scholarly journals Laboratory involvement in the diagnosis and monitoring of paroxysmal nocturnal hemoglobinuria: a case report

2021 ◽  
Vol 106 (106(812)) ◽  
pp. 89-92
Author(s):  
M.J. Ruíz-Márquez ◽  
J. Luis-Navarro
Keyword(s):  
Bone Marrow ◽  
Blood Cells ◽  
Paroxysmal Nocturnal Hemoglobinuria ◽  
Specific Treatment ◽  
Variable Number ◽  
Variable Degree ◽  
Effective Management ◽  
Hematopoietic Stem ◽  
Thrombotic Risk

Paroxysmal nocturnal hemoglobinuria is a rare non malignant clonal disease, caused by an acquired somatic mutation in a variable number of hematopoietic stem cells, whose consequence is an abnormal sensitivity of blood cells to complement-mediated lysis. It manifests as intravascular hemolytic anemia, a variable degree of bone marrow insufficiency and high thrombotic risk. The effective management of the disease is based on an adequate diagnosis and clinical and laboratory follow-up. Flow cytometry is the method of choice for diagnosis and monitoring of the patient. The only curative treatment is hematopoietic stem cell transplantation. Eculizumab is the first specific treatment approved for this disease. We present the case of a patient diagnosed with paroxysmal nocturnal hemoglobinuria, wo has recently started treatment with eculizumab. We show the clinical and analytical evolution during the first months of treatment as an assessment of is benefit.

Hematopoietic Stem Cell Transplantation following Reduced Intensity Conditioning for High Risk Patients with Paroxysmal Nocturnal Hemoglobinuria

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4407-4407
Author(s):  
Agata Mikolajewska ◽  
Haifa Kathrin Al-Ali ◽  
Nadezda Basara ◽  
Elliot Epner ◽  
Ernst Holler ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Stem Cell ◽  
High Risk ◽  
Stem Cell Transplantation ◽  
Paroxysmal Nocturnal Hemoglobinuria ◽  
Chronic Gvhd ◽  
Reduced Intensity Conditioning ◽  
Hematopoietic Stem ◽  
Reduced Intensity

Abstract Objectives: Paroxysmal nocturnal hemoglobinuria (PNH) is a non malignant acquired hematopoietic stem cell disorder that can cause severe complications such as arterial or venous thrombosis or deficient haematopoiesis. These patients have a high mortality rate and should be evaluated for allogeneic stem cell transplantation (SCT). However, conventional conditioning has been associated with high treatment related toxicity. We report here the extended follow up of 7 previously published and 4 additional patients with high risk PNH after allogeneic HCT with reduced intensity conditioning (RIC). Patients: Eleven patients (3 males) with a median time from diagnosis to SCT of 16 (range 4 to 59) months were treated with red blood cell transfusions (n=9), anticoagulation (n=3), or immunosuppression (n=10): cyclosporine A (CSA, n=3), azathioprin (n=1), mycofenolate mofetil (MMF, n=1), antithymocyte globulin (n=1) or systemic steroids (n=9) until SCT. High risk PNH was characterized by venous thromboses: sinus veins (n=1), liver veins (n=3), vena portae (n=1), mesenterial veins (n=1) or thrombosis of lower extremity (n=1); bone marrow failure (n=6); recurrent life threatening haemolysis (n=8) or infections (n=5). Seven patients had more than one high risk feature. The median age at SCT was 34 (range 22 to 49) years. Conditioning regimen consisted of 2 Gy total body irradiation (TBI) at day 0 and fludarabine (30 mg/m2) at day-4 to -2 followed by treatment with MMF and CSA. The stem cell donors were related (n=2), allele matched unrelated (n=7) or mismatched (n=2). Results: The median follow up was 43 (range 2–101) months after SCT. The median time until neutrophil recovery was 17 (range 0–29) days and 4/11 patients (36%) did not develop ANC<500/l. All but one patient (91%) showed primary donor engraftment with a median T-cell chimerism of 59 (range 38.3–99.3) % in the bone marrow at day 28 after SCT. The patient with primary graft failure received a second transplant from an alternative donor after RIC with 3 Gy TBI and showed stable engraftment. Six out of 11 (55%) patients developed grade II or III acute graft-versus-host disease (GvHD), which was treated with systemic steroids in 5 patients. Extensive chronic GvHD occurred in 3/11 (27%) of the patients. Three patients (27%) died of complications (pancreatitis with subsequent multiorgan failure, pseudomonas sepsis and haemorrhage) following steroid treatment for acute (n=1) and extensive (n=2) chronic GvHD 2, 12.5 and 14 months after SCT. The remaining 8 patients are alive and without clinical and laboratory evidence of PNH after a median follow up 61.5 (range 10–101) months after SCT. All surviving patients show an ECOG of 0–1 and 4/8 patients (50%) are off all immunsuppression. Conclusions: Allogeneic HCT with reduced intensity conditioning induces durable eradication of the PNH clone. The treatment related mortality even in high risk PNH with severe organ dysfunction was acceptable and due to complications after GVHD. All long term survivors have a good performance status and half of them are without any immunosuppression.

