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Matched and Mismatched Allogeneic Stem-Cell Transplantation From Unrelated Donors Using Combined Graft-Versus-Host Disease Prophylaxis Including Rabbit Anti–T Lymphocyte Globulin

From the Departments of Hematology & Oncology, Institute for Medical Statistics, Transfusion Medicine, Albert-Ludwigs University Medical Center, Freiburg, Germany.

Address reprint requests to Jürgen Finke, MD, Department of Hematology & Oncology, Albert-Ludwigs University Freiburg Medical Center, Hugstetter Str 55, D-79106 Freiburg, Germany; email: Finke{at}mm11.ukl.uni-freiburg.de.

	ABSTRACT

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Purpose: With improved HLA-typing techniques, it is presently unclear what degree of identity is necessary for successful unrelated-donor stem-cell transplantation (UD SCT). Here, we describe the outcome after matched and mismatched UD SCT using a graft-versus-host disease (GVHD) prophylaxis including high-dose rabbit anti–T lymphocyte globulin (ATG).

Patients and Methods: One hundred adult patients (median age, 37 years; range, 17 to 65 years) with hematologic malignancies underwent transplantation in early disease (first complete remission [CR1] or first chronic phase [CP1]; n = 34) or in advanced disease (second complete remission or second chronic phase, no remission, refractory; n = 66) with nondepleted bone marrow (n = 87) or peripheral-blood–derived (n = 13) stem cells from an HLA-A, HLA-B, HLA-DRB1*, or HLA-DQB1* identical (n = 75) or mismatched (one antigen, n = 21; two to three antigens, n = 4) unrelated donor. GVHD prophylaxis consisted of rabbit ATG before transplantation in addition to cyclosporine and short-course methotrexate.

Results: The cumulative incidence of acute GVHD °II-°IV was 21% (95% confidence interval [CI], 14% to 33%) and 20% (95% CI, 9% to 44%) and acute GVHD °III–°IV was 5.3% (95% CI, 2% to 14%) and 4% (95% CI, 0.6% to 28%) in HLA-matched and HLA-mismatched transplantations, respectively. The risk for extensive chronic GVHD was 43% (95% CI, 32% to 59%) and 44% (95% CI, 26% to 75%) for HLA-matched and HLA-mismatched patients, respectively. The risk of relapse at 4 years was 17% (95% CI, 7% to 43%) and 43% (95% CI, 31% to 60%) for CR1/CP1 and advanced disease patients, respectively. With a median follow-up of 1,068 days (range, 12 to 1,958 days), 3-year disease-free and overall survival for patients who underwent transplantation in CR1/CP1 was 63% (95% CI, 46% to 81%) and 75% (95% CI, 59% to 90%), respectively; and for patients with advanced disease, it was 34% (95% CI, 22% to 46%) and 39% (95% CI, 25% to 53%), respectively.

Conclusion: A certain degree of one antigen mismatching may not compromise the outcome after UD SCT when using this rabbit ATG in addition to standard GVHD prophylaxis regimen.

	INTRODUCTION

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ALLOGENEIC TRANSPLANTATION of hematopoietic stem cells (SCT) is increasingly used as curative treatment for patients with hematologic malignancies. Presently, more than 7 million donors are registered worldwide, thus increasing the chance to find an HLA-compatible donor within adequate time. Although the alloreactivity of donor T cells against residual malignant cells in the recipient is of major importance for long-term cure of the disease after allogeneic SCT, the flip side of the coin—graft-versus-host disease (GVHD)—is an important risk factor for morbidity and mortality. Mismatching within HLA-A, HLA-B, HLA-DRB1*, and HLA-DQB1* loci increases the risk of GVHD.^1,2 Therefore, optimal matching by high-resolution molecular typing of HLA class II and recently class I is commonly assumed to be a prerequisite for a successful outcome after unrelated-donor (UD) SCT in adult patients.³ However, the search for a completely matched donor may take time, too long for a patient with active leukemia. Furthermore, it is presently not known what degree of mismatching is acceptable in UD SCT.⁴ Other factors, such as type of GVHD prophylaxis, patient as well as donor age, a female donor for a male recipient, a positive cytomegalovirus serostatus, stem-cell source, diagnosis, and state of remission, may influence the incidence of GVHD and outcome after allogeneic SCT.^1,5–10 Recently, we have reported on our experience with a GVHD prophylaxis regimen using in vivo anti–T-lymphocyte globulin ([ATG] ATG-S; Fresenius, Graefelfing, Germany), which resulted in a low incidence of acute GVHD.¹¹ In this article, we extend our data on 100 consecutive patients receiving a first non–T-cell depleted SCT from an unrelated donor. We compared patients with an HLA-matched or HLA-mismatched graft. Our data contribute to the understanding of what degree of HLA mismatching may be acceptable provided adequate GVHD prevention strategies are instituted.

