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[我们抗信号识别颗粒(SRP)阳性的肌炎患者的临床特征及治疗反应]

[Clinical features and therapeutic response of our anti-SRP positive patients with myositis].

作者信息

Botos Balázs, Nagy-Vincze Melinda, Dankó Katalin

机构信息

I. Belgyógyászati Osztály, Borsod-Abaúj-Zemplén Megyei Központi Kórház és Egyetemi Oktatókórház Miskolc.

Belgyógyászati Intézet, Klinikai Immunológia Tanszék, Debreceni Egyetem Klinikai Központ Debrecen.

出版信息

Orv Hetil. 2017 Sep;158(35):1382-1389. doi: 10.1556/650.2017.30827.

Abstract

INTRODUCTION

Idiopathic inflammatory myopathies are a group of clinically heterogeneous diseases, which have been classified by myositis specific antibodies recently. The anti-SRP positive subset of this group is characterized by more severe clinical prognosis than other myositis specific antibody positive types.

AIM

Our goal was to compare 16 anti-SRP positive patients in the Division of Clinical Immunology, Department of Internal Medicine, University of Debrecen with 16 antibody negative ones.

METHOD

Muscle strength validated in both groups by the manual muscle test proved to be significantly decreased both before and after therapy (χ = 0.006 and 0.019) in the anti-SRP positive group.

RESULTS

Muscle-specific inflammatory laboratory parameters showed significant difference only in case of LDH-levels after therapy. Both groups showed good clinical response to first line steroid treatment, yet the significantly higher rate of second line administration suggests worse therapeutic response of the antibody positive group.

CONCLUSION

Based on these facts we determined poor clinical prognosis and therapeutic response of the anti-SRP positive group. Orv Hetil. 2017; 158(35): 1382-1389.

摘要

引言

特发性炎性肌病是一组临床异质性疾病,最近已根据肌炎特异性抗体进行分类。该组中抗信号识别颗粒(SRP)阳性亚组的临床预后比其他肌炎特异性抗体阳性类型更严重。

目的

我们的目标是比较德布勒森大学内科临床免疫科的16例抗SRP阳性患者和16例抗体阴性患者。

方法

通过徒手肌力测试验证,两组患者的肌力在治疗前后均显著下降(抗SRP阳性组中χ = 0.006和0.019)。

结果

肌肉特异性炎性实验室参数仅在治疗后的乳酸脱氢酶(LDH)水平方面存在显著差异。两组对一线类固醇治疗均显示出良好的临床反应,但二线治疗的显著更高比例表明抗体阳性组的治疗反应较差。

结论

基于这些事实,我们确定抗SRP阳性组的临床预后和治疗反应较差。《匈牙利医学周报》。2017年;158(35): 1382 - 1389。

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