Ham Test For Therapeutic Monitoring Of Eculizumab In Paroxysmal Nocturnal Hemoglobinuria

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4876-4876
Author(s):  
Miriam Arcavi ◽  
Fernanda Ceballo ◽  
Andres L. Brodsky ◽  
Nora Silvia Halperin ◽  
Norma Cantenys ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Stem Cell ◽  
Blood Cells ◽  
Paroxysmal Nocturnal Hemoglobinuria ◽  
Alternative Pathway ◽  
Specific Treatment ◽  
Chimeric Antibody ◽  
Intravascular Hemolysis ◽  
Hematopoietic Stem ◽  
Gold Standard Method

Abstract Introduction Paroxysmal nocturnal hemoglobinuria (PNH) is a rare acquired clonal disease, caused by an inactivating mutation in the PIG-A gene in a hematopoietic stem cell. The PIG-A gene encodes an enzyme required for glycosylphosphatidylinositol (GPI) anchor synthesis. Its inactivation results in a deficiency of many plasma membrane GPI-anchored proteins -including CD55 and CD59, natural inhibitors of the complement cascade- in the involved stem cell and all its progeny (the PNH clone). Intravascular hemolysis, anemia, thrombosis, acute and chronic renal damage, pulmonary hypertension, abdominal pain, esophagic spasm, erectile dysfunction -among others manifestations- are consequences of complement mediated damage of the sensitive PNH blood cells. In 2007 both the FDA and the EMA approved eculizumab, a monoclonal chimeric antibody targeted against C5 fraction of complement, as the first specific treatment of complement mediated PNH manifestations. Flow cytometry (FC) is the gold standard method for diagnosis. The former diagnostic test -the Ham test- is based on the susceptibility of PHN red blood cells (RBC), when they are incubated with both normal and patient sera to lysis mediated by the alternative pathway of complement (APC). APC is activated, in the Ham test, through sera acidification. Despite its physiopathological value, Ham test has been replaced with flow cytometry to diagnose PNH due to a much higher sensitivity and reproducibility. Aims To evaluate the Ham test in PNH treated patients, to monitor the eculizumab-mediated blockade of APC. Patients and methods Ham test was used to monitor APC blockade in the patient serum, testing the ability of the acidified patient serum to lyse his or her own PNH-RBC. Eight patients were diagnosed as PNH by FC and were treated with eculizumab. Six had a good therapeutic response, with decreased levels of both, LDH and the serum total complement hemolytic capacity (CH50). Ham test, in these six patients, showed hemolysis when PNH-RBC were mixed with normal acidified serum but absence of hemolysis when the acidified serum of eculizumab treated patient was added to the PNH-RBC. This result was called “blockade profile” and shows the “ex vivo” APC blockade, confirming thus the eculizumab success. The remaining two patients showed a persistent positivity of the Ham test at day 14 of eculizumab administration (as PNH-RBC lysis continued taking place with both normal and patient acidified sera). One patient demonstrated break through hemolysis occurring near the end of eculizumab dosing period as indicated by increase in LDH. As LDH may increase due to other possible factors (ie hepatic lesions) the positive Ham test confirmed that intravascular hemolysis was taking place, possibly due to a shorter eculizumab half life. An increase of the eculizumab dose to 1,200 mg/14 days reinstated lower LDH levels and the blockade profile in the Ham test (Table). There has been a single patient treated with eculizumab where LDH did not reduce. There was a persistently positive Ham test, elevated LDH and free hemoglobin levels and normal CH50 values despite a dose of 1,200 mg of eculizumab every 14 days (Table). A genetic study found in this case a C5 mutation, which seems responsible of the lack of response to eculizumab. Conclusions In our experience, the Ham test has proved to be a useful and economic method to monitor the effectiveness of eculizumab treatment in cases with high LDH levels due to either a) other causes than intravascular hemolysis, or b) no responsive patients due to pharmacokinetic (inadequate eculizumab concentration) or pharmacodynamic causes. Disclosures: Brodsky: Alexion Pharmaceuticals: Consultancy, Speakers Bureau. Colin:Alexion Pharmaceuticals: Consultancy.

