Journal
THROMBOSIS RESEARCH
Volume 203, Issue -, Pages 12-17Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.thromres.2021.04.018
Keywords
Antiphospholipid syndrome; Thrombosis; Thrombocytopenia; Neutrophil-to-lymphocyte ratio; MPV-to-lymphocyte ratio; Platelet-to-lymphocyte ratio
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In this study, we assessed the performance of MPV, PLR, NLR, and MPV-to-lymphocyte ratio in APS patients and found that baseline MPV and PLR may help identify APS patients according to their thrombotic or thrombocytopenic phenotype. These variables change during acute events and may reflect physiopathological or compensatory mechanisms in APS.
Objective: To assess the mean platelet volume (MPV), platelet-to-lymphocyte ratio (PLR), the neutrophil-tolymphocyte ratio (NLR) and the MPV-to-lymphocyte ratio, and to test them according to the clinical/serological status, shift through time and other comorbidities in APS. Methods: We included 96 primary APS patients according to the Sydney classification criteria and/or patients with thrombocytopenia and/or autoimmune hemolytic anemia who also fulfilled the serological criteria. We tested aCL, anti-82GP-I and aPS/PT antibodies and LA. We first registered the MPV and the aforementioned ratios within at least 6 months after an event of thrombosis or thrombocytopenia/AIHA (baseline determination), and during thrombosis/thrombocytopenia/AIHA onset when available (acute event). Results: A lower baseline MPV and a higher PLR characterized the thrombotic group (n = 74). The AUC for baseline PLR was 0.82 (p < 0.001): SE of 69%, SP 91%, PPV 96%, NPV 74%, LR+ 13.67 and LR- 0.19. During the acute event, both variables increased. The thrombocytopenic group (n = 66) had a higher baseline MPV and a lower PLR, and during an acute event the PLR decreased more deeply. The AUC for MPV was 0.64 (p = 0.02): SE 44%, SP 92%, PPV 86%, NPV 40%, LR+ 3.3 and LR- 0.85. These findings were not related with the aPL antibody profile status, titers or comorbidities. Conclusion: Basal MPV and PLR might help to identify APS patients according to their thrombotic or thrombocytopenic phenotype. These variables change during the acute events and might be the reflex of physiopathological or compensatory mechanisms in APS.
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