• 中国科学论文统计源期刊
  • 中国科技核心期刊
  • 美国化学文摘(CA)来源期刊
  • 日本科学技术振兴机构数据库(JST)

临床输血与检验 ›› 2025, Vol. 27 ›› Issue (4): 492-498.DOI: 10.3969/j.issn.1671-2587.2025.04.009

• 调查研究 • 上一篇    下一篇

东莞地区CD36抗原缺失型血小板献血者资料库的建立与分析*

何子毅1, 胡应明1, 贝孟辉1, 刘静2, 揭小梅1, 陈少彬1, 钟炽辉1, 梁华钦2   

  1. 1东莞市中心血站,广东东莞 523011;
    2广州血液中心临床输血研究所,广东广州 510410
  • 收稿日期:2025-02-18 出版日期:2025-08-20 发布日期:2025-08-22
  • 作者简介:何子毅,主要从事血液免疫学和输血传播疾病研究,(E-mail)zyhe_8@163.com。
  • 基金资助:
    *本课题受东莞市社会科技发展重点项目(No.20231800936012)、广州市医学重点学科项目(No.2025-2027)资助

Establishment and Analysis of the Database of CD36 Antigen-deficient Platelet Donors in Dongguan

HE Ziyi1, HU Yingming1, BEI Menghui1, LIU Jing2, JIE Xiaomei1, CHEN Shaobin1, ZHONG Chihui1, LIANG Huaqin2   

  1. 1Dongguan Blood Center, Dongguan 523011, Guangdong;
    2Guangzhou Blood Center, Guangzhou 5140410, Guangdong
  • Received:2025-02-18 Online:2025-08-20 Published:2025-08-22

摘要: 目的 建立东莞地区CD36抗原缺失型血小板献血者资料库并进行特点分析。方法 对565名纳入建库标准的献血者血样本采用流式细胞术进行血小板CD36抗原检测,对13例CD36抗原缺失型和187例纳入建库标准的献血者血样本采用三代基因测序分析技术进行基因序列检测。结果 流式细胞术共检出血小板CD36抗原缺失型13例,缺失型率为2.30%(13/565),其中Ⅰ型缺失型2例,占15.38%(2/13),Ⅱ型缺失型11例,占84.62%(11/13);CD36抗原缺失型率在性别、民族和ABO血型分布比较均无显著性差异(P>0.05);13例CD36抗原缺失型和187例CD36正常型血样本经三代基因序列测序,13例CD36缺失型中有7例发生基因突变,其中5例在外显子,2例在内含子区域,2例Ⅰ型未检出基因突变,发生基因突变均为Ⅱ型缺失型,且均为杂合子。187例CD36正常纳入建库标准献血者共检出27例CD36基因突变,CD36缺失型基因突变率(53.85%,7/13)高于CD36正常型基因突变率(14.44%,27/187)(P<0.05)。结论 本地区血小板CD36抗原缺失型频率除高于重庆地区外,与国内其他地区报道基本一致,适合采用血清学方法在本地区建立一支CD36抗原缺失型血小板献血者资料库,保障临床输血安全。

关键词: 血小板, CD36, 基因, 献血者, 血小板资料库

Abstract: Objective To establish a database of CD36 antigen-deficient platelet donors in Dongguan and analyze the characteristics. Methods Samples from 565 blood donors were tested for platelet CD36 antigen expression using flow cytometry. The gene sequences of 13 CD36-deficient samples and 187 samples from blood donors included in the database were analyzed using the third-generation gene sequencing (TGS). Results Flow cytometry detected CD36 deficiency in 13 cases, yielding a deficiency rate of 2.30% (13/565). Of these, 2 cases were type Ⅰ deficient (15.38%) and 11 cases were type Ⅱ deficient (84.62%). There was no significant difference in the rate of CD36 antigen deletion based on gender (P>0.05), ethnicity (Han vs. minority groups, P>0.05), or ABO blood group distribution (P>0.05). TGS revealed mutations in 7 of the 13 CD36 deficient samples, including 5 exons and 2 intron regions. Both type Ⅰ cases showed no detectable mutations, while all type Ⅱ cases exhibited heterozygous mutations. Additionally, 27 CD36 gene mutations were identified in 187 CD36 normal donors. The mutation rate in CD36 deficient donors (53.85%, 7/13) was significantly higher than that of CD36 normal donors (14.44%, 27/187) (P<0.05). Conclusion The frequency of platelet CD36 deficiency in Dongguan is higher than that reported in Chongqing but consists with findings from other Chinese regions. Establishing a serologically validated CD36-deficient platelet donor database in the area is recommended to enhance clinical transfusion safety.

Key words: Platelets, CD36, Gene, Blood donor, Platelet donor database

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