Long-Term Disease Control After Allogeneic Hematopoietic Stem Cell Transplantation in Primary Cutaneous T-Cell Lymphoma; Results From a Single Institution Analysis

Front Med (Lausanne). 2020 Jun 25:7:290. doi: 10.3389/fmed.2020.00290. eCollection 2020.

Abstract

Background: Allogeneic hematopoietic stem cell transplantation (alloHSCT) has been proposed as curative approach for advanced cutaneous T-cell lymphomas (CTCL). Currently, there is no established consensus for the management of disease relapse after alloHSCT. Results: Ten patients, previously treated with multiple lines of systemic treatment, received alloHSCT. Six patients had achieved partial response (PR, N = 5) and complete response (CR, N = 1) prior to HSCT. Post-HSCT, seven patients (N = 7) relapsed after a median time of 3.3 months (0.5-7.4 months) and were subsequently treated with radiotherapy (RT, N = 1), RT and adoptive T-cell transfer with EBV specific cells (N = 1), R-CHOP (N = 1) and interferon alpha-2a combined either with donor lymphocyte infusion (N = 1) or with brentuximab-vedotin (N = 1). One patient (N = 1) achieved PR only after reducing the immunosuppression. Two patients relapsed again and received interferon alpha-2a and brentuximab-vedotin, respectively. After a median follow-up time of 12.6 months (3.5-73.7 months) six patients were alive (60%) and four had deceased, three (N = 3) due to CTCL and one (N = 1) due to GVHD. Conclusion: Disease relapse after alloHSCT can be controlled with available treatments. For most patients who ultimately relapsed, reduction of immunosuppression and interferon alpha-2a either administered alone or in combination with another systemic agent were preferred. Although interferon alpha-2a, similarly to immunosuppression reduction, may be beneficial for the achievement of graft-vs.-lymphoma effect, the risk of simultaneous worsening of GVHD must be carefully evaluated and taken into consideration.

Keywords: Sézary syndrome; allogeneic stem cell transplantation; cutaneous T-cell lymphoma; interferon alpha-2a; mycosis fungoides.