本文通过分析风湿免疫疾病诊疗过程中存在的问题、患者特点等，阐明了培养住院医师医学人文精神的必要性，并提出了在临床实践过程中培养住院医师医学人文精神的主要内容，包括提升住院医师对常见风湿免疫疾病诊断治疗的认知了解，训练其掌握常见的风湿免疫专业操作技能，提高其医患沟通技巧。本文系统性地阐述了相关教学方法和考核手段，提出了采取包括案例教学法（CBL）、以团队为基础的学习（TBL）、以问题为中心的学习（PBL）、以病例讨论为主的互动式教学查房模式等多样化教学方法培养住院医师，并通过技能考核、理论考核及患者评价的方式检验教学质量与成果。

目的 分析系统性红斑狼疮(SLE)合并血栓性血小板减少性紫癜(TTP)患者的临床特点、诊治与预后.方法 回顾性分析13例SLE合并TTP患者的临床特征和实验室检查资料.结果 13例患者中,男4例,女9例.其中,5例诊断为SLE后确诊为TTP,8例同时诊断SLE和TTP.3例为SLE中度活动,10例为SLE重度活动.患者均出现血小板减少、微血管病性溶血性贫血和乳酸脱氢酶(LD H)水平升高.患者主要的临床症状包括发热(12例)、肾功能损害(11例)和神经系统异常(10例).7例患者接受糖皮质激素联合免疫抑制剂治疗,3例有效;6例患者接受血浆置换联合糖皮质激素及免疫抑制剂治疗,5例有效.6例患者长期随访病情稳定,5例死亡,2例失访.结论 SLE合并TTP患者常伴随SLE中、重度活动.当患者出现肾脏及神经系统症状时,应及时检测LDH水平与外周血涂片.糖皮质激素联合免疫抑制剂基础上早期联用血浆置换有利于改善SLE合并TTP患者预后.

选取南京鼓楼医院风湿免疫科诊治的1例抗黑色素瘤分化相关基因5（MDA5）抗体阳性DM伴多发皮下钙化结节患者进行讨论，并复习相关文献。本例患者的临床表现为全身多处皮肤红疹伴瘙痒、局部破溃、双下肢肌肉酸痛乏力、膝关节疼痛活动受限、四肢及躯干皮下结节，肌肉活检示炎症细胞浸润，肌电图示肌损改变，实验室检查示抗MDA5抗体阳性，胸部CT示双肺下叶轻度间质性改变，膝关节及其周围软组织彩色多普勒超声示膝关节皮下多发钙化灶。经激素、免疫抑制剂、地尔硫 、双膦酸盐治疗后皮疹明显好转，皮下结节未再增多。因此合并严重皮疹的抗MDA5抗体阳性DM患者需及时控制炎症减轻皮疹，并在早期关注有无皮下钙化表现，尽早治疗。

Objective To investigate the expression of transcription factor AT-rich interaction domain 3a (ARID3a) in peripheral blood B cells of patients with systemic lupus erythematosus (SLE) and its clinical significance. Methods Peripheral blood mononuclear cells were isolated from 17 SLE patients and 13 healthy controls. Then, the expression of ARID3a by B cells was determined by flow cytometry. Data was analyzed with independent sample t test. The correlations between the frequencies of ARID3a+ B cells and clinical indicators of SLE patients were assessed by Pearson cor relation analysis. The expression of ARID3a in kidney was detected by immunohistochemistry in 14 cases of lupus nephritis (LN). Results The percentages of ARID3a+ B cells in SLE patients [(51.6±3.2)%] were significantly higher than those in healthy controls [(32.6±3.4)%](t=4.0, P<0.01). There was a positive correlation between the percentages of ARID3a+ B cells in SLE patients and their 24-hour urinary protein (r=0.68, P<0.05). Furthermore, the percentages of ARID3a+ B cells in peripheral blood from patients with active LN[(62.3±4.3)%] were remarkably higher than that from patients without LN or with inactive LN [(43.3±2.8)%] (t=3.8, P<0.01). The expression of ARID3a in glomerula and tubules of LN patients markedly increased. Conclusion Elevated expression of transcription factor ARID3a in B cells may participate in the pathogenesis of LN. Key words: Lupus erythematosus, systemic; Lupus nephritis; B cells; AT-rich interaction domain 3a