Development of Paroxysmal Nocturnal Hemoglobinuria in Children with Aplastic Anemia

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 1499-1499 ◽  
Author(s):  
Atsushi Narita ◽  
Hideki Muramatsu ◽  
Yusuke Okuno ◽  
Yuko Sekiya ◽  
Kyogo Suzuki ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Aplastic Anemia ◽  
Paroxysmal Nocturnal Hemoglobinuria ◽  
Bone Marrow Failure ◽  
Subsequent Development ◽  
Poor Quality ◽  
Targeted Sequencing ◽  
Hematopoietic Stem ◽  
Bone Marrow Failure Syndromes

Abstract Introduction: Paroxysmal nocturnal hemoglobinuria (PNH) is a nonmalignant clonal disease of hematopoietic stem cells resulting from a somatic mutation in the PIGA gene. PNH frequently manifests in association with aplastic anemia (AA), in which PIGA mutations are believed to enable escape from the immune-mediated destruction by pathogenic T cells. Recent studies using next-generation sequencing have revealed that frequent somatic PIGA mutationsin AA patients are associated with a better response to IST and prognosis (Yoshizato et al N Engl J Med. 2015; 373: 35-47). However, clinical PNH is a progressive and life-threatening disease driven by chronic hemolysis that leads to thrombosis, renal impairment, poor quality of life, and death. Large studies in adults have reported that clinical PNH developed in 10%-25% of AA patients; however; the frequency of clinical PNH in children with AA has rarely been described. Here we aimed to elucidate the pathological link between PNH and AA in children. Methods: In total, 57 children (35 boys and 22 girls) diagnosed with acquired AA at our hospital between 1992 and 2010 were retrospectively studied. Patients who underwent hematopoietic stem cell transplantation as first-line treatment within 1 year after AA diagnosis and those with clinical PNH at AA diagnosis were excluded. Flow cytometry (FCM) was used to detect PNH CD13+/CD55−/CD59− granulocytes and PNH glycophorin A+/CD55−/CD59− red blood cells (RBCs). Clinical PNH was defined as the presence of intravascular hemolysis and ≥5% PNH granulocytes or PNH RBCs. Minor PNH clones were defined as those with >0.005% PNH granulocytes or >0.010% PNH RBCs. We performed targeted sequencing of bone marrow samples from patients with clinical PNH that were obtained at 2 time points: at AA diagnosis and after PNH development. The panel of 184 genes for targeted sequencing included most of the genes known to be mutated in inherited bone marrow failure syndromes and myeloid cancers, as well as PIGA. Results: The median patient age at AA diagnosis was 9.3 (1.2-17.8) years, and the median follow-up period was 123 (2-228) months. A total of 43 patients were screened for PNH clones by FCM after AA diagnosis, and 21 of these with minor PNH clones were identified. The median percentages of PNH granulocytes and PNH RBCs were 0.001% (0.000%-4.785%) and 0.000% (0.000%-3.829%), respectively. During follow-up, 5 patients developed clinical PNH after adolescence (15-22 years of age). The median time between AA diagnosis and PNH development was 4.9 (3.3-7.9) years. All clinical PNH patients were treated with IST for AA, and complete and partial response after 6 months were achieved in 1 and 4 patients, respectively. Gross hemoglobinuria was present in all clinical PNH patients, but thrombosis was not observed. The size of PNH clones varied greatly among patients: PNH granulocytes and PNH RBCs were 42.96% (10.04%-59.50%) and 48.87% (15.02%-90.80%), respectively. Oral cyclosporine A and intravenous eculizumab were administered to 3 and 1 patients, respectively; all patients showed sustained response as indicated by improvement in gross hemoglobinuria and normal blood counts after treatment. The remaining 1 patient underwent bone marrow transplantation from the HLA-identical mother and was alive without any complications. Overall, the 10-year probability of developing clinical PNH was 10.2% (95%CI, 3.6-20.7). Among 43 patients screened for PNH clones at AA diagnosis, the 10-year cumulative clinical PNH incidence was significantly higher in patients with minor PNH clones than in those without minor PNH clones at AA diagnosis [29% (95% CI, 10%-51%) vs. 0% (95% CI, 0%-0%); p = 0.015]. Among all clinical PNH patients, a total of 8 somatic PIGA mutations were detected (missense, 2; splice site, 2; and frameshift, 4). However, PIGA mutations were not detected at AA diagnosis even in patients who subsequently developed clinical PNH. Conclusion: In our cohort, the percentage of patients who eventually developed clinical PNH was comparable to that reported in adults in a previous study. Furthermore, the current study showed that the presence of minor PNH clones at AA diagnosis was a risk factor for the subsequent development of clinical PNH, although the clones were not detected by targeted sequencing. Thus, pediatric AA patients with PNH clones at AA diagnosis should undergo long-term periodic monitoring for potential clinical PNH development. Disclosures Kojima: SANOFI: Honoraria, Research Funding.

