以水肿为主要表现的系统性硬化症1例

笔者成功诊断1例76岁男性系统性硬化症患者。本患者主要表现为水肿,发病初期一直未明确诊断,对症支持治疗仅暂时缓解病情。水肿加重后查血清相关自身抗体示抗核抗体阳性,结合皮肤活检病理明确诊断为系统性硬化症。根据文献报道和笔者的临床经验,系统性硬化症临床表现复杂多样,缺乏特异性,早期诊断困难。对于临床上难以解释的水肿,应考虑本病的可能,重视患者皮肤的改变及血清相关自身抗体的检查,及早做出正确诊断。     

ST段抬高急性心肌梗死患者血清氧化低密度脂蛋白抗体-IgM水平与冠状动脉病变程度及住院期间预后的相关研究

目的：探讨血清氧化低密度脂蛋白抗体-IgM（ox-LDL-Ab IgM）水平在ST段抬高急性心肌梗死（STEMI）患者中与冠状动脉病变程度及近期预后的相关性。方法选取2008年8月至2009年5月诊断明确并行急诊经皮冠状动脉介入（PCI）治疗的STEMI患者95例,根据冠状动脉造影结果分为单支病变组、双支病变组及三支病变组,并以Gensini积分评价冠状动脉狭窄程度,分别测定血清ox-LDL-Ab IgM、丙二醛（MDA）、血脂,计算体质量指数（BMI）,统计患者住院期间心血管事件发生情况,分析ox-LDL-Ab IgM水平与冠状动脉病变程度及近期预后的关系。结果 STEMI患者血清ox-LDL-Ab IgM水平随冠状动脉病变支数增加而降低（P＜0.05）,但与Gensini积分无明显相关性（P＞0.05）;ox-LDL-Ab IgM水平与血脂、血糖水平等无明显相关性（P＞0.05）,与MDA水平呈显著负相关（r＝-0.319,P＜0.05）;ox-LDL-Ab IgM水平与患者住院期间心血管事件发生率呈显著负相关（r＝-0.708,P＜0.05）,logistic回归分析显示, ox-LDL-Ab IgM是STEMI患者住院预后的保护因素（OR＝-0.588,P＜0.05）。结论血清ox-LDL-Ab IgM水平可在一定程度上反映STEMI患者冠状动脉病变的严重程度。其可能通过调节机体氧化应激水平,减少LDL氧化修饰生成ox-LDL,从而减轻冠状动脉粥样硬化的面积,可能对STEMI患者近期预后具有保护作用。     

Australian consensus guidelines for the safe handling of monoclonal antibodies for cancer treatment by healthcare personnel

These consensus guidelines provide recommendations for the safe handling of monoclonal antibodies. Definitive recommendations are given for the minimum safe handling requirements to protect healthcare personnel. The seven recommendations cover: (i) appropriate determinants for evaluating occupational exposure risk; (ii) occupational risk level compared with other hazardous and non‐hazardous drugs; (iii) stratification of risk based on healthcare personnel factors; (iv) waste products; (v) interventions and safeguards; (vi) operational and clinical factors and (vii) handling recommendations. The seventh recommendation includes a risk assessment model and flow chart for institutions to consider and evaluate clinical and operational factors unique to individual healthcare services. These guidelines specifically evaluated monoclonal antibodies used in the Australian cancer clinical practice setting; however, the principles may be applicable to monoclonal antibodies used in non‐cancer settings. The guidelines are only applicable to parenterally administered agents.     

Renal transplantation in HLA sensitized patients: Traversing the immunological barrier

Successful renal transplantation across HLA barrier in sensitized individuals has been on the rise during the past decade, primarily due to improved desensitization regimes. The aim of this study was to share outcome of desensitization in renal transplant recipients with donor‐specific anti‐HLA antibodies (DSA). This was a retrospective analysis of all HLA immunized individuals who were prospective renal transplant recipients. All such patients underwent preconditioning as per the institutional desensitization protocol. Complement‐dependent cytoxicity‐based crossmatch (CDC‐XM), luminex‐based crossmatch (LM‐XM) and flowcytometry‐based crossmatch (FC‐XM) were done in all cases. If any of these tests turned out positive, single antigen bead assay (SAB) was performed. Desensitization for DSA was performed in 55 patients and all patients were followed‐up for 1 year to assess graft function and patient outcome. CDC‐XM being a less sensitive assay, could not detect incompatibility in 29 (52.73%) cases. After desensitization, even though SAB and LM‐XM results revealed an MFI within acceptable range, FC‐XM being an extremely sensitive assay, continued to give a positive result in eight (14.55%) cases. The mean ± SD number of pretransplant TPE were 3.44 ± 0.98 (2‐11). Out of 55, there were 10 patients who were lost to follow up. Patient and graft survival of 45 patients at 1 year was found to be 100%. Preconditioning for renal transplants in the form of immunosuppression with TPE is an extremely useful auxiliary for transplantation in HLA sensitized renal transplant recipients.     

Evolving concepts of pathogenesis of heparin‐induced thrombocytopenia: Diagnostic and therapeutic implications

Heparin‐induced thrombocytopenia (HIT) is an immune reaction to heparin. It often causes severe thrombosis which may lead to limb gangrene and thrombosis‐associated death. The concept of its pathogenesis has been evolving during the past five decades. Initially, HIT was thought to be caused by disseminated intravascular coagulation. Later it became clear that HIT was mediated by an immune mechanism whereby an IgG antibody induced platelet aggregation, release of procoagulant materials and consequently thrombus formation. The antigen comprises Platelet Factor 4 (PF4) and heparin which have a tendency to form ultralarge complexes. The HIT immune response has atypical features. IgG antibody appears early without IgM precedence and lasts transiently. One explanation is that there is prior priming by bacterial infection. Another unique characteristic is that it is processed as if it is a particulate antigen involving complement activation and B cells. Antigen‐presenting cells/monocytes are also involved but the role of T cells is controversial. Recent advances have provided new insights into the underlying mechanisms of HIT‐related thrombosis. Previously, platelets were believed to play a central role; their activation and consequently the induction of blood coagulation was the basis of the hypercoagulability in HIT. More recently, several studies have provided clear evidence that neutrophil and NETosis, monocytes and endothelial cells contribute significantly to the thrombosis in HIT. These new insights may result in development of better diagnostic laboratory assays and more effective treatments for HIT.