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 Table of Contents  
SPECIAL COMMUNICATION
Year : 2020  |  Volume : 5  |  Issue : 2  |  Page : 240-241

Clinical significance of C1q-human leukocyte antigen antibody in patients refractory to platelet transfusion


Beijing Red Cross Blood Center, Beijing, China

Date of Submission21-Oct-2020
Date of Decision21-Oct-2020
Date of Acceptance21-Oct-2020
Date of Web Publication13-Nov-2020

Correspondence Address:
Jia Yanjun
Beijing Red Cross Blood Center, Beijing
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2468-8398.300647

Rights and Permissions

How to cite this article:
Dongmei L, Jie W, Yuanyuan J, Dongmei W, Na L, Xiaoyan S, Yanjun J. Clinical significance of C1q-human leukocyte antigen antibody in patients refractory to platelet transfusion. Glob J Transfus Med 2020;5:240-1

How to cite this URL:
Dongmei L, Jie W, Yuanyuan J, Dongmei W, Na L, Xiaoyan S, Yanjun J. Clinical significance of C1q-human leukocyte antigen antibody in patients refractory to platelet transfusion. Glob J Transfus Med [serial online] 2020 [cited 2020 Nov 25];5:240-1. Available from: https://www.gjtmonline.com/text.asp?2020/5/2/240/300647

This special communication is reproduced with permission from Journal of Clinical Transfusion and Lab Medicine





  Introduction Top


Immunological factors are the main causes of platelet transfusion refractoriness (PTR), in addition to the quality of platelets and clinical factors, such as too few platelets, poor quality, improper preservation, fever, infection, splenomegaly, Disseminated Intra-vascular coagulation (DIC), and drug effects. Immunological factors mainly refer to the presence of human leukocyte antigen (HLA) antibody and/or human platelet antigen (HPA) antibody in PTR patients. According to literature reports, 30%–70% of panel-reactive antibody (PRA) patients with repeated platelet transfusion will have platelet transfusion failure, of which immunological factors account for about 20%–30%.

At present, for PTR patients with HLA and HPA antibodies, cross-matching blood test is needed to provide compatible platelets. However, we found that many PTR patients, especially highly sensitized patients, are often difficult to find compatible platelets. The reason may be that the antibody detected by enzyme-linked immunosorbent assay is HLA immunoglobulin G (IgG) total antibody including complement-binding antibody and noncomplement-binding antibody. Complement-binding antibody is a destructive antibody that can fix complement and bind to platelet surface in cytotoxic effect, but noncomplement-binding antibody does not lead to platelet destruction. It has been reported in many literatures that cytotoxic antibodies (i.e., antibodies that can bind to complement and produce cytotoxicity) play more important role in the rejection of heart transplantation and kidney transplantation than noncomplement-binding antibodies. In addition, an article from Stanford University also preliminarily showed that the single-antigen magnetic bead method (C1q-SAB) for detecting HLA antibodies that can bind to C1q complement is better than the SAB method for detecting total IgG-SAB method in detecting clinical related HLA antibodies, and its positive patients can obtain better Corrected Count Increment (CCI) value after cross-matching blood transfusion of platelets.

Therefore, this study intends to use C1q antibody detection technology to detect HLA antibodies that can fix complement, activate complement cascade reaction, and destroy platelets; provide compatible platelets for these PTR patients; observe the clinical effect after transfusion; analyze the role of C1q HLA antibody in PTR patients; and evaluate the feasible application of C1q antibody detection technology in the detection of PTR patients.

Objective

The specificity of HLA and HPA antibodies as well as C1q-HLA antibodies in patients with PTR was analyzed to determine the clinical significance of C1q-HLA antibody for PTR patients.


  Methods Top


LABScreen® Single Antigen (LSA) kit and C1qScreen™ kit were used to detect the specimens from HLA antibody-positive PTR patients to analyze the specificity of HLA and HPA antibodies, and whether these HLA antibodies could combine with complement component C1q.


  Results Top


In forty patients, ten patients (25%) had HPA antibodies which were mainly against glycoprotein GP IIb/IIIa [Table 1].
Table 1: Glycoprotein specificity of sera with broad reactivities against platelet glycoproteins

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In 39 cases of HLA-LSA-positive and 28 C1q-positive patients [Table 2], the percentage of PRA% and max mean fluorescence intensity of LSA-positive patients were significantly higher than those of C1q-positive patients [Figure 1] and [Figure 2]. There was no significant difference in the CCI value between C1q-positive and -negative patients [Figure 2] and [Figure 3] after random platelet transfusion. Different status of HLA antibodies had no significant effect on the difficulty of finding compatible cross-matched platelets for PTR patients.
Table 2: Patient characteristics at study entry and the positive % of C1q antibody

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Figure 1: The panel-reactive antibody (a) and max mean fluorescence intensity (b) of LABScreen® Single Antigen antibody positive and C1q antibody positive in the serum of patients refractory to platelet transfusion

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Figure 2: Probability of success for platelet cross-match at different LABScreen® Single Antigen Ab and C1q antibody

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Figure 3: The influence of C1q status on platelet transfusion response

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  Conclusion Top


The results of this study showed that there was no direct correlation between C1q-HLA antibodies and the clinical result of platelet transfusion. The occurrence of C1q-HLA antibodies may not increase the difficulty of finding compatible platelets for PTR patients.

For detailed article, log on to: Journal of Clinical Transfusion and Lab Medicine Available from: http://www.lcsxyjy.com/ CN/10.3969/j.issn. 1671-2587.2020.02.004.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.




    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1], [Table 2]



 

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