系统性红斑狼疮合并脑梗死1例

红斑狼疮是一种多发于青年女性的累及多脏器的自身免疫性炎症性结缔组织病。因其临床表现多样,常易误诊,在临床工作中曾经收治1例出现神经系统并发症,最后才明确诊断为系统性红斑狼疮合并脑梗死的患者,现报道如下：     

1例系统性红斑狼疮合并肺孢子菌肺炎的治疗报告

临床药师参与1例系统性红斑狼疮合并耶氏肺孢子菌肺炎患者的药学监护,在SMZ/TMP联合卡泊芬净经验性治疗后,患者因口服SMZ/TMP出现不良反应且不耐受,临床药师通过查阅文献,以卡泊芬净联合克林霉素治疗后患者临床症状明显改善.     

1例系统性红斑狼疮合并视网膜动脉闭塞的治疗并文献复习

目的：探讨系统性红斑狼疮（SLE）合并视网膜动脉闭塞的治疗方案。方法：通过1例本病的治疗情况，结合国内外文献复习．对SLE合并视网膜动脉闭塞的临床特点和治疗方案进行综合分析。结果：SLE合并视网膜动脉闭塞患者大多抗磷脂抗体阳性．抗凝治疗可以改善视网膜病变，防止血栓事件再次发生；免疫抑制剂治疗效果不明确；溶栓和阿司匹林治疗不能达到视网膜动脉再通和防止再次血栓形成；全视网膜光凝术或玻璃体切割可以延缓视力减退。结论：SLE合并视网膜动脉闭塞应接受长期抗凝治疗．必要时行全视网膜光凝术或玻璃体切割。     

系统性红斑狼疮合并胃肠道血管炎1例报告

系统性红斑狼疮（systemic lupus erythematosus ,SLE）是一种好发于青年女性的累及多器官的自身免疫性结缔组织病,常见的受累器官为皮肤、血液系统和肾脏,消化系统作为首发的靶器官相对少见。研究［1］发现,大约25％ ～ 50％ 患者有纳差、呕吐、腹痛、腹泻或腹水等消化系统表现,少数可并发急腹症,如肠梗阻、肠坏死、胰腺炎等,这些胃肠道表现大多与SLE 并发肠壁、肠系膜血管炎有关。     

男性系统性红斑狼疮合并急性心肌梗死1例

患者,男,50岁。主因阵发性胸痛4d,加重6h入院。缘于4天前患者无明显诱因出现胸部闷痛,以心前区为著,向左肩部放射,无汗出、恶心、呕吐等不适,含服“速效救心丸”10粒约3-5min症状缓解,未予诊治。入院6h前患者无明显诱因再次出现心前区闷痛,伴汗出,无恶心、呕吐,无头疼、头晕等,含服“速效救心丸”等药,症状持续不缓解,急收入我院。既往高血压病史6年,最高150/100mm Hg（1mm Hg=0133kPa）,自服降压药物（具体治疗不详）,血压控制可。系统性红斑狼疮、狼疮肾炎1年余,     

系统性红斑狼疮伴带状疱疹1例药学监护

目的 分析临床药师在系统性红斑狼疮(SLE)伴带状疱疹(HZ)患者的药学监护模式和监护重点.方法 临床药师通过参与1例SLE伴HZ患者的药物治疗,从药物选择、剂量调整及用药教育等方面提供药学监护.结果 医师采纳临床药师的建议,监测患者病情,及时调整药物治疗方案,使患者的临床症状缓解,好转出院.结论 通过全面的开展药学监...     

