Steroid Responsive T-Cell Mediated Pure Red Cell Aplasia Following Allogeneic Hematopoietic Stem Cell Transplantation

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 5498-5498
Author(s):  
Sandhya Kharbanda ◽  
James L. Zehnder ◽  
Bertil Glader

Abstract Pure red cell aplasia (PRCA) is an unusual complication following allogeneic hematopoietic stem cell transplantation (HSCT), the true incidence of which is not known. Almost all cases reported in the literature describe major ABO-incompatibility between the recipient and the donor as the major risk factor for this complication. Delayed recovery of reticulocyte counts and hypoplasia of erythroblasts in the marrow is attributed to incompatible hemagglutinins in recipients. There are reports of successful treatment of PRCA using different strategies include rapid tapering of calcineurin inhibitors, corticosteroids, donor lymphocyte infusion, rituximab, and/or plasma exchange. Additional causes of PRCA following allogeneic HSCT include parvovirus B19 infection and graft-versus-host disease (GVHD). The pathogenesis of PRCA in parvovirus infection is thought to be viral-mediated suppression of erythroid precursors in the bone marrow and this is due to the tropism of this virus for erythroid progenitor cells. Nonmyeloablative and reduced intensity conditioning regimens have been reported to have an increased risk of PRCA due to persistence of recipient lymphocytes. Here we report two cases of PRCA following allogeneic HSCT from major ABO mismatched donors. Both cases were correlated with the presence of a T-cell clone in the peripheral blood and bone marrow, and there was complete resolution of anemia with a short course of steroid treatment, as well as disappearance of the T-cell clone. Patient # 1 – A 24 year old female of Mediterranean descent underwent an HLA- 8/10 matched and major ABO-mismatched sibling donor bone marrow transplant for Sickle-Beta Thalassemia. She received a myeloablative but reduced toxicity conditioning regimen consisting of busulfan 16mg/kg, fludarabine 140mg/m2, cyclophosphamide 105mg/kg, and alemtuzumab 52mg/m2. Her immediate post-transplant course was relatively benign and significant for a mild CMV colitis which responded with resolution after treatment with anti-viral therapy. Her red cell transfusion needs had significantly decreased to every four weeks by day 130. However, at day 146 from HSCT, she started requiring red cell transfusions every two weeks, with a drop in the reticulocyte count to 0.6%. No antibodies were detected, and the patient was negative for parvovirus B19 and did not have any evidence of GVHD. However, her bone marrow showed an marked erythroid hypoplasia, and was positive for a T-cell clone with gamma chain gene rearrangement in the T-cell receptor. Due to a new onset of transfusion need, she was treated with a short course of steroids with an excellent response and disappearance of the T-cell clone from peripheral blood. She remained on immunosuppression during this entire period with a calcineurin inhibitor. Patient# 2 – A 10 year old Hispanic girl underwent a 10/10 HLA-matched and major ABO-mismatced sibling donor bone marrow transplant for idiopathic acquired severe aplastic anemia. Her preparative regimen consisted of 200 mg/kg of cyclophosphamide and 16mg/kg of rabbit-anti-thymocyte globulin. Her immediate post-transplant course was complicated by E.coli bacteremia. She had prompt engraftment and became transfusion independent on day 86. A cyclosporine taper was initiated at day 100 but held at day 119 when anemia was first noted. Peripheral blood showed a T-cell clone with gamma and beta chain gene rearrangement. She was started on a moderate dose of steroids with a good response, and has been tapered down to physiologic replacement dose of steroids with normal Hb and transfusion independence. With the resolution of anemia, the gamma chain gene rearrangement is not seen in the T-cell clonality assay, however, the beta chain gene rearrangement persists. To our knowledge, this is the first report of a T-cell mediated PRCA following allogeneic HSCT. Moreover, the PRCA was steroid responsive and not associated with GVHD in both the patients. Disclosures: No relevant conflicts of interest to declare.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3269-3269
Author(s):  
Serena Rupoli ◽  
Gaia Goteri ◽  
Renzo Ranaldi ◽  
Capretti Roberta ◽  
Anna Rita Scortechini ◽  
...  

