Risk factors for post‐transplant lymphoproliferative disease in patients with cystic fibrosis

Saueressig, Mauricio Guidi; Boussaud, Véronique; Amrein, C.; Guillemain, R.; Souilamas, Jihane; Souilamas, Rédha

doi:10.1111/j.1399-0012.2011.01464.x

Cited by 19 publications

(21 citation statements)

References 26 publications

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“…The risk of PTLD has been shown to be related to the EBV donor (D) and recipient (R) serostatus [16], with the risk increasing from R+ to R-/D- and from R-/D- to R-/D+ in kidney transplant recipients. In a series of lung transplant recipients with cystic fibrosis, 7 of the 8 patients with PTLD were R- [17]. However, in our study, all but 1 recipient were adults and most were EBV+, as are more than 90% of normal adults [18].…”

Section: Discussionmentioning

confidence: 78%

Lymphoproliferative Disorders after Lung Transplantation: Clinicopathological Characterization of 16 Cases with Identification of Very-Late-Onset Forms

Montpréville

Pavec²,

Ladurie³

et al. 2015

Respiration

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Background: The incidence of posttransplant lymphoproliferative disorders (PTLD) has recently declined, but late cases are increasingly reported in lung transplant recipients. Objectives: We present our experience with PTLD after lung transplantation, attempting to examine the distinguishing characteristics of early versus late cases. Methods: We have reviewed clinical and pathological data of all cases occurring in our institution between 2001 and 2014. Results: Patients, aged 15-63 years, were mostly (12/16) Epstein-Barr virus (EBV) seropositive at the time of transplantation. Eleven early cases, occurring 9.4 ± 5.2 months after transplantation and mostly (9/11) prior to 2010, had EBV+ diffuse large B-cell lymphomas. Lungs and/or thoracic lymph nodes were often involved (n = 8). Treatments included reduction of immune suppression (n = 11), rituximab (n = 8) and chemotherapy (n = 7). Two patients are in complete remission at 26 and 216 months. Nine patients died 8.0 ± 6.5 months after PTLD diagnosis. Of the 5 cases with late PTLD occurring 4-23 years (mean ± SD: 10.4 ± 7.7) after transplantation (and 3/5 after 2009), 1 had pulmonary lymphomatoid granulomatosis (only endothoracic case), 1 cutaneous large T-cell lymphoma, 2 had anaplastic large cell lymphomas, and 1 Hodgkin's disease. Two of the 5 cases were EBV-, including one followed by a second EBV+ PTLD after 8 years of complete remission. Two patients were alive and well (follow-up: 44 and 151 months), one having suffered from EBV-related cholestatic hepatitis 6 years after the PTLD. Conclusion: Our small experience shows a trend toward (very) late occurrence, associated with more unusual clinicopathologic features, but not with a worse prognosis.

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Section: Discussionmentioning

confidence: 78%

Lymphoproliferative Disorders after Lung Transplantation: Clinicopathological Characterization of 16 Cases with Identification of Very-Late-Onset Forms

Montpréville

Pavec²,

Ladurie³

et al. 2015

Respiration

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“…Figure details a flowchart of the basis that studies were excluded. Of the 14 studies, a total of 164 PTLD lung transplant patients were analyzed for outcomes and characteristics data. Table shows studies that provided treatments and treatment outcomes for PTLD in LTR.…”

Section: Resultsmentioning

confidence: 99%

Systematic review and meta‐analysis of post‐transplant lymphoproliferative disorder in lung transplant recipients

Cheng

Moore

Iasella

et al. 2018

Clinical Transplantation

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A systematic review of papers in English on post-transplant lymphoproliferative disorder (PTLD) in lung transplant recipients (LTR) using MEDLINE, EMBASE, SCOPUS, and Cochrane databases was performed. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) recommendations were strictly adhered to. Pooled odds ratios (pOR) were calculated from a random-effects model, and heterogeneity among studies was quantitated using I values. Fourteen studies published from 2005 to 2015 were included in the meta-analysis. One hundred and sixty-four lung transplant recipients were included. LTRs who received single vs bilateral were associated with a 7.67-fold risk of death after PTLD (6 studies with 64 LTRs; pOR 7.67 95% CI 1.98-29.70; P = .003). pOR of death for early onset PTLD (<1 year post-LT) vs late onset (>1 year post-LT) was not different (3 studies with 72 LTRS; pOR 0.62, 95% CI 0.20-1.86, P = .39). Standardized mean difference (SMD) in time from transplant to PTLD onset between LTRs who died vs alive was not different (9 studies with 109 LTRs; SMD 0.03, 95% CI -0.48-0.53, P = .92). Survival in polymorphic vs monomorphic PTLD and extranodal vs nodal disease was similar (4 studies with 31 LTRs; pOR 0.44, 95% CI 0.08-2.51; P = .36. 6 studies with 81 LTRs; pOR 1.05 95% CI 0.31-3.52, P = .94). This meta-analysis demonstrates that single LTRs are at a higher risk of death vs bilateral LTRs after the development of PTLD.

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“…Early presentation within the first year after lung transplantation is associated with primary EBV infection in a seronegative, naïve patient [6, 21, 22] and pediatric thoracic transplant recipients [23, 24], underlying cystic fibrosis diagnosis likely due to EBV seronegative status [6, 21], primary CMV infection [4], higher rejection frequency [25], and use of induction therapy at time of transplant [4, 25, 26]. In general, later onset PTLD was associated with extent of exposure to higher levels of immunosuppression, older recipient age, and male gender [4].…”

Section: Clinical Presentation Of Ptld After Lung Transplantationmentioning

confidence: 99%

Posttransplant Lymphoproliferative Disease after Lung Transplantation

Neuringer

2013

Clinical and Developmental Immunology

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Posttransplant lymphoproliferative disease (PTLD) after lung transplantation occurs due to immunosuppressant therapy which limits antiviral host immunity and permits Epstein-Barr viral (EBV) replication and transformation of B cells. Mechanistically, EBV survives due to latency, escape from cytotoxic T cell responses, and downregulation of host immunity to EBV. Clinical presentation of EBV may occur within the lung allograft early posttransplantation or later onset which is more likely to be disseminated. Improvements in monitoring through EBV viral load have provided a means of earlier detection; yet, sensitivity and specificity of EBV load monitoring after lung transplantation may require further optimization. Once PTLD develops, staging and tissue diagnosis are essential to appropriate histopathological classification, prognosis, and guidance for therapy. The overall paradigm to treat PTLD has evolved over the past several years and depends upon assessment of risk such as EBV-naïve status, clinical presentation, and stage and sites of disease. In general, clinical practice involves reduction in immunosuppression, anti-CD20 biologic therapy, and/or use of plasma cell inhibition, followed by chemotherapy for refractory PTLD. This paper focuses upon the immunobiology of EBV and PTLD, as well as the clinical presentation, diagnosis, prognosis, and emerging treatments for PTLD after lung transplantation.

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Risk factors for post‐transplant lymphoproliferative disease in patients with cystic fibrosis

Cited by 19 publications

References 26 publications

Lymphoproliferative Disorders after Lung Transplantation: Clinicopathological Characterization of 16 Cases with Identification of Very-Late-Onset Forms

Lymphoproliferative Disorders after Lung Transplantation: Clinicopathological Characterization of 16 Cases with Identification of Very-Late-Onset Forms

Systematic review and meta‐analysis of post‐transplant lymphoproliferative disorder in lung transplant recipients

Posttransplant Lymphoproliferative Disease after Lung Transplantation

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