移植后淋巴组织增生性疾病的影像学表现

目的探讨移植后淋巴组织增生性疾病的影像学特点,以提高对该疾病的认识与影像学诊断水平。方法通过文献复习的方法,对移植后淋巴组织增生性疾病在腹部、胸部、头颈部和中枢神经系统的影像学表现及其流行病学特征、发病机理与病理类型进行全面综述。结果移植后淋巴组织增生性疾病是移植后主要由EB病毒感染和免疫抑制治疗引起的一组不同病理类型的淋巴组织增生性疾病。在影像学检查中发现可疑病灶通常为诊断该病的第一线索,不同部位的移植后淋巴组织增生性疾病具有各自不同的影像学特点。结论熟悉移植后淋巴组织增生性疾病及其影像学特点对于诊断该疾病、明确活检取样部位以及评估治疗效果方面有着重要的意义。     

肝移植术后淋巴组织增生性疾病的诊治进展

移植后淋巴组织增生性疾病是人体实体器官移植和骨髓移植后的严重并发症之一.病理表现为淋巴细胞增生紊乱并形成淋巴瘤,其发病与受者免疫功能抑制及EB病毒感染相关.随着器官移植在我国的迅速发展,对肝移植术后淋巴组织增生性疾病的临床研究进展将逐步深入,我们将介绍肝移植术后淋巴组织增生性疾病的病因、发病机制、诊断和治疗等方面的研究...     

移植后淋巴组织增生性疾病的临床研究进展

移植后淋巴组织增生性疾病（PTLD）是人体实体器官移植和骨髓移植后的严重并发症之一，病理表现为淋巴细胞增生紊乱，形成淋巴瘤，其发病与受者免疫功能抑制及Epstein Barr（EB）病毒感染相关，PTLD的发生率低（1％～10％），目前国内偶见个案报道。下面就PTLD的临床研究进展作一综述。     

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.     

器官移植受者EB病毒感染和移植后淋巴增殖性疾病临床诊疗专家共识

<正>1前言近年来,外科手术技术、免疫抑制药物、预防性抗感染药物、移植前供/受者风险评估等的发展已显著降低了实体器官移植(solid organ transplant,SOT)术后并发症发生率和死亡率,但感染及因此引发的相关疾病在SOT受者中仍较常见[1-2]。其中与EB病毒(epstein-barr virus,EBV)感染相关的移植后淋巴增殖性疾病(post-transplant lymphoproliferative     

器官移植术后的合理免疫抑制与监测(续)——2008年美国移植大会(ATC)内容综述

3.恶性肿瘤:2004年的一项研究表明,采用抗淋巴细胞抗体诱导治疗能使发生移植后淋巴细胞增殖性疾病(PTLD)的相对危险(RR)增加(RR=1.78,P＜0.01),但与新生肿瘤的发生可能无关(RR=1.07,P＞0.05).     

脾移植前去除成熟树突状细胞预防移植排斥反应的体外研究

目的 建立治疗性单抗溶液持续灌注大鼠脾脏模型,应用抗大鼠树突状细胞单克隆抗体（ＷＺＤ）降低大鼠移植脾的免疫原性。方法 以ＷＺＤ溶液持续灌注移植脾,筛选最佳方案并观察灌注后混合淋巴细胞培养（ｍｉｘｄｅ ｌｙｍｐｈｏｃｙｔｅ ｃｕｌｔｕｒｅ,ＭＬＣ）淋巴细胞增殖情况及脾细胞的超微结构,以及灌注后移植脾细胞的免疫组化情况。结果 ＷＺＤ灌注组ＭＬＣ淋巴细胞增殖能力明显降低,与对照组及应ＣｓＡ组相比差异有显     

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、...     