系统性红斑狼疮猝死1例报告

1病例报告患者,男,31岁。因发热伴头痛4d入院。患者于3年前发现患有系统性红斑狼疮,长期服用糖皮质激素等药物治疗,1年前并发脉管炎,双下肢有大面积的溃疡面。于4d前无明显诱因出现发热,     

1例系统性红斑狼疮

病例资料：患者女 ,２６岁。患者于２０００年１２月３１日剖宫产１男婴 ,产后无特殊不适。入院前１月 (即２００１年４月 )无诱因出现腰痛、下肢浮肿。化验尿提示有蛋白。曾诊断为急性肾炎。经治疗症状无明显好转。随之出现发热 ,体温高达４００Ｃ ,伴有心悸、胸闷、气促 ,夜间平卧困难。既往无高血压病及风湿热病史。入院查 :体温在３９～４００Ｃ ,半坐位 ,痛苦病容 ,皮肤无红斑。口唇无发绀 ,颈静脉无怒张。双肺呼吸音粗 ,未闻及干湿性罗音 ,右下肺呼吸音减弱。心浊音界向左下扩大 ,各瓣膜听诊区未闻及杂音。双下肢无浮肿。入院后摄胸片…     

抢救系统性红斑狼疮合并多器官功能衰竭1例

1病案摘要 患者，女，27岁，因咳嗽、咳痰、发热3d，胸闷、气喘1d，于2009年12月28日来院急诊。胸片示两下肺片絮状高密度影、心影明显增大；CT示双肺多发絮状、结节状密度增高影。当天上午10：40收入病房。患者既往有系统性红斑狼疮（SLE）、慢性肾功能不全病史8年，高血压2年余，长期使用免疫抑制剂（糖皮质激素、马替麦考酚脂等）及降压保肾治疗。     

系统性红斑狼疮合并横贯脊髓炎临床分析(附1例报告)

目的 :加强对系统性红斑狼疮 (SLE)合并横贯性脊髓炎 (TM)的认识。方法 :报告 1例系统性红斑狼疮合并横贯性脊髓炎并复习文献。结果 :总结SLE合并TM的临床表现、诊断及治疗。结论 :TM是一个少见但严重的SLE的并发症。     

妊娠合并系统性红斑狼疮的临床分析

目的探讨妊娠与系统性红斑狼疮（SLE）病情的相互影响及SLE患者妊娠时机的选择及妊娠期的处理。方法回顾性调查惠州市中心人民医院收治的31例妊娠合并SLE患者，其中选择性妊娠18例，非选择性妊娠13例，妊娠期予不同剂量泼尼松控制病情。分析比较2组患者妊娠期病情的变化和妊娠的结局。结果选择性妊娠组中6例在孕期出现狼疮活动，非选择性妊娠组的13例均出现较为严重的狼疮并发症。非选择性妊娠组的妊娠丢失率、早产率较选择性妊娠组显著增高（P〈0.05），而新生儿存活率及新生儿体质量则较选择性妊娠组显著下降（P〈0.05）。结论对妊娠合并SLE患者而言，妊娠和SLE互为不利因素；在SLE病情缓解期选择发妊娠并合理治疗将使母婴安全性明显增高。     

大剂量羟氯喹治疗系统性红斑狼疮 并发难治性血小板减少1例

目的观察大剂量羟氯喹联合糖皮质激素治疗系统性红斑狼疮并发难治性血小板减少病人的治疗效果及其不良反应。方法 2010年 9月 13日收住阜阳市人民医院系统性红斑狼疮并发难治性血小板减少病人 1例,对大剂量糖皮质激素、丙种球蛋白以及多种免疫抑制剂治疗无效,应用大剂量羟氯喹(硫酸羟氯喹 0.6 g/d)联合糖皮质激素(醋酸泼尼松 20 m/d)治疗。结果大剂量羟氯喹联合激素对此例系统性红斑狼疮并发难治性血小板减少显示出良好的治疗效果并可以长期维持血小板数量,且未见明显不良反应发生。结论大剂量羟氯喹成功治疗 1例系统性红斑狼疮并发难治性血小板减少。     

系统性红斑狼疮合并妊娠35例临床分析

目的探讨系统性红斑狼疮合并妊娠的临床特点、孕产期处理及妊娠结局。方法对35例系统性红斑狼疮合并妊娠的临床资料进行回顾性分析。结果孕期SLE病情活动者13例（活动组）,非活动者22例（非活动组）。活动组患者子痫前期发生率38.46%,胎儿生长受限发生率69.23%,非活动组发生子痫前期0例,胎儿生长受限发生率13.64%,两组分别比较差异有统计学意义（P均〈0.05）。活动组患者胎膜早破、胎儿窘迫、产后出血、早产的发生率及胎儿丢失率均高于非活动组,但差异均无统计学意义（P均〉0.05）。结论妊娠期SLE患者易出现产科并发症,加强孕期母婴监护,正确使用肾上腺皮质激素,多数患者能获得良好的结局。     