	PATIENTS AND METHODS

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Patients
Between November 1995 and December 1999, 100 adult patients with hematologic malignancies received a bone marrow or peripheral-blood stem-cell graft as a first transplantation from an unrelated donor after an ATG- and cyclosporine-containing GVHD prophylaxis. All patients, except for two, received high-dose total-body irradiation (TBI) or alkylating agent–containing conditioning regimen. Patients who had undergone previous autologous or allogeneic SCT were not included; seven patients who were not receiving ATG within the early phase of this time period were also not included. Patient characteristics are listed in Table 1. The median age was 37 years (range, 17 to 65 years). Thirty-four patients underwent transplantation in first complete remission (CR1) of acute leukemia or first chronic phase (CP1) of chronic myelogenous leukemia (CML), and 66 patients were either untreated or refractory and relapsing or in second complete remission (CR2) or in advanced phase.

Seventy-five patients received transplantations from an HLA-A, HLA-B, HLA-DRB1*, or HLA-DQB1* identical donor. For 25 patients only, a mismatched donor was found. In 21 donor-recipient pairs, one single allele difference within the same cross-reactive group for class I loci, and minor and micro differences for DRB1* and DQB1*, respectively, were accepted. In three patient-donor pairs, two differences were accepted, and in one pair, three differences were accepted (Table 2).

GVHD Prophylaxis
All patients received rabbit ATG (Fresenius, Graefelfing, Germany), produced by immunizing rabbits with the T-lymphoblastic cell line Jurkat, within the last 3 days before transplantation, as described previously.¹¹ The first 21 patients received 3 x 30 mg/kg bw/d (total, 90 mg/kg bw), and consecutively, because of frequent side effects, the dose was reduced to 20 mg/kg bw/d (total 60 mg/kg bw). Three patients received 80 mg/kg total dose, and in 12 patients with advanced leukemia, the effective dose applied was 20 to 40 mg/kg bw. Before starting the ATG infusion and 2 hours later, patients received 100 mg of prednisone intravenous prophylactically and ranitidine and clemastine.

All patients received cyclosporine 2.5 mg/kg intravenously twice daily starting day -3. Ninety-two patients received additional short-course methotrexate days +1, +3, and +6. Four patients did not receive methotrexate because of toxicity, and four patients received mycophenolate mofetil (CellCept; Roche, Basel, Switzerland) 2 x 1 g/d instead of methotrexate. During the first part of the time period, 50 patients received additional prednisone starting day +7, as reported previously¹³; however, since June 1997, prednisone was omitted in patients not in CR1 or CP1 before bone marrow transplantation (Table 1).

Statistical Analysis
Data were evaluated as of May 2, 2001, and follow-up of patients was complete. End points were incidence and severity of acute GVHD, incidence of chronic GVHD, incidence of relapse, disease-free survival (DFS), and overall survival. Disease-free survival time was defined as time from transplantation to relapse or death of any cause. Overall survival time was defined as time from transplantation to death of any cause. The probability of GVHD and relapse was estimated by cumulative incidence rates, where death without GVHD or death without relapse was considered a competing event, respectively. Disease-free and overall survival were estimated by the Kaplan-Meier method. No statistical tests were performed. Results with corresponding 95% confidence intervals (CIs) are presented in a descriptive manner. Data analysis was performed using the Statistical Analysis System (SAS) version 6, 1990 (SAS Institute Inc, Cary, NC). Kaplan-Meier estimates were calculated by the procedure LIFETEST. For the calculation of cumulative incidence rates, self-written SAS macros were used.¹⁴

	RESULTS

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Engraftment
Three patients died before engraftment of WBC more than 1,000/µL because of diffuse alveolar hemorrhage, herpes simplex virus sepsis, and aspergillosis at days +12, +15, and +15, respectively. One patient with end-stage myelofibrosis and splenomegaly and blast crisis died from pneumonia on day +36 without engraftment after bone marrow transplantation from a matched donor. All other patients were engrafted with leukocytes more than 1,000/µL on median day +15 (range, day +10 to +29). Secondary graft failure occurred at day +36 in a CML patient who underwent transplantation in accelerated phase from a three-loci HLA-A, HLA-DRB1*, and HLA-DQB1* mismatched marrow donor (patient 980340 in Table 2). Unsupported platelet counts of more than 20,000/µL were reached on median day 24 (range, day 9 to 150). Thirteen patients died before platelet engraftment.