scholarly journals Paroxysmal nocturnal hemoglobinuria clone in bone marrow of patients with pancytopenia

Blood ◽  
1995 ◽  
Vol 85 (5) ◽  
pp. 1371-1376 ◽  
Author(s):  
H Nakakuma ◽  
S Nagakura ◽  
N Iwamoto ◽  
T Kawaguchi ◽  
M Hidaka ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Flow Cytometry ◽  
Blood Cells ◽  
Paroxysmal Nocturnal Hemoglobinuria ◽  
Unknown Origin ◽  
Diagnostic Value ◽  
Follow Up Study ◽  
Early Appearance ◽  
Pnh Clone

The lack of glycosylphosphatidylinositol (GPI)-anchored membrane proteins such as decay-accelerating factor (DAF) and CD59 on blood cells has a diagnostic value in paroxysmal nocturnal hemoglobinuria (PNH). Because PNH often develops in patients with aplastic anemia (AA), we attempted to detect a PNH clone in the bone marrow (BM) of patients with AA and pancytopenia before affected cells were evident in the peripheral blood (PB). We used flow cytometry with monoclonal antibodies against DAF and CD59 for the detection of the clone. Affected cells were observed in the BM of 3 of 7 patients with AA and 1 of 3 patients with pancytopenia of unknown origin, but not in their PB. All 8 patients with apparent PNH had affected cells in their BM and PB. On the basis of the early appearance of the PNH clone in the BM, a prospective 4-month follow-up study of the PB cells was performed. The study showed the release of affected mature cells first in granulocytes, then in monocytes, and finally in lymphocytes. Ham's test was positive before affected erythrocytes were detected by flow cytometry. Our findings indicate that detection of the PNH clone in BM could be predictive of the development of PNH in patients with AA and pancytopenia.

scholarly journals The Platelet Millionaire: A Rare Cause of Thrombocytosis in an Adolescent

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 5391-5391
Author(s):  
Ritika Walia ◽  
Theresa Sepulveda ◽  
Sharon Wretzel ◽  
Philip H Brandt
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Biopsy ◽  
Primary Care Physicians ◽  
Conflicts Of Interest ◽  
Abdominal Ultrasound ◽  
Cell Transplant ◽  
Peripheral Smear ◽  
Hematopoietic Stem ◽  
Marrow Fibrosis

