肾移植术后淋巴增殖性疾病的诊治体会

目的探讨肾移植术后淋巴细胞增殖性疾病(PTLD)的发病原因、临床特点、诊治方法及预后。方法回顾性分析2000年1月至2019年1月海军军医大学长征医院2844例肾移植受者中术后并发PTLD的13例受者的临床资料,收集受者性别、年龄、血肌酐、药物浓度、糖尿病、肾移植术后有无移植肾功能延迟恢复、急性排斥反应和免疫抑制剂方案的使用等相关资料。13例PTLD受者中,男11例,女2例,确诊时年龄为55岁(31~78岁)。结果PTLD病变位置分布在肺部1例,胃肠道8例,区域淋巴结2例,皮肤1例,颅内1例,均病理诊断为弥漫性大B淋巴细胞淋巴瘤,距肾移植手术中位时间为86个月(12~204个月)。76.9%受者病理组织EB病毒检测呈阳性。确诊后给予免疫抑制剂减量为主的综合治疗,无法耐受利妥昔单抗+CHOP(R-CHOP)方案化学药物治疗的受者切换为利妥昔单抗+来那度胺(R2)方案,2例受者肺部感染死亡,完全缓解10例,部分缓解1例,病情进展1例,总有效率91.6%。结论肾移植术后淋巴细胞增殖性疾病进展迅速,病死率高,与EB病毒感染密切相关,减少免疫抑制剂用量是综合治疗的核心,根据受者耐受性选择合理的化学药物治疗方案,R2方案为无法耐受一线R-CHOP方案的受者更多选择。     

肾移植术后放线菌病一例

患者男性，36岁，因慢性肾功能不全于1993年3月在我院行尸肾移植术。术后肾功能正常。服用三联免疫抑制剂抗排斥治疗，环孢素A8mg·kg-1／d，硫唑嘌呤50mg／d，泼尼松20mg／d。1995年2月无明显诱因出现右下腹包块，逐渐增大至6cm×7cm，表面皮肤形成两处长条形脓肿约2cm×5cm，并破溃，脓液中可见到黄白色颗粒，CT显示包块位于腹壁，与腹腔脏器及移植肾无联系，提示为腹壁炎性包块。活检病理报告为“炎性包块”。即在硬膜外麻下行包块切除术。术后切口愈合良好，治愈出院。病理报告：放线菌病。1996年3月在原肿块生长部位又出现包块，并迅…     

肾移植后并发获得性免疫缺乏综合征一例

近几年来 ,获得性免疫缺乏综合征 (艾滋病 ,ＡＩＤＳ)的流行范围不断扩大 ,肾移植术后由于免疫抑制药物的应用 ,增加了机会感染与肿瘤发病率 ,ＡＩＤＳ的发病率也明显增加 ,但在我国罕见报道。我们发现 1例肾移植术后 4年并发ＡＩＤＳ ,现报道如下。患者为男性 ,2 5岁 ,因慢性肾功能衰竭、尿毒症收住我院。住院 1周后因诊断合并有急性病毒性肝炎 (丙型 ) ,而转肝炎病专科医院治疗 ,期间输血 3次共 60 0ｍｌ,丙型肝炎抗体转阴、肝功能正常后 ,于 1 996年 6月再次入我院。经积极术前准备 ,于 1 996年 7月行同种异体肾移植术。患者术后恢复良好…     

肾移植术后克隆氏病一例

目前，克隆氏病的病因尚不明确，可能与免疫反应有关，糖皮质激素及免疫抑制剂是主要治疗方法之一。本院1例患者于肾移植术11年后并发克隆氏病，给予病变肠段切除治疗，但最终因全身多脏器功能衰竭死亡。报道如下：     