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。     

EB病毒感染及相关移植后淋巴组织增殖性疾病诊疗进展

移植后淋巴组织增殖性疾病(post-transplant lymphoproliferative disease,PTLD)是实体器官移植(solid organ transplantation,SOT)或异基因造血干细胞移植(allogeneic hematopoietic stem cell transplantation,alloHSCT)受者因免疫抑制状态而发生的淋巴组织或浆细胞从良性组织增生为恶性肿瘤的淋巴系统增殖性疾病,其中>70%的PTLD与EB病毒(epsteinbarr virus,EBV)感染相关[1],EBV感染导致的淋巴组织增殖性疾病(EBV-PTLD)是导致器官移植受者死亡的主要原因。     

心脏移植术后发生移植后淋巴组织增生性疾病二例并文献复习

目的探讨心脏移植术后发生移植后淋巴组织增生性疾病（PTLD）的发病原因、临床表现、病理特点及防治措施。方法1997年1月至2013年12月,浙江省人民医院心胸外科共开展心脏移植18例,其中2例发生PTLD。回顾性分析2例患者的临床资料并进行文献复习。结果2例患者心脏原位移植术后使用以环孢素为基础的三联免疫抑制方案。从移植术后到确诊PTLD的时间分别为12年和9年。患者均以颈部淋巴结肿大为临床表现,病理活检均提示“非霍奇金恶性淋巴瘤,B细胞源性,弥漫性大B细胞淋巴瘤”。在调整免疫抑制方案的基础上,给予美罗华＋半剂量CHOP化疗方案。随访至2013年12月,2例患者生活工作均正常。结论对于心脏移植术后确诊为PTLD的患者,半剂量CHOP方案化疗既不影响心脏移植的抗排斥反应,又能有效控制肿瘤的进展;美罗华可增强化疗药物作用。因此,美罗华＋半剂量CHOP化疗方案是治疗PTLD的优选方案。     

Posttransplantation lymphoproliferative disorder--the great mimic in liver transplantation: appraisal of the clinicopathologic spectrum and the role of Epstein-Barr virus.

Case series describing posttransplantation lymphoproliferative disorder (PTLD) after liver transplantation (LTx) have been limited in number because of the rarity of the disorder. The prevalence of Epstein-Barr virus (EBV) infection and its detection, the clinical and histological diversity of disease, and survival have varied. The aim of this study is to define the clinical and pathological spectrum of PTLD after LTx, and evaluate EBV prevalence, impact of infection, and patient survival. A retrospective analysis of all LTx recipients at our institution diagnosed with PTLD from January 1990 until May 2005, recording clinical presentations, times of presentation after transplantation, histological findings, results of EBV assessment, and survival, as well as the interrelationship of these variables. Among 621 LTx recipients were 22 cases of PTLD in 21 patients, of whom 5 were children and 16 were adults. Extranodal disease was present in 17 of 22 cases (77%) involving a wide variety of organ systems, while 5/22 (23%) had lymphadenopathy. The spectrum of PTLD histopathology was equally varied. In situ hybridization for EBV showed negativity in 8 of 13 (62%) and positivity in 5 of 13 (38%) cases tested. Neither time interval from transplantation to presentation (median 33 months) nor mortality (average 32%) was influenced by EBV status. In conclusion, PTLD in LTx recipients is predominantly extranodal and can involve a wide variety of organ systems, which may confound initial diagnosis. The lymphoproliferative histological spectrum is also diverse. Nowadays, PTLD is frequently EBV-negative, and EBV status does not appear to influence clinical or pathological presentation, or survival.     

肝移植术后淋巴组织增生性疾病的诊断和治疗(附1例报告及文献复习)

目的探讨肝移植术后淋巴组织增生性疾病(posttransplant lymphoproliferative disease,PTLD)的诊断和治疗。方法回顾性分析1例肝移植后PTLD的临床表现、诊断和治疗过程,并复习相关文献。结果 2003年10月至2011年12月在中山大学附属第三医院肝移植中心随访的336例肝移植术后患者中有1例发生PTLD,发生率为0.3%。该例患者的临床表现不典型,主要表现为反复发热、腹部不适、多处淋巴结肿大和肝脏占位病变等,淋巴结活组织检查提示B细胞源性非霍奇金淋巴瘤淋巴瘤,确诊为PTLD。经减少免疫抑制剂用量、抗炎,对症支持治疗无效后死亡。结论肝移植术后PTLD的临床表现不典型,易被误诊或延误诊断,预后甚差。治疗以减少免疫抑制剂用量、抑制淋巴细胞增殖、对症支持治疗为主。     

Post‐transplant lymphoproliferative disorder following kidney transplantation: a population‐based cohort study