GVHD
The cumulative incidence of acute GVHD °I-°IV for matched and mismatched transplantations was 37% (95% CI, 28% to 50%) and 52% (95% CI, 36% to 76%), respectively (Fig 1A); the incidence of acute GVHD °II-°IV was 21% (95% CI, 14% to 33%) and 20% (95% CI, 9% to 44%), respectively (Fig 1B). Acute GVHD °III–°IV was seen in 5.3% matched (95% CI, 2% to 14%) and 4% mismatched transplantations (95% CI, 0.6% to 28%) (Fig 1C). The incidence of death before acute GVHD was 15% and 8% for matched and mismatched transplant patients, respectively. In 79 patients (58 matched, 21 mismatched) surviving beyond day 100, the cumulative risk of developing chronic GVHD was 59% (95% CI, 48% to 74%) and 67% (95% CI, 49% to 90%) for matched and mismatched transplant patients, respectively (Fig 2A); the risk for extensive chronic GVHD was 43% (95% CI, 32% to 59%) and 44% (95% CI, 26% to 75%), respectively (Fig 2B). The cumulative incidence of death before chronic GVHD was 15% for matched and 14% for mismatched transplant patients.

View larger version (25K): [in this window] [in a new window]   Fig 1. Incidence of acute graft-versus-host disease (aGVHD) in mismatched (solid line) and matched transplants (dashed line): (A) °I-°IV; (B) °II-°IV; and (C) °III–°IV.

View larger version (33K): [in this window] [in a new window]   Fig 2. Incidence of chronic graft-versus-host disease (cGVHD) in mismatched (solid line) and matched transplants (dashed line): (A) limited and extensive cGVHD and (B) extensive cGVHD.

View larger version (25K): [in this window] [in a new window]   Fig 3. (A) Disease-free and (B) overall survival rate. Kaplan-Meier estimates for 34 patients with early disease (solid line) and 66 patients with advanced disease (dashed line).

View larger version (28K): [in this window] [in a new window]   Fig 4. (A) Transplantation-related mortality (incidence of death before relapse) estimates, and (B) relapse rate estimates for patients with early disease (solid line) and patients with advanced disease (dashed line).

	DISCUSSION

TOP ABSTRACT INTRODUCTION PATIENTS AND METHODS RESULTS DISCUSSION REFERENCES

 
Here we present an analysis of mature data of a large patient cohort with special consideration on the degree of HLA mismatching and outcome after UD SCT. UD-derived grafts are increasingly used for allogeneic transplantation. In adult patients, standard GVHD prophylaxis with cyclosporine and methotrexate results in a higher incidence of mortality because of GVHD in UD SCT compared with matched-sibling transplantation, and optimal DNA-based matching is assumed to improve outcome after UD SCT.^15–18 Previously undetected HLA differences in class I or minor antigens possibly contribute to the increased risk of GVHD in UD SCT.¹⁹ The National Marrow Donor Program (NMDP) reported on 1,423 patients with CML who received transplantations from unrelated donors, and patients in first chronic phase had a 47% 3-year DFS.⁸ Better results were seen in younger patients less than 35 years in the first year after initial diagnosis of CML.^8,9 The use of tacrolimus instead of cyclosporine has been shown to significantly decrease the risk of acute GVHD °II-°IV from 74% to 56% in UD SCT in a randomized trial.²⁰ In a single-center study, T-cell depletion with anti-CD6 monoclonal antibodies resulted in an acute GVHD °II-°IV rate of 42% after UD SCT.²¹ Mortality for the first 100 days after transplantation was 19%, and all 14 patients older than 50 years did not survive. Using unmodified marrow grafts and adding anti–T-lymphocyte globulin to the standard GVHD prophylaxis of cyclosporine and short-course methotrexate, we and others observed a low incidence of severe acute GVHD comparable with results obtained in matched-sibling donor transplantation.^11,22,23