肾移植术后淋巴漏24例

目的 探讨肾移植患者术后发生淋巴漏的原因及治疗方法。方法 回顾性分析1999年1月至2004年12月间24例肾移植术后淋巴漏患者的临床资料，总结其发生原因和治疗方法。结果 24例患者发生淋巴漏的持续时间均〉2周，其中5例超过1个月。通过持续引流，并辅以抗生素预防感染，19例患者于治疗15-22d后痊愈；其余5例持续引流4周，引流量始终〉100ml／d，经引流管注入葡萄糖和注射用红霉素共50ml进行硬化治疗，隔日1次，经2～8次治疗后，引流量逐渐减少，分别于术后35-54d治愈出院。术后随访4个月～6年，均未发现淋巴囊肿。结论 肾移植手术操作失误和急性排斥反应是发生淋巴漏的主要原因。采用持续引流及硬化疗法可有效治疗肾移植后淋巴漏。     

肾移植术后皮肤血管角质瘤一例

患者 ,男性 ,4 6岁。于 2 0 0 1年 1月 4日因慢性肾小球肾炎、慢性肾功能衰竭尿毒症期在我院行同种异体肾移植术。术后肾功能恢复良好 ,常规服用泼尼松、霉酚酸酯和环孢素三联免疫抑制剂抗排斥。患者分别于术后 2 0 0 1年 8月、2 0 0 2年 8月 ,发生急性排斥反应而返院 ,接受甲泼尼龙冲击治疗后肾功能恢复。半年前患者不慎烫伤右小腿内踝方 ,经治疗后伤口愈合。 5个月前因又发生移植肾急性排斥反应 ,再次使用甲泼尼龙冲击治疗。右小腿原来伤口处出现溃破且红肿 ,皮损迅速向四周蔓延并波及足、大腿 ,同时发现右腹股沟淋巴结肿大。分别取右内踝…     

肾移植后并发晚发型淋巴组织增生性疾病一例

移植后淋巴组织增生性疾病(PTLD)是实体器官或造血干细胞移植后的一种严重并发症.文献显示,PTLD的总发生率不足2%~([1]),肾移植后PTLD发生率约1%~([2]).PTLD常发生于肾移植后1年内,也可在10年后发生~([3]).我科收治1例肾移植后晚发型PTLD,报告如下.     

肾移植术后并发人乳头瘤病毒感染一例

患者，女性，42岁，2000年5月30日因尿毒症在我院行肾移植术。术后常规服用环孢素A（CsA）＋霉酚酸酯（MMF）＋泼尼松（Pred）三联免疫抑制剂。定期复查肝、肾功能均正常。2006年12月停服CsA，改他克莫司（FK506）胶囊2mg，每天2次口服。于2007年1月发现外阴赘生物伴疼痛，于2007年1月5日首次来本科就诊。患者肾移植术后每2个月左右过性生活1次，无不良的性接触史，     

大肠良性淋巴组织增殖一例

大肠良性淋巴组织增殖亦称良性淋巴样息肉病,国内少见,临床报道不多,极易和肠道多发性息肉病混淆。为提高对本病的认识,正确的诊断及治疗,现将本例介绍如下。患者女,19岁。因腹痛、腹泻、便血3个月,于     

肾移植术后免疫抑制剂致急性肾血管毒一例

免疫抑制剂引起急性肾血管毒(AVT)的病理改变不典型时,极易与急性血管型排异相混淆.现回顾分析1例AVT的临床和病理资料.     

Post-transplant lymphoproliferative disorders after live donor renal transplantation

