Lymphocyte subset recovery following allogeneic bone marrow transplantation: CD4+-cell count and transplant-related mortality

Talmadge, James E.

doi:10.1038/sj.bmt.1705871

Cited by 9 publications

(5 citation statements)

References 18 publications

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“…However, these studies did not test CD4+ counts at onset of cGvHD. Independently from cGvHD, in transplanted patients, a fast and robust recovery of CD4+ counts at early time-points after HSCT was associated with low TRM (38,39). This is possibly linked to the protection from opportunistic infections mediated by T cells early after transplant.…”

Section: Discussionmentioning

confidence: 97%

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Immune Reconstitution-Based Score for Risk Stratification of Chronic Graft-Versus-Host Disease Patients

et al. 2021

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IntroductionAllogeneic stem cell transplantation survivors are at a relevant risk of developing chronic GvHD (cGvHD), which importantly affects quality of life and increases morbidity and mortality. Early identification of patients at risk of cGvHD-related morbidity could represent a relevant tool to tailor preventive strategies. The aim of this study was to evaluate the prognostic power of immune reconstitution (IR) at cGvHD onset through an IR-based score.MethodsWe analyzed data from 411 adult patients consecutively transplanted between January 2011 and December 2016 at our Institution: 151 patients developed cGvHD (median follow-up 4 years). A first set of 111 consecutive patients with cGvHD entered the test cohort while an additional consecutive 40 patients represented the validation cohort. A Cox multivariate model for OS (overall survival) in patients with cGvHD of any severity allowed the identification of six variables independently predicting OS and TRM (transplant-related mortality). A formula for a prognostic risk index using the β coefficients derived from the model was designed. Each patient was assigned a score defining three groups of risk (low, intermediate, and high).ResultsOur multivariate model defined the variables independently predicting OS at cGvHD onset: CD4+ >233 cells/mm3, NK <115 cells/mm3, IgA <0.43g/L, IgM <0.45g/L, Karnofsky PS <80%, platelets <100x103/mm3. Low-risk patients were defined as having a score ≤3.09, intermediate-risk patients >3.09 and ≤6.9, and high-risk patients >6.9. By ROC analysis, we identified a cut-off of 6.310 for both TRM and overall mortality.In the training cohort, the 6-year OS and TRM from cGvHD occurrence were 85% (95% CI, 70-92) and 13% (95% CI, 5-25) for low-risk, 64% (95% CI, 44-89) and 30% (95% CI, 15-47) for intermediate-risk, 26% (95% CI, 10-47), and 42% (95% CI, 19-63) for high-risk patients (OS p<0.0001; TRM p = 0.015).The validation cohort confirmed the model with a 6-year OS and TRM of 83% (95% CI, 48-96) and 8% (95% CI, 1-32) for low-risk, 78% (95% CI, 37-94) and 11% (95% CI, 1-41) for intermediate-risk, 37% (95% CI, 17-58), and 63% (95% CI, 36-81) for high-risk patients (OS p = 0.0075; TRM p = 0.0009).ConclusionsIR score at diagnosis of cGvHD predicts GvHD severity and overall survival. IR score may contribute to the risk stratification of patients. If confirmed in a larger and multicenter-based study, IR score could be adopted to identify patients at high risk and modulate cGvHD treatments accordingly in the context of clinical trial.

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Section: Discussionmentioning

confidence: 97%

“…In the training set, the 3-year cGvHD incidence was 35% (95% CI, 29-40%) with 27% moderate-severe cGvHD (95% CI, 22-32%), while in the validation set, it was 36% (95% CI, 27-45) with 33% moderate-severe (95% CI, [24][25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40][41][42].…”