In this article, we extend our previous data¹¹ and report on a large consecutive cohort of patients who received UD SCT using in vivo rabbit anti-T cell globulin. With our protocol, we did not observe an increase in acute GVHD in 25 patients who underwent transplantation from donors with HLA class I or II differences compared with the patients with a complete HLA-A, HLA-B, HLA-DRB1*, and HLA-DQB1* match. Both groups were balanced regarding factors influencing GVHD, such as cytomegalovirus, donor-recipient sex mismatch, age, graft source, or disease. More recently, the terms cross-reactive group for HLA class I alleles and minor or micro differences in DRB1* and DQB1* have been challenged, and presently, any differences in these HLA loci are regarded as such, independent of the level of resolution. The value of DNA typing for class I alleles in UD SCT has to be shown, and it is still not known which differences in HLA typing will be acceptable without negatively influencing the outcome. Despite the relatively small numbers, it seems that mismatching as indicated in our patient series does not increase the incidence of clinically relevant GVHD. However, secondary graft failure after marrow transplantation and busulfan conditioning in a patient with advanced CML and a three-antigen mismatch indicates the limits of mismatching. Possibly, a peripheral-blood derived graft and/or high-dose TBI could counteract the rejection vector in this situation more effectively. It has to be kept in mind that the majority of our mismatched patients had only a single difference, and no conclusions regarding mismatches in several HLA loci can be drawn.

The overall low rate of clinically relevant acute GVHD observed in our patient series compares favorably with results obtained with the standard GVHD prophylaxis cyclosporine and methotrexate.^8,15,24 Several agents contribute to the GVHD prevention strategy; apart from cyclosporine and short course methotrexate, half of the patients received additional corticosteroids. However, our own and others’ experiences suggest that the addition of corticosteroids is not sufficient to decrease the rate of acute GVHD in UD SCT,^25,26 and prophylactic use of corticosteroids was omitted since June 1997 in advanced disease patients to possibly reduce the risk of infections. We attribute the overall low incidence of GVHD in the matched as well as mismatched patient groups to the in vivo use of anti–T-cell globulin. The ATG used in our patients is a polyclonal rabbit immunoglobulin G that has been raised by immunization with the T-lymphoblastic leukemia cell line Jurkat. This agent binds dose-dependently not only to T but also to B and other cells and is likely to be different in its spectrum compared with either rabbit or horse sera that have been produced by immunization with thymocytes. Therefore, when comparing trials using ATG, not only do differences in the dose and schedule applied need to be kept in mind, but as importantly, possible differences in the potency and the spectrum of cellular targets also have to be noted. For most of these different sera, optimal doses for the use in SCT and their definite role have to be defined in randomized trials. Ideally, these agents contribute to a more rapid immunologic tolerance after transplantation, allowing a safe reduction of immunosuppressive therapy. However, increased rates of opportunistic infections and relapse rates may be the flip side of the coin. This dose-dependent side effect is especially prominent with the highly immunosuppressive antithymocyte globulins, otherwise used successfully for the treatment of severe aplastic anemia.

Using a serum different from that used by us, Bacigalupo et al²⁷ reported a low incidence of severe acute and chronic GVHD in patients receiving a higher dose compared with patients receiving a lower dose or no polyclonal rabbit antithymocyte globulin. However, this did not translate to a better survival because a higher rate of fatal infections was observed. With the in vivo application of the monoclonal antibody Campath-1H directed against the CD52 antigen, ubiquitously expressed on lymphocytes, efficient GVHD prophylaxis has been demonstrated in allogeneic SCT; however, long-term follow-up data are lacking.²⁸

Late opportunistic infections and relapse, especially in the advanced-disease patient group, remain a concern. Remarkably, in the CR1/CP1 patient group, we observed relapse of disease more than 2 years after transplantation. However, all four patients responded to donor lymphocyte infusions, with three patients obtaining CRs. Therefore, long-term monitoring of minimal residual disease seems to be important because early intervention with donor lymphocytes or other measures are likely to be successful in these patients.

In conclusion, we have shown that adding this particular rabbit ATG to a standard cyclosporine and methotrexate GVHD prophylaxis results in a low incidence of severe acute GVHD, and with this regimen, a certain degree of single-antigen mismatching may not compromise the outcome after UD SCT. Our data add to the experience to define the role of HLA mismatching in UD SCT. This approach may extend the availability of unrelated donors for patients in need.

	ACKNOWLEDGMENTS

 
We are thankful for the fruitful collaboration in patient care with J.Th. Fischer, F. Hirsch, and J. Mezger, and for the dedicated work of the team from transplant ward Löhr. We thank E. Lenartz for transplant coordination, U. Tritschler and S. Zehbe for technical assistance, I. Matt for documentation work, and Professor R. Mertelsmann for continuous support.

	REFERENCES

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Submitted March 25, 2002; accepted October 4, 2002.

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This Article Abstract Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Save to my personal folders Download to citation manager Rights & Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Finke, J. Articles by Bertz, H. Search for Related Content PubMed PubMed Citation Articles by Finke, J. Articles by Bertz, H. Social Bookmarking                            What's this?