系统性红斑狼疮合并尿路感染的临床分析

目的探讨系统性红斑狼疮（SLE）合并尿路感染的临床特点。方法对金华市中心医院243例SLE患者中合并尿路感染的95例患者（占SLE总数的39．1％）SLE疾病活动指数、白细胞和血小板水平、血清补体（C3、C4）、红细胞沉降率、抗双链DNA及24h尿蛋白等数据、患者临床表现及相关危险因素进行分析。结果SLE合并尿路感染患者各项生理指标均出现异常,67例出现抗双链DNA升高[平均值为（67±22）U／m1],占70．5％;54例出现白细胞减少[平均值为（2．7±0．5）×10^9／L],占56．8％;51例红细胞沉降率增大[平均值为（35±18）ram／1h],占53．7％;47例血小板减少[平均值为（81±12）×10^9／L],占49．5％;42例补体C3减少[平均值为（577±213）mg／L],占44．2％;41例补体C4减少[平均值为（89±24）mg／L],占43．2％;39例24h尿蛋白增加[平均值为（4．1±1．0）g],占41．0％。发生大肠杆菌感染69例,占尿路感染总数的72．6％;混合感染81例,占85．3％。Logistic回归分析结果：Sledal评分、血白细胞和血小板减少均与尿路感染的发生显著相关（OR：3．274,OR=2．454,OR=2．133,P〈0．01或P〈0．05）。结论SLE患者易合并尿路感染,且以复杂性尿路感染为主,大肠杆菌为尿路感染的主要致病菌。     

系统性红斑狼疮合并妊娠分析

目的探讨患者在妊娠时患有系统性红斑狼疮（SLE）对母亲和胎儿的影响。方法在对2011年12月～2012年2月来本院住院的SLE合并妊娠患者的临床资料进行回顾性分析和比较。结果在50例SLE患者中共妊娠56次。医生按照选择性妊娠与非选择性妊娠分为两组，选择性妊娠组29例，活产24例，早产3例，低出生体质量儿2例，妊娠期疾病出现活动6例；非选择性妊娠组21例，活产12例，早产6例，低出生体质量儿2例，妊娠期疾病出现活动11例。选择性妊娠组活产率明显高于非选择性妊娠组，早产率明显低于非选择性妊娠组，妊娠期间疾病活动明显少于非选择性妊娠组。结论由于SLE患者选择适当的妊娠时机，并在妊娠期间加强风湿免疫科及产科的监护，这不仅可以提高活产率，也大大降低妊娠期间病情活动和早产率。     

妊娠合并系统性红斑狼疮83例临床分析

目的探讨妊娠合并系统性红斑狼疮(SLE)患者孕期原有疾病的变化与对母婴结局的影响。方法 2010年1月~2015年12月瑞金医院收治的妊娠合并SLE患者共83例。美国风湿病学会1997年推荐的SLE分类为诊断标准,分成三组:A组妊娠发生在SLE稳定6个月以上,蛋白尿<0.5g;B组妊娠时距SLE活动期<6个月;C组妊娠期新发SLE。结果在A组中,76.47%的孕妇妊娠到足月,80.39%活产。B组和C组的妊娠结局差很多。B组的妊娠复发率高达42.19%。妊娠期新发的SLE的妊娠结局比较差,但在妊娠晚期发生的SLE的结局改善很多。SLE在妊娠期的复发率较高,即便是在稳定期内妊娠,复发率可达33.33%。结论 SLE患者妊娠时发生妊娠期高血压疾病、早产、低出生体重儿的几率在SLE病情活动时明显增加,建议在病情稳定半年以上受孕,可获得最佳妊娠结局。     

急性心肌梗死并发急性脑梗死28例临床分析

目的 探讨急性心肌梗死并发急性脑梗死的诊断及治疗方法.方法 回顾性分析226例急性心肌梗死并发28例急性脑梗死患者的临床资料.结果 28例患者在救治期间,平均住院时间为32 d,其中治愈21例,好转3例,出现失语1例,出现肢体瘫痪1例,死亡2例.结论 急性心肌梗死并发急性脑梗死是临床急症,应快速反应、及时发现,抓住其治疗有效期,根据临床症状及早进行头颅CT检查,从而减少致残率和病死率,提高抢救成功率.     