Abstract In patients with early Mycosis Fungoides (MF), a dominant T-cell receptor (TCR) gene rearrangement can be detected in the skin in 50–75% of cases, while in 15–40%, an identical T-cell clone is detectable also in the peripheral blood This may indicate an unfavourable subset of patients. We observed on omogeneus group of early MF patients all receiving the some protocol. The purpuose of this study were: - T-cell receptor gene rearrangement analisys of peropheral blood samples; - evaluation of the prognostic impact of T-cell monoclonality on CR and relapse rate. 44 patients diagnosed as having MF at early stage (25 M, 19 F; mean age 58.7 yrs, range 34–77; 11 in stage IA, 28 in stage IB, 5 in stage IIB) and showing a dominant T cell clone in the skin lesions at diagnosis, were included in the present study. Peripheral blood samples were collected for DNA extraction at diagnosis. PCR amplification for TCRγ gene was performed as previously reported by Ashton-Key et al. (1997) in all 44 cases both in peripheral blood and skin and reduplicated: amplification products were visualised by 10% polyacrylamide gel electrophoresis. Peripheral blood samples were considered positive for a circulating T cell clone only if the monoclonal signals in peripheral blood and skin were reproducible and overlapping. All patients received the same treatment, consisting of a combination protocol with low-dose IFNα + PUVA for 14 months, and then followed up. Clinical response to the therapy and further disease recurrences were registered. After a mean time of 6.02 months (range, 1–21), 7 patients failed to respond to combination therapy, while 37 obtained a clinical complete remission (CCR). Among them, 15 experienced a disease recurrence during the follow-up (mean time, 29.8 months, range, 1–77 months). PCR analysis of TCRγ gene showed in the peripheral blood the same T-cell clone detected in the skin in 16 cases (36.4%). Failure to obtain a CCR was found in 3 out of 28 cases without a T cell clone in peripheral blood (10.7%) and in 4 out 16 cases with a circulating T cell clone (25%; c2 test: P=0.41, NS). Disease recurrence was observed in 9 out of 25 cases without a T cell clone in peripheral blood (36%) and in 6 out of 12 cases with a circulating T cell clone (50%; c2 test: P=0.65, NS). Disease-free survival curves plotted by Kaplan-Meier method showed that patients with and without a circulating T cell clone did not behave differently and that half of the patients would have experienced a relapse after a similar period of time (34 and 36 months, respectively, for patients with TCRg+ and − peripheral blood; log rank test, P=0.79). PCR analysis of TCRγ gene rearrangement analysis has allowed us to detect monoclonality in the peripheral blood in 36% of early MF cases with a documented monoclonality in the skin. At this stage of the disease a circulating T cell clone could indicate a subset of patients in which skin-directed therapies are more likely to fail to completely eradicate the malignant cells. Interestingly, our data seems to show that the negative influence of a circulating clone can be bypassed by the combination of a skin-directed therapy like PUVA and the systemic immunoregulatory effects of IFNα.


1987 ◽  
Vol 165 (4) ◽  
pp. 1000-1015 ◽  
Author(s):  
Z Chen ◽  
D Le Paslier ◽  
J Dausset ◽  
L Degos ◽  
G Flandrin ◽  
...  

T cell rearranging gene gamma (TRG gamma) and T cell antigen receptor beta (TCR beta) chain gene rearrangement and transcription were studied in a series of patients with B-lineage acute lymphoblastic leukemia (ALL), in which the Ig H chain genes are rearranged and the surface phenotype reproduces the stages of normal pre-B maturation. For comparison, polyclonal T cells from peripheral blood of healthy donors and blast cells from 19 cases of T lineage ALL were also studied. In this study we demonstrate the presence of a clonal rearrangement of the TRG gamma in 18 of the 22 B-lineage ALL cases and establish that this rearrangement, which generally involves the J gamma 1 region, is often monoallelic and appears different from the biallelic J gamma 2 rearrangement frequently seen in T-cell ALLs. In 9 of 22 cases, we found rearrangement of the genes of the TCR beta chain, which never involved the J beta 1 region. Conversely, the TRG gamma were seen in germline configuration in all 19 cases of B chronic lymphoid malignancies. In none of the 9 AML cases studied was TRG gamma and TCR beta chain gene rearrangement found. The TCR beta chain genes were rearranged in one B cell chronic lymphocytic leukemia (CLL). We also show that in B-lineage ALL, the cells probably use the same V gamma genes for TRG gamma rearrangements as the malignant cells in T-ALL and the polyclonal T cells. In none of the 13 B-lineage ALL cases investigated by Northern analysis was TCR beta mRNA expression detected, whereas a weak expression of TRG gamma transcripts was found in two of these cases. The correlations between surface phenotype, rearrangement of TRG gamma, TCR beta, and Ig H chain genes were analyzed. The significance of rearrangement of TRG gamma and TCR beta chain genes in B or pre-B cells is also discussed.


Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 1306-1306
Author(s):  
Olga Zimmermannova ◽  
Ondrej Hrusak ◽  
Eva Fronkova ◽  
Marketa Kubricanova Zaliova ◽  
Ester Mejstrikova ◽  
...  