Objectives: Primary myelofibrosis is rare in pediatrics, often manifesting as persistent idiopathic thrombocytosis.Transitions from pediatric to adult medical care can be complicated by workup requiring invasive procedures. J.M., an 18-year-old healthy male, presented for excessive gingival bleeding after wisdom tooth extraction. Workup revealed persistent thrombocytosis to 1,165K, prompting a referral to hematology-oncology. A peripheral smear was notable for many platelets but normal RBC morphology. He had splenomegaly on abdominal ultrasound and a decreased von-Willebrand's activity to antigen ratio, suggesting acquired vWD. A bone marrow biopsy was advised; however, J.M. became lost to follow up for over 9 months owing to self-reported anxiety about the procedure. He remained asymptomatic in this interim until he re-presented to clinic for easy bruising, with no other evidence of bleeding at the time. The biopsy was pursued, revealing hypercellular marrow for age with left shifted granulocytic and erythroid maturation, abnormal megakaryocytes, and 3% blasts. This was consistent with primary early myelofibrosis (PMF), positive for MF-1, CALR, and TP53 mutations and negative for JAK2 and BCR-ABL. He was transitioned to adult hematology, maintained on baby aspirin, and referred for potential allogeneic hematopoietic stem cell transplant (HSCT). PMF is characterized by marrow fibrosis due to secretion of fibroblast growth factor by clonally proliferative megakaryocytes. It is a disease of adulthood, with 67 years being the median age at diagnosis. Only 100 cases have been reported in children, most of which are secondary to AML, ALL or other malignancies.1 Most patients present with complications of extramedullary hematopoiesis or bleeding.2 Diagnosis is suggested by a leukoerythroblastic picture on peripheral smear and confirmed with a bone marrow biopsy "dry tap" revealing marrow fibrosis.3 Prognosis in pediatric PMF is difficult to predict but outcomes tend to be worse;4 TP53 mutation is rare and based on limited adult studies may portend a poorer prognosis.5 Our young patient with this rare mutation was therefore referred for HSCT evaluation. Further complicating this case was J.M.'s anxiety, which delayed definitive diagnosis by biopsy. He only agreed to it when, at the med-peds clinic, the concept of local pain management was discussed. Anticipation of upcoming procedures by primary care physicians and close follow-up is especially important for patients transitioning from pediatric to adult providers. Disclosures No relevant conflicts of interest to declare.

scholarly journals Complement sensitivity of paroxysmal nocturnal hemoglobinuria bone marrow cells

Blood ◽  
1980 ◽  
Vol 55 (6) ◽  
pp. 1040-1046 ◽  
Author(s):  
J Tumen ◽  
LB Kline ◽  
JW Fay ◽  
DC Scullin ◽  
EG Reisner ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Paroxysmal Nocturnal Hemoglobinuria ◽  
Bone Marrow Cells ◽  
Myeloid Cell ◽  
Erythroid Cell ◽  
Hematopoietic Stem ◽  
Increased Sensitivity ◽  
Complement Lysis ◽  
Increased Susceptibility

Abstract Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired disorder in which erythrocytes, granulocytes, and platelets are defective, as shown by increased susceptibility of RBCs, WBCs, and platelets to complement- mediated lysis in vitro. The purpose of this study is to determine the sensitivity to complement lysis of PNH and non-PNH erythroid and myeloid precursors using the release of 59Fe and myeloperoxidase as specific markers to monitor the lytic action of complement on erythroid and myeloid cell precursors, respectively. Erythroid cell precursors in four of four PNH patients demonstrated increased sensitivity to complement-mediated lysis. Myeloid cell precursors in four of five PNH patients also exhibited increased sensitivity to complement and antibody. In addition, CFU-c growth was below normal in the marrow of seven PNH patients. These findings support the hypothesis that the defect in PNH occurs at the level of the hematopoietic stem cell.

scholarly journals Syngeneic bone marrow transplantation without conditioning in a patient with paroxysmal nocturnal hemoglobinuria: in vivo evidence that the mutant stem cells have a survival advantage