Section: Chronic Gvhd Features According To Nih Classificationmentioning

confidence: 99%

Immune Reconstitution-Based Score for Risk Stratification of Chronic Graft-Versus-Host Disease Patients

et al. 2021

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“…Of all factors analyzed thus far, CD4 1 counts may provide the most readily available and predictive marker of the restoration of immune competence following HCT. Although the predictive value of low CD4 1 counts has not been as extensively studied in recipients of HCT as they have in HIV infection, several studies have demonstrated that CD4 1 recovery is associated with diminished infectious risk and improved transplant outcomes [56][57][58][59]. When T cell regeneration occurs via the ontogenic or thymic-dependent pathway, there is a substantial rise in CD4 1 T cell numbers, with recovery of naïve CD4 1 and CD8 1 T cells and diversification of the T cell repertoire [60].…”

Section: Background To Hct Including Posttransplant Immune Recoverymentioning

confidence: 99%

Guidelines for Preventing Infectious Complications among Hematopoietic Cell Transplantation Recipients: A Global Perspective

Tomblyn¹,

Chiller²,

Einsele³

et al. 2009

Biology of Blood and Marrow Transplantation

1,573

1,540

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“…Data from the entire group showed a 75% long-term survival, which is higher than that reported in a majority of individual series, likely as a result of a reporting bias. A recent survey from the Italian Transplant Group (GITMO) on 23 PNH patients transplanted between 1988 and 2006 showed a 6-month treatment-related mortality of 26% and an overall survival of 70%, with a median follow-up of 107 months (Santarone et al 2008). A similar retrospective study is currently ongoing within the European Blood and Marrow Transplantation (EBMT) group, and promises to provide useful information for evidence-based decision making; preliminary results confirm an overall survival in the range of 55%–65%, with older age and acute GvHD significantly affecting the outcome, and apparently comparable results between sibling and unrelated transplants.…”

Section: Management: the Pre-eculizumab Eramentioning

confidence: 99%

Paroxysmal nocturnal hemoglobinuria: pathophysiology, natural history and treatment options in the era of biological agents

Risitano¹

2008

BTT

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Paroxysmal nocturnal hemoglobinuria (PNH) is a clonal non-malignant hematological disease characterized by the expansion of hematopoietic stem cells (HSCs) and progeny mature cells, whose surfaces lack all the proteins linked through the glycosyl-phosphatidyl inositol anchor. This defect arises from an acquired somatic mutation in the X-linked phosphatidylinositol glycan class A gene, with subsequent clonal expansion of the mutated HSCs as a result of a concomitant, likely immune-mediated, selective pressure. The disease is characterized by complement-mediated chronic intravascular hemolysis, resulting in hemolytic anemia and hemosiderinuria; capricious exacerbations lead to recurrent gross hemoglobinuria. Additional cardinal manifestations of PNH are a variable degree of bone marrow failure and an intrinsic propensity to thromboembolic events. The disease is markedly invalidating, with chronic symptoms requiring supportive therapy – usually including periodical transfusions; possible life-threatening complications may also ensue. The biology of PNH has been progressively elucidated in the past few years, but therapeutic strategies remained unsatisfactory for decades, the only exception being stem cell transplantation, which is restricted to selected patients and retains significant morbidity and mortality. Recently, a biological agent to treat PNH has been developed – the terminal complement inhibitor eculizumab – which has been tested in a number of clinical trials, with exciting results. All the data from worldwide clinical trials confirm that eculizumab radically modifies the symptoms, the biology, and the natural history of PNH, strongly improving the quality of life of PNH patients.

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Lymphocyte subset recovery following allogeneic bone marrow transplantation: CD4+-cell count and transplant-related mortality

Cited by 9 publications

References 18 publications

Immune Reconstitution-Based Score for Risk Stratification of Chronic Graft-Versus-Host Disease Patients

Immune Reconstitution-Based Score for Risk Stratification of Chronic Graft-Versus-Host Disease Patients

Guidelines for Preventing Infectious Complications among Hematopoietic Cell Transplantation Recipients: A Global Perspective

Paroxysmal nocturnal hemoglobinuria: pathophysiology, natural history and treatment options in the era of biological agents

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