@article {Tanboone448作者= {Jantima Tanboon井上渡和Shinya Hirakawa Hisateru Tachimori Shinichiro Hayashi和Satoru野口Shigeaki铃木和直子Okiyama Manabu藤Ichizo Nishino},标题= {Anti-Mi-2皮肌炎的病理特征},体积={96}={3},页面= {e448——e459} = {2021}, doi = {10.1212 / WNL。出版商0000000000011269}= {Wolters Kluwer健康,公司代表美国神经病学学会},文摘={目的识别特征的病理特征皮肌炎(DM)与anti-Mi-2相关自身抗体(anti首页-Mi-2 DM)。方法我们回顾了188名肌肉活检的患者(1)病理诊断为糖尿病通过myxovirus-resistant的表情肌质蛋白和(2)血清学阳性1 5 DM-specific自身抗体(DMSAs) (anti-Mi-2 n = 30;其他DMSAs, n = 152)或-为所有5 DMSAs (n = 6)。然后,我们相比anti-Mi-2 DM患者的病理和免疫组织化学特点与non-Mi-2 DM和anti-synthetase综合症患者(屁股)(n = 212)使用t测试,Fisher精确检验和逻辑回归模型。anti-Mi-2 DM患者结果显示显著更高的严重程度分数比non-Mi-2 DM患者肌肉纤维和炎症域。围的出现坏死,增加perimysial碱性磷酸酶活动,和sarcolemmal膜攻击复杂沉积更频繁anti-Mi-2 DM患者(p < 0.01)。Bonferroni调整后,没有明显差异的百分比之间的上述特性anti-Mi-2 DM患者和那些屁股\ (p > 0.01)。结论围坏死和perimysial病理学特性之前报道的屁股,在anti-Mi-2 DM患者很常见。我们的研究结果不仅有助于区分anti-Mi-2 DM与其他糖尿病亚型也显示重叠的可能性机制anti-Mi-2 DM和ASS.Classification证据之间的这项研究二类提供证据证明DM患者的肌肉活检anti-Mi-2自身抗体更容易展示更高的严重程度分数在肌肉纤维和炎症域。ACP =酸性磷酸酶;高山=碱性磷酸酶;ARS = aminoacyl-transfer RNA合成酶;屁股= anti-synthetase综合症;CK =肌酸激酶;考克斯=细胞色素C氧化酶; DM=dermatomyositis; DMSA=DM-specific autoantibody; ENMC-DM=European Neuromuscular Centre DM workshop; H\&E=hematoxylin \& eosin; IFN1=type I interferon; ILD=interstitial lung disease; IMPP=immune myopathies with perimysial pathology; MAC=membrane attack complex; MDA5=melanoma differentiation-associated gene 5; mGT=modified Gomori trichrome; MHC=major histocompatibility complex; MHCn=neonatal myosin heavy chain; MxA=myxovirus resistance protein A; NXP-2=nuclear matrix protein 2; PFA=perifascicular atrophy; PFN=perifascicular necrosis; PM-ALP=perimysial connective tissue ALP activity; PM-Fr=perimysial connective tissue fragmentation; SAE=small ubiquitin-like modifier activating enzyme; TIF1-γ=transcription intermediary factor 1-γ}, issn = {0028-3878}, URL = {//www.ez-admanager.com/content/96/3/e448}, eprint = {//www.ez-admanager.com/content/96/3/e448.full.pdf}, journal = {Neurology} }