Blood ◽  
1996 ◽  
Vol 88 (2) ◽  
pp. 742-750 ◽  
Author(s):  
M Endo ◽  
PG Beatty ◽  
TM Vreeke ◽  
CT Wittwer ◽  
SP Singh ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Paroxysmal Nocturnal Hemoglobinuria ◽  
Pathological Process ◽  
Survival Advantage ◽  
Hematopoietic Stem ◽  
Glycosyl Phosphatidylinositol ◽  
Normal Expression ◽  
Marrow Infusion

A 10-year-old girl with paroxysmal nocturnal hemoglobinuria (PNH) received an infusion of syngeneic bone marrow without preparative marrow ablation or immunosuppression. Following transplant, the patient became asymptomatic in concordance with an increase in the percentage of peripheral blood cells with normal expression of glycosyl phosphatidylinositol-anchored proteins (GPI-AP). However, molecular analysis suggested engraftment of a relatively small number of donor stem cells and persistence of an abnormal stem cell with mutant PIG-A. During 17 months of observation, the percentage of cells with normal GPI-AP expression gradually decreased, while intravascular hemolysis progressively increased. Approximately 16.5 months post-transplant, the patient once again became symptomatic. Together, these results indicate that syngeneic marrow infusion provided a clinical benefit by increasing the proportion of erythrocytes with normal expression of GPI- anchored complement regulatory proteins without supplanting the abnormal stem cells. However, evidence of insidious disease progression following the marrow infusion implies that the abnormal stem cells have a survival advantage relative to the transplanted stem cells. Thus, these studies contribute in vivo data in support of the hypothesis that PNH arises as a consequence of a pathological process that selects for hematopoietic stem cells that are GPI-AP-deficient.

scholarly journals Acquired XO/XY clones in bone marrow of a patient with paroxysmal nocturnal hemoglobinuria (PNH)

Blood ◽  
1976 ◽  
Vol 47 (4) ◽  
pp. 611-619 ◽  
Author(s):  
J Whang-Peng ◽  
T Knutsen ◽  
EC Lee ◽  
B Leventhal
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Hematopoietic Stem Cells ◽  
Y Chromosome ◽  
Paroxysmal Nocturnal Hemoglobinuria ◽  
Hematopoietic Stem ◽  
Cytogenetic Studies ◽  
History Of ◽  
Aging Phenomenon

Abstract Cytogenetic studies showed both 45XO and 46XY clones in the bone marrow of a 76-yr-old male with a 17-yr history of paroxysmal nocturnal hemoglobinuria (PNH). 55Fe incorporation studies demonstrated that both clones involved the hematopoietic stem cells. The loss of the Y chromosome may reflect an aging phenomenon, rather than be related to the PNH.

scholarly journals Peripheral Red Blood Cell Split Chimerism as a Consequence of Intramedullary Selective Apoptosis of Recipient Red Blood Cells in a Case of Sickle Cell Disease

2014 ◽  
Vol 6 (1) ◽  
pp. e2014066 ◽  
Author(s):  
Marco Marziali ◽  
Antonella Isgrò ◽  
Pietro Sodani ◽  
Javid Gaziev ◽  
Daniela Fraboni ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Red Blood Cells ◽  
Sickle Cell ◽  
Sickle Cell Anemia ◽  
Blood Cells ◽  
Marrow Transplant ◽  
Mixed Chimerism ◽  
Radical Cure ◽  
Hematopoietic Stem ◽  
Hematopoietic Chimerism

Allogeneic cellular gene therapy through hematopoietic stem cell transplantation is the only radical cure for congenital hemoglobinopathies like thalassemia and sickle cell anemia. Persistent mixed hematopoietic chimerism (PMC) has been described in thalassemia and sickle cell anemia. Here, we describe the clinical course of a 6-year-old girl who had received bone marrow transplant for sickle cell anemia. After the transplant, the patient showed 36% donor hematopoietic stem cells in the bone marrow, whereas in the peripheral blood there was evidence of 80%  circulating donor red blood cells (RBC). The analysis of apoptosis at the Bone Marrow  level suggests that Fas might contribute to the cell death of host erythroid precursors. The increase in NK cells and the regulatory T cell population observed in this patient suggests that these cells might contribute to the condition of mixed chimerism.

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