Post‐transplant lymphoproliferative disorder (PTLD) incidence is difficult to determine, mainly because both early and other lesions may go unrecognized and unregistered. Few studies have included systematic pathology review to maximize case identification and decide more accurately PTLD frequency after long‐term post‐transplantation follow‐up. A retrospective population‐based cohort study including all kidney transplant recipients at two Danish centres (1990–2011; population covered 3.1 million; 2175 transplantations in 1906 patients). Pathology reports were reviewed for all patient biopsies to identify possible PTLDs. Candidate PTLDs underwent histopathological review and classification. Seventy PTLD cases were identified in 2175 transplantations (3.2%). The incidence rate (IR) after first transplantation was 5.4 cases per 1000 patient‐years (95% CI: 4.0–7.3). Most PTLDs were monomorphic (58.5%), or early lesions (21.5%). Excluding early lesions and patients <18 years, IR was 3.7 (95% CI: 2.9–5.5). Ten patients with PTLD were retransplanted, 2 developing further PTLDs. Post‐transplant patient survival was inferior in patients with PTLD, while death‐censored graft survival was not. Using registry data together with extensive pathological review and long follow‐up, a rather high incidence of PTLD was found.     

Primary Central Nervous System Posttransplant Lymphoproliferative Disease in a Bilateral Transfemoral Lower Extremity Transplantation Recipient

Posttransplant lymphoproliferative disorder (PTLD) is a heterogeneous group of clinical and pathological entities characterized by malignant lymphoid cell proliferation occurring after solid organ transplantation, with frequent extranodal involvement. Central nervous system (CNS) involvement occurs in 7–15% of the cases and it is a significant negative prognostic factor. A case of primary CNS (PCNS) PTLD in the first bilateral lower limb transplant recipient is presented.     

Clinical characteristics and outcomes of PTLD following intestinal transplantation

Post‐transplant lymphoproliferative disease (PTLD) has the highest incidence following intestinal transplantation (ITx). Our center has seen a recent increase in PTLD. Our aim was to review a single‐center PTLD experience with a focus on clinical characteristics and outcomes. We completed a retrospective review of biopsy‐proven PTLD cases using a prospectively maintained database of 115 ITx recipients transplanted between 1991 and 2014. Nineteen (17%) ITx recipients developed 25 PTLD cases during a median follow‐up time of 6.4 (1.6‐14.6) years. The incidence of early PTLD was 6% (n = 7). There was a trend toward increased risk of PTLD in children compared with adults (P = .11) and a significantly increased risk of PTLD in re‐ITx compared with primary ITx recipients (P = .03). Most PTLD cases were diagnosed between 2010 and 2014 (n = 14). All early PTLD cases were EBV+ on in situ hybridization. Overall graft and patient survival are 68% and 74%, respectively. Second episodes of PTLD were diagnosed in 43% of surviving pediatric patients. Our program has a low incidence of early PTLD with overall excellent graft and patient survival following diagnosis. However, we have also seen a rising incidence of late PTLD. The cause of the increase is unknown as no major changes in immunosuppression protocols have occurred since 1999.     

Early onset post-transplant lymphoproliferative disease is associated with allograft localization

Post-transplant lymphoproliferative disease (PTLD) is a major complication after solid organ transplantation. We analyzed incidence, patient characteristics, clinical presentation, and prognostic factors for treatment outcome and survival of PTLD patients transplanted at our center. Records from adult kidney and lung transplant recipients, transplanted between January 1985 and December 2002 with a histologically confirmed diagnosis of PTLD, were retrieved. Histology was reviewed and prognostic factors for treatment outcome were evaluated by multivariable analysis. Of 1354 kidney and 206 lung transplants, PTLD was diagnosed in 40 transplant recipients (2.6%). Lung transplant recipients had a significantly higher incidence of PTLD (8.3%) than kidney transplant recipients (1.7%). Sites of presentation were highly heterogeneous. Notably, PTLD localized in the allograft occurred significantly earlier after transplantation than PTLD localized outside the allograft (p = 0.001). This was true for lung (p = 0.006) as well as for kidney transplant recipients (p = 0.03). In multivariable Cox regression, performance status (p = 0.01) and advanced stage (p = 0.04) were factors negatively predictive for response to first-line treatment. Only performance status remained as negative predictive factor for survival (p = 0.002) and freedom from tumor progression (p = 0.01). In conclusion, the allograft is significantly more often involved as primary site of PTLD presentation during the first post-transplant year. This may have clinical consequences and give new insights in pathogenesis of PTLD. Performance status and stage are important risk factors for outcome of PTLD.     

