Liam’s Chimerism Results

  • Mysticlimber13

    Liams graft results aren’t what we wanted:( CD3 Tcell 76% donor CD33 10% donor CD56 NK function 40% donor CD19 8% nothing seems 2 make sense
    (about 31 minutes ago)



I have so much anger right now. I’m paralyzed with fear as the reality of this horrible disease really sinks in. U try 2 become emotionless
(about 55 minutes ago)


DAY+ 200 – 11/29/11        DNA Chimerism Analysis – Blood

(CD3+) T Cell                       76% donor origin (24% host)

(CD33+) Myeloid Cells           10% donor origin (90% host)

(CD56+) NK Cells               40% donor origin (60% host)

(CD19+) B Cells                        8% donor origin (92% host)


DAY+ 138 – 09/27/11        DNA Chimerism Analysis – Blood

(CD3+) T Cell                       62% donor origin (38% host)

(CD33+) Myeloid Cells           23% donor origin (77% host)

(CD56+) NK Cells               71% donor origin (29% host)

(CD19+) B Cells                      22% donor origin (78% host)


DAY +28 – 06/14/11        DNA Chimerism Analysis

(CD3+) T Cell                       59% donor origin (41% host)

(CD33+) Myeloid Cells           100% donor origin (0% host)

(CD56+) NK Cells               100% donor origin (0% host)

(CD19+) B Cells                      100% donor origin (0% host)


Chimerism analysis is important for monitoring post-transplant outcome and for determining appropriate therapy after transplantation. Since it is the basis for providing early treatment decisions, chimerism analysis requires sensitive and reliable techniques to detect the presence of donor leukocytes in the hosts’ peripheral blood or bone marrow. As lymphoid and myeloid engraftment is asynchronous, lineage-specific chimerism analysis is necessary. This requires the specific enrichment of myeloid and lymphoid cells prior to performing chimerism analysis (e.g. by PCR-based detection of donor- or recipient-specific mini-satellite DNA sequences).


Chimerism in nonmalignant diseases

Allogeneic stem cell transplantation is the only curative treatment option for many patients with inherited or acquired nonmalignant diseases as thalassemia, sickle cell disease, immunodeficiency diseases, osteopetrosis, storage diseases, severe aplastic anemia, bone marrow failure syndromes and others (for a review, see Section IV in Thomas et al34). The aim of the procedure in these diseases is to achieve sustained engraftment to (i) improve the hematopoietic function, to (ii) correct the immune competence and/or to (iii) increase or normalize the respective enzyme shortage. Therefore a priori, it is not necessary to replace the recipient hematopoietic system completely. The implementation of a state of mixed chimerism is mostly sufficient to substantially improve the patient’s well being. Thus, to reduce toxic side effects, most conditioning regimens are less myeloablative and thereby mixed chimerism is more likely.60,61,62,63 As a consequence, graft rejection or nonengraftment remained the major causes of treatment failures in this diseases. Sensitization to minor histocompatibility antigens by prior blood product transfusion might increase this danger. The rapid development of complete chimerism in NK and T cells seems to play an important role in achieving sustained engraftment especially in patients who were treated with a dose reduced conditioning regimen.64,65,66,67


Pediatric Transplants

Increasing mixed chimerism and the risk of graft loss in children undergoing allogeneic hematopoietic stem cell transplantation for non-malignant disorders

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