TY - T1的病理特征Anti-Mi-2皮肌炎JF -神经学乔-神经病学SP - e448 LP - e459做- 10.1212 / 首页WNL。0000000000011269六世- 96 - 3盟Jantima Tanboon AU -井上渡盟Shinya Hirakawa盟Hisateru Tachimori Satoru野口AU - Shinichiro Hayashi盟盟- Shigeaki铃木盟直子Okiyama AU - Manabu藤盟Ichizo Nishino Y1 - 2021/01/19 UR - //www.ez-admanager.com/content/96/3/e448.abstract N2 -目标识别特征的病理特征皮肌炎(DM)与anti-Mi首页-2相关自身抗体(anti-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。围坏死的存在,增加了perimysial碱性磷酸酶活动,和sarcolemmal膜攻击复杂沉积更频繁的anti-Mi-2 DM患者(p & lt;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比;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; ASS=anti-synthetase syndrome; CK=creatine kinase; COX=cytochrome C oxidase; 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 ER -