4.2 Article

Abnormal platelet phenotypes in patients with myelodysplastic syndromes

Journal

INTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY
Volume 42, Issue 4, Pages 371-379

Publisher

WILEY
DOI: 10.1111/ijlh.13191

Keywords

flow cytometry; MDS; phenotype; platelets

Categories

Funding

  1. National Natural Science Foundation of China [81170472] Funding Source: Medline
  2. Application Bases and Advanced Technology Research Program of Tianjin [14JCYBJC27200, 09JCYBJC112 00] Funding Source: Medline
  3. Key National Natural Science Foundation of Tianjin [16JCZDJC35300] Funding Source: Medline
  4. Key Technology Research and Development Program of Tianjin [18ZXDBSY00140] Funding Source: Medline

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Introduction Hemorrhage and infection are two main causes of death in patients with myelodysplastic syndromes (MDS), and it is becoming increasingly clear that platelet dysfunction can also affect the process of hemostasis and anti-infection. The aim of this study was to evaluate activation function and immune-related function of platelets in MDS. Methods We included 29 MDS patients and divided them into different subgroups (low-risk group and high-risk group; untreated group and treated group; pretransfusion group and post-transfusion group) according to IPSS-R score, hypomethylating agents (HMAs) therapy, and platelet transfusion history. Platelet light scatter properties, expression of CD41a, activation-associated phenotypes (CD62p and CD63), and immune-associated phenotypes (CD154 and TLR4) were detected by multiparameter flow cytometry. Results Expression of CD41a was decreased (P < .05), and no difference was found in platelet light scatter properties between MDS patients and healthy subjects (P > .05). Significantly decreased expression frequency and intensity of activation phenotype CD63 were found in patients with MDS (P < .05). Low-risk MDS showed lower expression frequency while high-risk MDS showed reduced mean fluorescence intensity (MFI) of CD63. Decreased expression of CD154 and TLR4 was found in MDS patients (P < .05) which was significantly elevated after HMAs therapy (P < .05). Particularly, MFI of CD154 and TLR4 reduced in high-risk MDS patients (P < .05). Conclusion Myelodysplastic syndromes patients displayed defective expression of both activation- and immune-associated platelet phenotypes, with differential mechanisms between low-risk and high-risk groups regarding phenotype alterations. The findings confirmed impaired platelet phenotypes in MDS which may assist in the diagnosis and identification of MDS patients.

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