Abstract Abstract 1306 Introduction Acute lymphoblastic leukemia (ALL) can rarely be manifested before its diagnosis as pancytopenia and bone-marrow aplasia followed by spontaneous transient hematological remission. A leukemic clone can be detected during this particular period, making it possible to follow its dynamics in size, as well as independent changes leading to the overt disease. Patients and methods We initially selected 5 cases of ALL, in which the pre-diagnostic period of anemia had occurred. In all pre-diagnostic samples, the immunoglobulin (Ig) and/or T-cell receptor (TCR) gene rearrangements were investigated using quantitative real-time PCR. In addition, SNP array and FISH were performed in some cases in order to reveal other aberrations specific to leukemia. To backtrack the preleukemic cells three different approaches were employed - qPCR, FISH and next generation sequencing (NGS). Results Immunoreceptor gene rearrangements were detected in all 5 patients in the diagnostic sample. At least one of the diagnostic rearrangements was found in all preleukemic bone-marrow samples. The levels of positivity differed from 10−1 to 10−6. In 3 patients more than one pre-diagnostic sample was made available for our examination. A surprising dynamics in the size of the leukemic clone was revealed by the investigation. Although a steady increase of blasts was expected, particularly high levels occurred in the first available preleukemic samples (10% and more clonal Ig/TCR positive cells compared to the diagnosis, in 4/5 of patients), followed by remarkable decrease 1 to 3 months before the diagnosis in 3 patients with more than one sample available. This dynamics points to possible immune system interventions during preleukemic phase. In 2 patients NGS (targeted to Ig/TCR gene rearrangements, Adaptive Biotechnologies, Seattle) was applied. The acquired data correlated with the results of qPCR backtracking. In addition, more detailed information was gained about gene rearrangement spectra as well as about possible immunological background of the leukemia progression. In both these patients, the examination revealed a significant fraction of non-malignant γΔ T cell-clone carrying an identical Vg9-Jg1.2 gene rearrangement, which has been reported previously to play an important role in anti-tumour and anti-microbe immune responses. Interestingly, the dynamics of this particular clone seemed to correlate negatively with the leukemic cell levels, pointing out its putative role in tumour surveillance. Consequently, SNP array was performed to define the aberrations acquired, followed by FISH investigation to confirm the above conclusions. While some aberrations were confirmed already in the pre-diagnostic samples (namely ETV6 deletion in the patient with ETV6/RUNX1 positive ALL), others occurred in the diagnostic sample, yet not in the preleukemic cells several months before the diagnosis. Conclusion Preleukemic cells present during the aplastic phase preceding leukemia onset are not just a gradually growing clone. Their specific dynamics has been shown, which supports our previous data acquired during the investigation of secondary leukemias. Furthermore, at least in some cases, this clone indeed should be considered ‘preleukemic’ as it is to undergo at least one more hit or subclonal selection to progress into an active disease. Disclosures: No relevant conflicts of interest to declare.


Blood ◽  
1999 ◽  
Vol 94 (4) ◽  
pp. 1409-1417 ◽  
Author(s):  
J. Marcus Muche ◽  
Ansgar Lukowsky ◽  
Jürgen Heim ◽  
Markus Friedrich ◽  
Heike Audring ◽  
...  

Clinical, immunohistological, and molecular biological data suggest the chronic dermatosis small plaque parapsoriasis (SPP) to be a precursor of mycosis fungoides (MF). However, most data are contradictory and confusing due to inexact definition of SPP. Recently, clonal T cells were detected in skin and blood samples of early MF. Because demonstration of identical T-cell clones in skin and blood of SPP patients would indicate a close relationship of SPP to MF, we investigated the clonality of skin and blood specimens from 14 well-defined SPP patients. By a polymerase chain reaction (PCR) amplifying T-cell receptor γ rearrangements and subsequent high-resolution electrophoresis, clonal T cells were detected in 9 of 14 initial and 32 of 49 follow-up blood samples, but in 0 of 14 initial skin specimens. Even a clone-specific PCR showing the persistence of the initial blood T-cell clone in 20 of 20 follow-up samples, failed to detect the T-cell clone in the skin. In 2 patients, the clonal T cells were shown to be CD4+. For the first time, the majority of SPP patients was shown to carry a T-cell clone in the peripheral blood. Although a relation between circulating clonal T cells and SPP cannot directly be proven by the applied techniques, our results indicate blood T-cell clonality to be a characteristic feature of SPP and CTCL because analysis of multiple controls and clinical workup of our SPP patients excluded other factors simulating or causing a clonal T-cell proliferation. A sufficient cutaneous antitumor response but also an extracutaneous origin of the T-cell clones might explain the failure to detect skin infiltrating clonal T cells.


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