The development of post-transplant lymphoproliferative disorders (PTLD) is a well-recognized complication of solid organ transplantation in patients receiving immunosuppressive therapy. The literature on PTLD in live renal allograft recipients is scarce and most of the data pertains to PTLD in cadaveric transplants. As live donor grafts form the mainstay of transplantation programme in India, this study was carried out to define the profile of PTLD in live donor renal allograft recipients. On retrospective evaluation, nine cases of PTLD amongst 1700 live donor allograft recipients from January 1989 to August 2004, were detected at a tertiary care hospital in north India. The clinicopathological features of these cases were evaluated. Mean age at diagnosis of PTLD was 38 yr with median post-transplant latency period of 7 yr. All cases were from extra-renal sites, five being in ileum/jejunum, three in retroperitoneal lymph nodes and one in epididymus. All cases received cyclosporin, azathioprine and prednisolone in varying combinations as immunosuppressive therapy. One case was treated for rejection by anti-thymocyte globulin. Seven patients were seronegative for Epstein-Barr virus at the time of diagnosis. All were B-cell monomorphic PTLD, classifiable as B-cell diffuse large cell lymphomas, with five extranodal and three nodal lymphomas. Management included reduction in immunosuppression, acyclovir therapy, surgical excision and chemotherapy. On follow-up, four patients died, two presented with recurrence, two were in remission and one was lost to follow-up. This study comprising of live related/unrelated renal allograft recipients observed late onset high grade monomorphic PTLD with paucity of early onset polymorphic lesions. Long post-transplant latency period, aggressive behaviour and poor response to treatment necessitate long-term cancer surveillance to facilitate early detection and newer therapeutic strategies to improve the outcome in these patients.     

Intermediate syndrome after organophosphate intoxication in patient with end-stage renal disease

A 42-year-old woman with a 24-year history of systemic lupus erythematous and lupus nephritis for 8 years who had been receiving regular hemodialysis for 4 years for nonoligoric end-stage renal disease (ESRD) ingested about 100 mL of 40.8% chlorpyrifos in a suicide attempt. On admission to our emergency department, she was drowsy. Gastric lavage, activated charcoal, pralidoxime (PAM), and atropine were administered 4 h later. Her consciousness level improved gradually with treatment, which included hemodialysis. However, on the second hospital day, intermittent fever to 38.4 degrees C, sore throat, and trismus were noted. About 45 h after chlorpyrifos ingestion, the patient developed profound motor paralysis followed by respiratory arrest, consistent with the diagnosis of intermediate syndrome (IMS), even with adequate atropine and PAM. Chorealike involuntary movements of her upper limbs were noticed on the fifth day. Intermittent tonic-clonic seizures, each attack lasting for 3 to 5 min, appeared on the 13th day, which responded well to intravenous diazepam and phenytoin. She was discharged on the 18th day. This case suggests that patients with ESRD suffering chlorpyrifos intoxication are at risk of IMS. Prompt endotracheal intubation, intensive care, and hemodialysis are necessary for life support.     

Cardiovascular disease after renal transplantation

Cardiovascular disease (CVD) is common after renal transplantation. In the absence of controlled intervention trials, the strength of evidence that modifying a risk factor will reduce the incidence of CVD in renal transplant recipients must rest on: (1) evidence from studies in the general population, (2) observational studies linking the risk factor to CVD in renal transplant recipients, and (3) studies showing that the risk factor can be safely and effectively treated in transplant patients. Accordingly, the evidence is strong that hyperlipidemia should be treated after renal transplantation. Evidence is very suggestive that pretransplant screening for CVD, treatment of hypertension, the use of low-dose aspirin, and smoking cessation will also help to reduce the incidence of posttransplant CVD. Less compelling are data suggesting that intensive glucose control in diabetics will safely decrease the incidence of CVD. Although there is little evidence that treatment of erythrocytosis will reduce CVD, hematocrits above 55% to 60% should probably be treated to prevent venous thrombosis. Vitamins for reducing homocysteine, antioxidant vitamins, and prophylaxis for potentially atherogenic infections are therapies that warrant additional study. In summary, the best current approach to reducing the high incidence of posttransplant CVD is to aggressively identify, and then systematically treat modifiable risk factors.     

肺移植术后淋巴组织增生性疾病的研究进展

移植后淋巴组织增生性疾病(PTLD)是肺移植术后可致死性并发症,与年龄、免疫抑制水平、爱泼斯坦-巴尔病毒(EBV)感染等密切相关。降低免疫抑制水平、利妥昔单抗治疗、T细胞免疫治疗是其常见的治疗手段。随着肺移植在中国的迅速发展,肺移植术后PTLD也引起高度关注。本文就肺移植术后发生PTLD的危险因素、病理分型、临床表现、诊断、治疗、预后和预防做一综述,旨在为肺移植术后PTLD发生、发展的早期监测和管理提供参考。