Serum CLEC4G level and its clinical application value in atopic dermatitis patients
10.3969/j.issn.1006-5725.2023.21.019
- VernacularTitle:特应性皮炎患者血清C型凝集素结构域家族4成员G水平及其意义
- Author:
Xiang CHEN
1
;
Zuiming JIANG
;
Sheng LI
;
Min GU
;
Xitao ZHOU
;
Wenhui LUO
;
Hui LIN
;
Manling TANG
Author Information
1. 株洲市中心医院检验医学中心(湖南株洲 412007)
- Keywords:
atopic dermatitis;
CLEC4G;
interleukin-33;
immunoglobulin E
- From:
The Journal of Practical Medicine
2023;39(21):2808-2811
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the serum C-type lectin domain family 4 member G(CLEC4G)level and its clinical value in patients with Atopic Dermatitis(AD).Methods The blood samples of 60 AD patients and 29 control patients were collected,and CLEC4G,Interleukin-33(IL-33),total immunoglobulin E(tIgE),specific IgE(specific IgE),and eosinophil levels were detected.The correlation between CLEC4G level and clinical data of AD patients and IL-33 was analyzed.The risk of AD was evaluated by Logistic regression analysis of CLEC4G,IL-33 and other indicators.Results Compared with the control group,the serum CLEC4G level in AD patients was significantly decreased(359.4±57.3 vs.521.8±48.1)pg/mL.There was no significant difference in CLEC4G level between child-hood,adolescent and adult,male and female AD patients.Compared with tIgE≤100 kU/L group,CLEC4G level was significantly decreased in 100～200 kU/L group and tIgE≥200 kU/L group,but there was no significant difference between 100～200 kU/L group and tIgE≥200 kU/L group.Serum CLEC4G level decreased significantly only in the moderate AD group,but had no significant difference among the other groups.The serum level of IL-33 was increased in AD patients,but there was no significant correlation between CLEC4G and IL-33(r = 0.090,P = 0.495).Age less than 14 years old and IL-33 were risk factors for the incidence of AD,with OR values of 2.756 and 1.241,95%CI of 1.076～7.060 and 1.030～1.495,respectively.CLEC4G was a protective factor for AD(OR = 0.890,95%CI:0.809～0.979).Conclusion CLEC4G may be a protective factor independent of IL-33 mediated AD pathogenesis.
