结节病是以非干酪样坏死性上皮样细胞肉芽肿为病理特征的系统性疾病[1],以中青年发病为主,全球发病率约为2～160/10万[2],我国发病率尚不清楚.结节病可累及全身各个组织器官,90％以上患者会出现肺及纵隔淋巴结受累,30％～50％的患者出现胸外受累,包括眼、皮肤、肝、脾、淋巴结、唾液腺、心脏、神经系统及肌肉骨骼等,其中骨结节病非常罕见,在结节病中的发生率小于5％[3].

Objective:To elucidate the correlation between peripheral blood levels of pentraxin 3 (PTX3) and fibroblast growth factors 2 (FGF2) and clinical manifestations, immunological indexes and disease activity of systemic lupus erythematosus (SLE) patients.Methods:The correlation between peripheral blood levels of PTX3 and FGF2 and clinical manifestations, immunological indexes and disease activity of SLE pa-tients was determined. T test, Mann-Whitney U test and Spearman's rank correlation coefficient were analyzed statistically. Results:Plasma PTX3 levels were significantly higher in SLE patients than in healthy controls (3 191±2 423) pg/ml vs (755±432) pg/ml, t=5.595, P<0.01) . The titer of PTX3 in patients with hematologic in-volvement was higher than that in the patients without [(3 810±2 840) pg/ml vs (2 493±1 830) pg/ml, t=2.008, P=0.049). Plasma PTX3 concentration in SLE patients was positively correlated not only with the level of 24 h urine protein ( r=0.498 6, P=0.005 9), but also with ESR ( r= 0.376, P=0.007) and systemic lupus erythematosus disease activity index (SLEDAI) scores ( r=0.405, P=0.003). On the contrast, plasma PTX3 concentration in SLE patients was negatively correlated with complement 3 ( r=-0.405, P=0.005). Increased serum PTX3 levels accompanied by increased serum FGF2 levels was observed. Plasma FGF2 concentration in SLE patients was positively correlated with SLEDAI scores ( r=0.326, P=0.019), but negatively correlated with level of comple-ment 3 ( r=-0.414, P=0.004) and complement 4 ( r=-0.451, P=0.007). Levels of FGF2 were higher in patients with positive anti-NuA antibody [(138±91) pg/ml vs (59±68) pg/ml, t=2.996, P=0.004 2), anti-dsDNA antibody [(120±96) pg/ml vs (56±58) pg/ml, t=3.583, P=0.000 7] and anti-rRNP antibody (151±109) pg/ml vs (63±61) pg/ml, t=3.757, P=0.000 4) than in patients with negative of these antibodies. Conclusion:The levels of PTX3 and FGF2 in peripheral blood may play a role in determining the disease activity and clinical phenotype of SLE, and can help doctors to make diagnosis and treatment decisions.

OBJECTIVE:The clinical features of rheumatic patients with coronavirus disease 2019 (COVID-19) have not been reported. This study aimed to describe the clinical features of COVID-19 in rheumatic patients and provide information for handling this situation in clinical practice.METHODS:This is a retrospective case series study. Deidentified data, including gender, age, laboratory and radiological results, symptoms, signs, and medication history, were collected from 2326 patients diagnosed with COVID-19, including 21 cases in combination with rheumatic disease, in Tongji Hospital between 13 January and 15 March 2020.RESULTS:Length of hospital stay and mortality rate were similar between rheumatic and non-rheumatic groups, while the presence of respiratory failure was more common in rheumatic cases (38% vs 10%, p<0.001). Symptoms of fever, fatigue and diarrhoea were seen in 76%, 43% and 23% of patients, respectively. There were four rheumatic patients who experienced a flare of rheumatic disease during hospital stay, with symptoms of muscle aches, back pain, joint pain or rash. While lymphocytopaenia was seen in 57% of rheumatic patients, only one patient (5%) presented with leucopenia in rheumatic cases. Rheumatic patients presented with similar radiological features of ground-glass opacity and consolidation. Patients with pre-existing interstitial lung disease showed massive fibrous stripes and crazy-paving signs at an early stage. Five rheumatic cases used hydroxychloroquine before the diagnosis of COVID-19 and none progressed to critically ill stage.CONCLUSIONS:Respiratory failure was more common in rheumatic patients infected with COVID-19. Differential diagnosis between COVID-19 and a flare of rheumatic disease should be considered.TRIAL REGISTRATION NUMBER:ChiCTR2000030795.

系统性血管炎是一组以血管炎症为特征的全身性自身免疫性疾病,其临床表现和病理特征复杂多变,取决于受累血管的部位和类型.根据主要受累血管的类型,2012年Chapel Hill共识会议(CHCC)对多种血管炎进行了命名和定义,是目前使用最为广泛的血管炎命名系统.文章详细阐述了系统性血管炎的分类,并对系统性血管炎的定义、病因、流行病学和诊断进行了概述.

目的:研究维生素A(VA)缺乏对3 w龄大鼠的脂质过氧化和抗氧化系统的影响.方法:健康Wistar雄性大鼠33只,按体重随机分为A(VA完全缺乏组),B(VA轻度缺乏组),C(VA正常对照组)三组.每组11只,实验期为84 d.观察指标有:血清VA,血清、肝脏及脑组织的超氧物岐化酶(SOD)活性,全血、肝脏及脑组织的谷胱甘肽过氧化物酶(GSH-Px)活性,血清、肝脏及脑组织的丙二醛(MDA)含量,并采用电子自旋共振(electron spin resonance,ESR)和自旋捕捉技术直接测定大鼠肝组织中的氧自由基.结果:A、B组大鼠血清、肝脏及脑组织SOD活性明显下降,全血、肝脏及脑组织GSH-Px活性明显降低,血清、肝脏及脑组织MDA含量显著升高,ESR图谱出现了N-H偶合的三组双峰波.结论:VA完全或轻度缺乏均可以使大鼠脂质过氧化反应明显增强,而抗氧化能力明显减弱.

目的探讨缺锌对大鼠脑肌醇磷脂信号转导系统的影响.方法24只Wistar大鼠,雌雄各半,按体重随机分为A(缺锌组),B(自由进食组),C(配对饲养组)三组,每组8只,实验期40天,测定脑锌和血锌含量,并观察缺锌对大鼠脑组织内磷脂酶C(PLC)活性,蛋白激酶C(PKC)活性,钙调蛋白(CaM)含量,及钙依赖性蛋白激酶Ⅱ(CaMKⅡ)活性的影响.结果A组大鼠血清和脑锌含量明显降低,同时A组大鼠大脑皮层和海马中PLC,PKC,CaMKⅡ活性亦明显低于B组和C组.A组大鼠脑组织CaM含量明显低于B组,与C组无显著性差异.结论缺锌可以抑制肌醇磷脂信号转导系统.