Graft versus host disease in autologous stem cell transplantation

Citation
Gh. Marin et al., Graft versus host disease in autologous stem cell transplantation, J EXP CL C, 18(2), 1999, pp. 201-208
Citations number
15
Categorie Soggetti
Oncology
Journal title
JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
ISSN journal
03929078 → ACNP
Volume
18
Issue
2
Year of publication
1999
Pages
201 - 208
Database
ISI
SICI code
0392-9078(199906)18:2<201:GVHDIA>2.0.ZU;2-7
Abstract
Relapse remains the major cause of mortality in haematological malignancies treated with autologous stem cell transplantation (ASCT). Graft versus tum our reaction (GVT) associated to autologous graft versus host disease (GVDH ) may contribute to eliminate minimal residual disease (MRD) after ASCT. Eighty patients with several diagnostics were submitted to ASCT. After stem cell infusion, patients randomised in 4 groups. Groups were treated as fol lows: Group A received either a IFN (alpha Interferon - 1.000.000 U/d), Cyc losporine A (CSA - 1 mg/-kg/d intravencus) for 28 days, and granulocyte-mac rophage colony stimulating factor (GM-CSF250/m2/d) until engraftment; B: CS A (same dose and way) and GM-CSF; C: CSA (1 mg/kg/d orally) and GM-CSF and D: only GM-CSF. Patients were inspected daily and if skin rash was detected , a skin biopsy was obtained at that moment, otherwise biopsies were obtain ed at day 21 after ASCT. GVHD was positive in 23 patients (13 from group A and 10 from group B). All cases were grades I and II. A majority of CD4+ T lymphocytes was seen in s kin infiltrates. No significant differences were seen in WBC and platelets engraftment times, antibiotic administration or hospitalisation days requir ed among the four groups. With a median follow up of 18 months, there were no differences in disease free survival (DFS) or overall survival (OS) betw een the patients who developed GVHD and the others. However, considering th at myeloma cells do not express antigen MCH II, which is necessary for GVT effect, we excluded patients with multiple myeloma (MM) from survival analy sis, thus obtaining a significant difference in OS results between patients who developed GVHD and those in whom this reaction was not observed (81% v s 58% p:0.05). We conclude that pharmacological induction of GVHD in ASCT is possible with CSA administration (1 mg/kg/d i.v.). Development of GVHD showed a better o utcome for patients in our study except for those patients with MM. This re sults must be confirmed by a longer follow up of our patients and further s tudies.