ABSTRACT
The clinical course of hematopoietic stem cell transplantation (HSCT) recipients was retrospectively analyzed to determine whether carriage of methicillin-resistant Staphylococcus aureus (MRSA) is a risk factor for MRSA infection during the neutropenic period. We studied four patients in whom MRSA colonies developed before HSCT. Two patients were previously diagnosed as having MRSA infection and two were carriers of MRSA. We tried to eliminate MRSA before HSCT and succeeded in eradication in two patients. MRSA infection did not develop in one patient who received prophylactic administration of vancomycin (VCM), but MRSA-induced phlegmon developed during neutropenia in one patient who did not receive prophylaxis. Of the other two patients who had been persistently positive for MRSA, MRSA did not develop in one patient who received prophylaxis, but the another patient who did not receive prophylaxis died from MRSA-induced sepsis in the early post-transplant period. We therefore recommend that MRSA be eliminated by prophylactic administration of anti-MRSA drugs such as VCM before HSCT when patients have persistent MRSA.
Subject(s)
Drug Resistance, Bacterial , Hematopoietic Stem Cell Transplantation/adverse effects , Methicillin , Staphylococcal Infections/prevention & control , Staphylococcus aureus/physiology , Adolescent , Adult , Anti-Bacterial Agents/therapeutic use , Humans , Male , Neutropenia , Retrospective Studies , Risk , Staphylococcal Infections/etiology , Vancomycin/therapeutic useABSTRACT
In the present study, we investigated the inhibitory natural killer cell receptor (NKR) expression of CD94/NKG2A on PBMC after allogeneic bone marrow transplantation (BMT). The proportion of CD94 expression on PBMC was higher in patients without chronic graft-versus-host disease (cGVHD) and also in cGVHD patients with good response to conventional immunosuppressive therapy than in cGVHD patients with poor response. Also, the proportions of CD94+/CD3+ cells and CD94+/CD8+ cells were higher in cGVHD patients showing good response. In addition, the proportion of NKG2A-expressing cells was higher in patients without cGVHD than in patients with cGVHD. Therefore, chronic allostimulation after allo-BMT may augment the proportion of CD94/NKG2A-positive cells, and these cells may play some role in the regulation of alloresponse in some patients.
Subject(s)
Antigens, CD/metabolism , Lectins, C-Type , Leukocytes, Mononuclear/immunology , Membrane Glycoproteins/metabolism , Transplantation, Homologous/immunology , Bone Marrow Transplantation/immunology , CD3 Complex , CD8-Positive T-Lymphocytes , Case-Control Studies , Graft vs Host Disease/blood , Graft vs Host Disease/immunology , Hematologic Neoplasms/blood , Hematologic Neoplasms/complications , Hematologic Neoplasms/therapy , Humans , Killer Cells, Natural/cytology , Killer Cells, Natural/metabolism , NK Cell Lectin-Like Receptor Subfamily C , NK Cell Lectin-Like Receptor Subfamily D , Receptors, Immunologic/metabolism , Receptors, Natural Killer Cell , T-Lymphocytes , Treatment OutcomeABSTRACT
We have sequentially investigated the expression of natural killer cell inhibitory receptors (KIRs) for HLA-C (CD158b) on peripheral blood mononuclear cells (PBMC) in three patients with extensive chronic graft-versus-host disease (cGVHD) after allogeneic bone marrow transplantation (alloBMT). Clinical symptoms of cGVHD were not cured and worsened in the first patient whose CD158b-positive cells increased to 18.5% during cGVHD and decreased to 9.4% at 8 months after transplantation. On the other hand, cGVHD was cured and did not relapse in the second patient whose CD158b-positive cells increased up to 45.9% during cGVHD and sustained 19.4% at 8 months after transplantation. In contrast, CD158b-positive cells were less than 10% during the course of cGVHD in the third patient, and her cGVHD did not respond to treatment. Therefore, it appears that chronic allostimulation augments the expansion of CD158b-positive cells and these expanded CD158b-positive cells may have some role in the control of alloresponse in some patients.
