a benefit of continued monitoring of CD4 cell counts in patients with both high CD4 cell counts and sustained viral suppression.12, 13, 14, 15, 16 Cessation of CD4 monitoring would, on one hand, avoid misinterpretations of random fluctuations in CD4 cell counts and, on the other hand, allow substantial cost-savings.
    Methods Data were analyzed with SPSS®22.0 and GraphPad®5. The results were considered statistically significant when p < 0.05.
    Discussion In accordance with current guidelines, both viral load and CD4 cell counts are monitored in patients with antiretroviral therapy in high-income settings, at least every 6–12 months. Viral load monitoring is the preferred approach to access treatment efficacy and detect adherence problems. The added value of CD4 cell count monitoring in patients with continuous viral suppression has been recently questioned. In this study, we assessed the probability of maintaining a CD4 count over 200 cells/μL during continuous viral suppression. Our results are in agreement with recent published papers12, 13, 14, 15, 16: we have found that the probability of a CD4 count <200 cells/μL in an HIV-infected patient with continuous viral suppression and CD4 counts ≥300 cells/μL was very low. All patients with CD4 counts >300 cells/μL and continuous viral suppression maintained CD4 count >200 cells/μL during the follow-up period (after exclusion of those with a non-HIV cause for CD4 lymphopenia). A number of factors other than HIV infection influence CD4 cell counts. Significant changes in the total white cell count can lead to marked changes in the absolute CD4 cell count. Certain medications or infections associated with leukopenia may result in depression of the absolute CD4 cell count. In contrast, specific medications or infections which lead to leucocytosis can result in elevated CD4 cell count. In our study, we found that 60.7% of patients that experienced a CD4 dip had an identifiable non-HIV cause for CD4 lymphopenia, making it predictable.