Subject(s)
Cord Blood Stem Cell Transplantation/methods , Fetal Blood/transplantation , Precursor Cell Lymphoblastic Leukemia-Lymphoma/therapy , Adult , Antiretroviral Therapy, Highly Active , CD4 Lymphocyte Count , CD4-Positive T-Lymphocytes/cytology , Disease-Free Survival , Female , Fusion Proteins, bcr-abl/metabolism , HIV Infections/complications , HIV Infections/drug therapy , HIV Seropositivity , Humans , Reverse Transcriptase Polymerase Chain ReactionABSTRACT
Herpes simplex virus (HSV) infection in adult patients who underwent cord blood transplantation (CBT) from unrelated donors was studied. None of nine HSV-seronegative patients developed HSV disease after CBT. Of 28 HSV-seropositive patients, seven (25%) developed HSV disease at a median of 92 days after CBT (range, 52-239 days). The cumulative incidence of HSV disease in HSV-seropositive patients was 27% at 12 months after CBT. The manifestations of HSV disease included gingivostomatitis (three patients), herpes labialis (two patients), localized herpes facialis of the nose (one patient), and disseminated eczema herpeticum (one patient). HSV disease recurred in two patients as gingivostomatitis and disseminated eczema herpeticum. All the patients responded to antiviral therapy. The presence of grade II-IV acute graft-versus-host disease (GVHD) was significantly associated with a higher rate of HSV disease after CBT (51 vs 8%, P=0.015). These results suggest that the recovery of HSV-specific immune responses is delayed in patients who develop grade II-IV acute GVHD after CBT.
Subject(s)
Cord Blood Stem Cell Transplantation/adverse effects , Herpes Simplex/etiology , Adult , Female , Graft vs Host Disease , Hematologic Diseases/complications , Hematologic Diseases/therapy , Herpes Simplex/epidemiology , Herpes Simplex/pathology , Humans , Incidence , Japan , Male , Middle Aged , Probability , Risk Factors , Transplantation, Homologous , Treatment Outcome , Whole-Body IrradiationABSTRACT
We report a case of acute myeloblastic leukemia (AML)-M2 (by French-American-British classification) with t(8;21) (q22:q22) that was complicated with severe pneumonia. The patient tested positive by fluorescence in situ hybridization (FISH) for AML1 splitting and positive by reverse transcriptase polymerase chain reaction (RT-PCR) for chimeric AML1/MTG8 messenger RNA (mRNA), which indicated splitting of the MTG8 gene on chromosome 8 (q22) and the AMLI gene on chromosome 22 (q22). High-dose methylprednisolone was administered, and the leukemic cells disappeared without chemotherapy, although dysplastic hematopoietic cells were observed transiently after the first therapy. After the disappearance of leukemic cells, FISH for AML1 splitting was negative, and real-time PCR results for quantitative chimeric AML1/ MTG8 mRNA were less than the detectable level, however, RT-PCR results for AML1/MTG8 mRNA remained positive. These findings suggest that the patient acquired morphological, cytogenetic. and possibly molecular genetic remission by the synergistic effects of severe infection and high-dose methylprednisolone.
Subject(s)
Anti-Inflammatory Agents/administration & dosage , Leukemia, Myeloid, Acute/complications , Methylprednisolone/administration & dosage , Pneumonia/drug therapy , Aged , Cytogenetic Analysis , Female , Humans , Leukemia, Myeloid, Acute/diagnosis , Leukemia, Myeloid, Acute/genetics , Pneumonia/etiology , Remission, SpontaneousABSTRACT
A 43-year-old man with a 7-year history of low antinuclear factor titer developed Basedow's disease and autoimmune hemolytic anemia (AIHA) simultaneously. Such simultaneous occurrence of these autoimmune disorders has been reported only rarely. Administration of methimazole for Basedow's disease and prednisolone for AIHA was effective for ameliorating both conditions. The patient had the HLA DR2, DRB1 1501 and DPB1 0501 alleles, suggesting a genetic predisposition for these diseases.
Subject(s)
Anemia, Hemolytic, Autoimmune/etiology , Graves Disease/etiology , Adult , Humans , MaleABSTRACT
Two cases of non-Hodgkin's lymphoma (NHL) generated within 6 months in first degree relatives, a father and a son, are presented. The NHL was a diffuse large B-cell type in the father and a small cleaved follicular type in the son. Cytogenetic and molecular studies of the lymphoma cells revealed the rearrangement of the immunoglobulin heavy chain (JH) gene in both patients, the mutation of p53 gene in the father and t(14; 18) (q32; q21) in the son. Both patients had low serum immunoglobulin levels. It is not known whether the occurrence of NHL in this family was incidental or pathogenetically related, since there was no clear common molecular abnormality between the father and the son. The pathogenetic mechanism of this familial occurrence of NHL is discussed.
