Subject(s)
Multiple Myeloma/mortality , Multiple Myeloma/therapy , Adult , Aged , Aged, 80 and over , Antineoplastic Agents/therapeutic use , Female , Hematopoietic Stem Cell Transplantation , Humans , Japan/epidemiology , Kaplan-Meier Estimate , Male , Middle Aged , Proportional Hazards Models , Retrospective StudiesABSTRACT
BACKGROUND: Varicella zoster virus (VZV) reactivation following hematopoietic stem cell transplantation (SCT) is common. To help reduce its incidence and to identify predictive factors for VZV reactivation after autologous SCT (auto-SCT), we conducted a retrospective analysis in patients with hematologic malignancy at our hospital. METHODS: We conducted a single-hospital observational trial with a retrospective case-control analysis of post-auto-SCT VZV reactivation in patients with malignant lymphoma (ML) and multiple myeloma (MM) between January 2001 and December 2010, in the Department of Hematology at our hospital. First, we analyzed the cumulative incidence of VZV reactivation during the post-SCT period. Second, we conducted a case-control analysis to identify the risk factors for VZV reactivation within 1 year after SCT. Univariate analyses were performed using Fisher's exact test for categorical variables. A multivariable model and logistic regression were used to assess the risk factors for VZV reactivation. RESULTS: We included 97 patients in this study. The median duration of follow-up was 1027 days. Forty-two patients experienced VZV reactivation after SCT, while 29 (69.0%) experienced reactivation within 1 year after SCT. The cumulative incidence was 30.7% at 1 year and 51.2% for the total observation period. Multivariate analysis showed that engraftment after day 10 was an independent risk factor for VZV reactivation (P = 0.03). CONCLUSIONS: Our study showed a high incidence of VZV reactivation in the first year after auto-SCT in ML and MM patients. Patients with delayed engraftment are at high risk for VZV reactivation and should be considered for prolonged VZV prophylaxis.
Subject(s)
Herpes Zoster/etiology , Herpesvirus 3, Human/physiology , Lymphoma/therapy , Multiple Myeloma/therapy , Peripheral Blood Stem Cell Transplantation , Virus Activation , Adult , Aged , Case-Control Studies , Female , Follow-Up Studies , Herpes Zoster/diagnosis , Herpes Zoster/epidemiology , Herpes Zoster/virology , Humans , Incidence , Logistic Models , Male , Middle Aged , Retrospective Studies , Risk Factors , Transplantation, AutologousABSTRACT
Lymphoproliferative disease of granular lymphocytes (LDGL) is a disorder characterized by the clonal expansion of granular lymphocytes. It has recently been shown that the clonal expansion of granular lymphocytes occurs in patients with paroxysmal nocturnal hemoglobinuria (PNH) in a subclinical fashion. To test the possibility that LDGL patients share a PNH phenotype, we obtained peripheral blood cells from 20 patients with LDGL and examined the expression of the glycosylphosphatidyl inositol (GPI)-anchored proteins, CD55 and CD59. Compared with normal controls, however, a defective expression of CD55/59 was not observed on either granulocytes or erythrocytes from LDGL patients. An unexpected finding was the significantly lower CD55/59 expression on granular lymphocytes from patients with CD16(+)CD56(-) phenotype LDGL than from patients with CD16(+)CD56(+) phenotype LDGL, or natural killer (NK) and NK/T lymphocytes from healthy individuals. The positive correlation between the expression of CD56 and CD55/59 might have some relevance to the functional properties of the CD56(+) subset of large granular lymphocytes.
Subject(s)
CD55 Antigens/biosynthesis , CD59 Antigens/biosynthesis , Gene Expression Regulation , Killer Cells, Natural/metabolism , Lymphoproliferative Disorders/metabolism , T-Lymphocytes/metabolism , Female , Hemoglobinuria, Paroxysmal/metabolism , Hemoglobinuria, Paroxysmal/pathology , Humans , Killer Cells, Natural/pathology , Lymphoproliferative Disorders/pathology , Male , T-Lymphocytes/pathologyABSTRACT
Numerous crystalline inclusions were observed in glomerular and tubular epithelial cells in a 46-year-old female patient with multiple myeloma and renal dysfunction. On light microscopy, epithelial cells were filled with homogenous materials and were remarkably swollen. Infiltrations of histiocytes with expanded cytoplasm were also seen in the interstitium of the kidney and bone marrow. On electron microscopy, cytoplasmic inclusions had crystalline structure showing rhomboid and oval shapes. Immunofluorescence study revealed that these cells were positive for IgG-kappa. The combination chemotherapy followed by autologous stem cell transplantation led to a partial resolution of her renal dysfunction, continued by a slight reduction in the number of crystalline-containing podocytes at the second renal biopsy. Crystal inclusions in the kidney are rarely found and cause renal impairment in multiple myeloma.
