B B Nkambule1, G M Davison2, H Ipp1. 1. Division of Haematology, Department of Pathology, Stellenbosch University and NHLS, Tygerberg, South Africa. 2. Department of Biomedical sciences, Faculty of Health and wellness sciences, Cape Peninsula University of Technology, Bellville, South Africa.
Abstract
INTRODUCTION: Cardiovascular disease and thrombotic events have emerged as major causes of mortality in people living with HIV. Activated platelets play a key role in both inflammation and thrombosis. Haematology analysers measure a variety of platelet indices, which could be surrogate markers of platelet activation. Flow cytometry offers the discrimination of platelet subpopulations and evaluation of the activation status of platelets. This study aimed to measure platelet indices in untreated HIV infection and to evaluate their relationship with markers of immune activation and disease progression. MATERIALS AND METHODS: One hundred and eighty-five antiretroviral therapy (ART)-naïve HIV-infected and 145 HIV-negative healthy individuals were recruited. Platelet indices measured using the ADVIA 2120 platform consisted of platelet count (PLT ×10(9) /L), mean platelet volume (MPV fL), platelet distribution width (PDW%) and plateletcrit (PCT%). These were correlated with CD4 count, %CD38 on CD8+ (CD38/8) T cells, viral load, fibrinogen, D-dimers and CD31+ platelet CD62P and CD36 expression, determined using flow cytometry. RESULTS: The HIV group had decreased MPV levels [median 7.7 (7.1-8.3) vs. control group 8.4 (7.8-9.2), P < 0.0001], which correlated with PCT% (r = 0.3038, P = 0.0013), viral load (r = 0.2680, P = 0.0177) and PDW% (r = 0.2479, P = 0.0257). Additionally, the MPV correlated with CD4 count r = -0.2898, P = 0.0075. The HIV group had decreased PDW%, 49.35 (46.40-52.65) vs. control group, 53.90 (50-56.80), P = 0.0170. In addition, the PDW% showed correlations with D-dimers (r = 0.443, P = 0.03) and %CD36 (r = -0.3666, P = 0.0463). CONCLUSION: Platelet indices may offer a rapid and affordable method for monitoring platelet activation and disease progression in patients with HIV.
INTRODUCTION:Cardiovascular disease and thrombotic events have emerged as major causes of mortality in people living with HIV. Activated platelets play a key role in both inflammation and thrombosis. Haematology analysers measure a variety of platelet indices, which could be surrogate markers of platelet activation. Flow cytometry offers the discrimination of platelet subpopulations and evaluation of the activation status of platelets. This study aimed to measure platelet indices in untreated HIV infection and to evaluate their relationship with markers of immune activation and disease progression. MATERIALS AND METHODS: One hundred and eighty-five antiretroviral therapy (ART)-naïve HIV-infected and 145 HIV-negative healthy individuals were recruited. Platelet indices measured using the ADVIA 2120 platform consisted of platelet count (PLT ×10(9) /L), mean platelet volume (MPV fL), platelet distribution width (PDW%) and plateletcrit (PCT%). These were correlated with CD4 count, %CD38 on CD8+ (CD38/8) T cells, viral load, fibrinogen, D-dimers and CD31+ platelet CD62P and CD36 expression, determined using flow cytometry. RESULTS: The HIV group had decreased MPV levels [median 7.7 (7.1-8.3) vs. control group 8.4 (7.8-9.2), P < 0.0001], which correlated with PCT% (r = 0.3038, P = 0.0013), viral load (r = 0.2680, P = 0.0177) and PDW% (r = 0.2479, P = 0.0257). Additionally, the MPV correlated with CD4 count r = -0.2898, P = 0.0075. The HIV group had decreased PDW%, 49.35 (46.40-52.65) vs. control group, 53.90 (50-56.80), P = 0.0170. In addition, the PDW% showed correlations with D-dimers (r = 0.443, P = 0.03) and %CD36 (r = -0.3666, P = 0.0463). CONCLUSION: Platelet indices may offer a rapid and affordable method for monitoring platelet activation and disease progression in patients with HIV.
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