Epstein–Barr Virus‐Related Post‐Transplant Lymphoproliferative Disorders: Pathogenetic Insights for Targeted Therapy

Post‐transplant lymphoproliferative disorder (PTLD) is a spectrum of major, life‐threatening lymphoproliferative diseases occurring in the post‐transplant setting. The majority of PTLD is of B‐cell origin and is associated with several risk factors, the most significant being Epstein‐Barr virus (EBV) infection. EBV's in vitro transforming abilities, distinctive latency, clonality within the malignant cells and response to targeted therapies implicate a critical role in the biology of PTLD. This minireview focuses on EBV‐related PTLD pathogenesis, in particular the interplay between aspects of the EBV life cycle and latency with nonviral factors resulting in the wide spectrum of histology and clinical presentations encountered in PTLD. With the increased prevalence of transplantation a rise in the incidence of PTLD may be expected. Therefore the importance of laboratory and animal models in the understanding of PTLD and the development of novel therapeutic approaches is discussed.     

Epstein-Barr virus serology and posttransplant lymphoproliferative disease in lung transplantation.

BACKGROUND: Posttransplant lymphoproliferative disease (PTLD) is now a widely recognized complication of lung transplantation. In the current study, we present our experience with PTLD over a 15-year period, which includes the incidence rates in 242 lung allografts and the relative risk of developing PTLD in 146 patients with known pretransplantation Epstein-Barr virus (EBV) status. METHODS: Inpatient and outpatient charts of 300 consecutive lung transplant recipients between 1984 and 1999 were retrospectively reviewed. RESULTS: Twelve cases of PTLD were observed for a total incidence rate of 5.0%. Ten of these patients had pretransplantation EBV testing, and the consequent increase in relative risk for patients who were EBV negative was 6.8-fold. The mean time between organ transplantation and tissue diagnosis of PTLD was 17.6 months. Total 1-year survival rate from the time of diagnosis for the cohort was 58%, whereas 2-year survival rate was 50%. Median survival for the six patients who died was 4.5 months. CONCLUSIONS: These data suggest that although EBV seronegativity does carry a 6.8-fold increase in the relative risk of developing PTLD, long-term survival despite the development of PTLD can be achieved, and thus EBV seronegativity by itself should not be considered a contraindication to lung transplantation.     

Posttransplantation lymphoproliferative disorder in pediatric liver transplantation

INTRODUCTION: The aim of this study was to evaluate the clinical features of risk factors for posttransplantation lymphoproliferative disorder (PTLD) in pediatric liver transplantation. MATERIALS AND METHODS: Between June 1996 and June 2002, among 41 pediatric patients who underwent liver transplantation, 7 died in the postoperative period. Thirty-five patients, including 1 patient who died of PTLD, were reviewed. Based on the serology results, patients were divided into a high-risk group (EBV-naive recipients of EBV-positive grafts) and a low-risk group (patients other than those in the high-risk group). RESULTS: Five of 41 patients (12.2%) developed PTLD. All of them belonged to the high-risk group. The incidence of PTLD in the high-risk group was 31.3% (5 of 16). The mean duration between operation and diagnosis for PTLD was 9.8 months. Primary EBV infection developed at a median of 6 months after transplantation. Three of 5 patients developed rejection before the diagnosis of PTLD. One patient was diagnosed with laryngeal and gastrointestinal PTLD, whereas the other 4 had gastrointestinal PTLD. They experienced the following symptoms and signs: anemia (100%), hypoalbuminemia (100%), fever (80%), diarrhea (80%), gastrointestinal bleeding (80%), and anorexia (60%). CONCLUSION: The common features of PTLD development were as follows: (1) EBV-positive donors placed into EBV-naive recipients, (2) primary EBV infection approximately 6 months after transplantation, (3) young age, 1 year old at operation, and (4) requirement for intensive posttransplantation immunosuppression.