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Platelets. 2019 Oct 13:1-7. doi: 10.1080/09537104.2019.1678114. [Epub ahead of print]

Influence of antiretroviral therapy and cardiovascular disease on the immature platelet fraction in patients living with HIV.

Author information

1
Department of Medicine I, Technical University of Munich, School of Medicine, University Hospital Klinikum rechts der Isar , Munich , Germany.
2
DZHK (German Centre for Cardiovascular Research), Partner Site Munich Heart Alliance , Munich , Germany.
3
Department of Medicine II, Technical University of Munich, School of Medicine, University Hospital Klinikum rechts der Isar , Munich , Germany.
4
DZIF (German Center for Infection Research), partner site Munich , Munich , Germany.
5
Department of Dermatology and Allergology, Technical University of Munich, School of Medicine, University Hospital Klinikum rechts der Isar , Munich , Germany.
6
Medizinisches Versorgungszentrum am Karlsplatz, HIV Clinical Care and Research Center , Munich , Germany.
7
School of Medicine, Institute for Medical Informatics, Statistics and Epidemiology, Technical University of Munich , Munich , Germany.

Abstract

Cardiovascular disease is an important contributor to morbidity and mortality in people living with HIV . The immature platelet fraction (IPF) is increased in HIV-negative patients with cardiovascular disease and evidence suggests that an enlarged IPF is associated with adverse cardiovascular events. In this multi-center observational study, we aimed to investigate how the IPF in people living with HIV is influenced by antiretroviral therapy and cardiovascular disease. Subjects without cardiovascular disease that received antiretroviral therapy showed a smaller IPF accompanied by lower D-dimer and C-reactive protein (CRP) levels compared to therapy-naïve subjects (mean IPF: 2.9% vs. 3.9%, p = .016; median D-dimer: 252 µg/L vs. 623 µg/L, p < .001; median CRP: 0.2 mg/dL vs. 0.5 mg/dL, p = .004). No significant differences for the IPF, D-dimer or CRP were found between subjects on antiretroviral therapy with documented cardiovascular disease and therapy-naïve subjects. In conclusion, we observed a reduction in the IPF among subjects on therapy only in the absence of cardiovascular disease. In contrast, subjects receiving therapy that had documented cardiovascular disease showed an IPF comparable to therapy-naïve subjects. Future studies are needed to investigate if an enlarged IPF may serve as a biomarker in predicting adverse cardiovascular events in people living with HIV.

KEYWORDS:

Antiretroviral therapy; HIV; blood platelets; cardiovascular diseases; immature platelets; inflammation

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