B-cell-targeted therapy for systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is a complex disease characterised by numerous autoantibodies and clinical involvement in multiple organ systems. The immunological events triggering the onset of clinical manifestations have not yet been fully defined, but a central role for B cells in the pathogenesis of this disease has more recently gained prominence as a result of research in both mice and humans. Both antibody-dependent and -independent mechanisms of B cells are important in SLE. Autoantibodies contribute to autoimmunity by multiple mechanisms, including immune complex-mediated type III hypersensitivity reactions, type II antibody-dependent cytotoxicity, and by instructing innate immune cells to produce pathogenic cytokines such as interferon-alpha, tumour necrosis factor and interleukin-1. Suggested autoantibody-independent B-cell functions include antigen presentation, T-cell activation and polarisation, and dendritic-cell modulation. Several of these functions are mediated by the ability of B cells to produce immunoregulatory cytokines, chemokines and lymphangiogenic growth factors, and by their critical contribution to lymphoid tissue development and organisation, including the development of ectopic tertiary lymphoid tissue. Given the large body of evidence implicating abnormalities in the B-cell compartment in SLE, a recent therapeutic focus has been to develop interventions that target the B-cell compartment by multiple mechanisms.Rituximab, a mouse-human chimeric monoclonal antibody against CD20 that specifically depletes B cells, has been studied the most extensively. Although promising open-label data await confirmation in ongoing multicentre placebo-controlled trials, a number of preliminary conclusions can be drawn. The adequacy of peripheral B-cell depletion depends on achieving high and sustained serum rituximab concentrations, pharmacokinetics that can be varied with treatment dose and factors that may affect drug clearance, such as human anti-chimeric antibodies. In SLE patients with effective B-cell depletion, the clinical response can be significant, with favourable responses observed in a diverse array of disease manifestations. Moreover, rituximab appears to have the potential to induce clinical remission in severe, refractory disease. B-cell depletion has the potential to induce disease amelioration by inhibiting autoantibody production and/or by interfering with other B-cell pathogenic functions. The fact that clinical improvement correlates with B-cell depletion and precedes by several months any decline in serum levels of relevant autoantibodies suggests a predominant effect of autoantibody-independent functions of B cells, although the subset of patients with disease remission ultimately also experience autoantibody normalisation. Significant questions remain about rituximab therapy in SLE, including the immunological determinants of treatment response and remission, the role of combination therapy, and the safety of repeated courses of rituximab. In addition, the efficacy and role of other B-cell-depleting approaches, such as humanised anti-CD20 antibodies and anti-CD22, remain to be defined.Another B-cell-targeted therapeutic approach is to block costimulatory interactions between T and B cells. Blockade of the CD40-CD40 ligand pathway has met with variable clinical benefit and unfortunate thromboembolic complications, although inhibition of the B7 pathway with cytotoxic T-lymphocyte antigen-4Ig is currently under early investigation in SLE clinical trials. Preliminary data on the treatment of SLE with belimumab, a fully human monoclonal antibody that specifically binds to and neutralises the B-lymphocyte stimulator (BLyS or B-cell-activating factor [BAFF]), are now available. In a phase II double-blind, placebo-controlled trial of the safety and efficacy of three different doses administered in addition to standard therapy, belimumab was well tolerated but reportedly did not meet primary efficacy endpoints. Blockade of BAFF is still viewed as a promising therapeutic approach and additional agents that interfere with the BAFF pathway are under study.Overall, therapies targeting B cells appear to be promising in the treatment of SLE, provide additional evidence for the importance of B cells to disease pathogenesis, and will continue to elucidate the diverse roles of B cells in this disease.