11/495. Cytotoxicity against lymphoblastoid cells mediated by a T-cell clone from an aplastic anaemia patient: role of CD59 on target cells.In an attempt to elucidate the pathogenic role of a CD4 cytotoxic T-cell clone NT4.2 isolated from the bone marrow of a patient with cyclosporine-dependent aplastic anaemia, we characterized the T-cell clone as well as its cytotoxicity against an autologous Epstein-Barr (EB) virus-transformed B-lymphoblastoid cell line (LCL). NT4.2 expressed BV21 BJ2.7 with a complementarity-determining region (CDR) 3 motif of SQGQGEVEQY which was homologous to that of a T-cell clone isolated from a patient with connective tissue disease. NT4.2 started to lyse LCL cells within 2 h and exerted maximal cytotoxicity within 3 h of incubation. The cytotoxicity required the presence of divalent cations and was not associated with dna fragmentation of the target cells. Anti-CD59 monoclonal antibodies (MoAb) blocked the cytotoxicity to the same degree as anti-CD3, HLA-DR or CD2 mAb. Flow cytometric analysis of the peripheral blood of this patient during remission after cyclosporine therapy revealed 1.7% of granulocytes to be deficient in CD59. These findings indicate that NT4.2 exerts its cytotoxicity through a perforin-mediated pathway, not a Fas/Fas ligand-dependent pathway, and that haemopoietic stem cells lacking CD59 may evade cytotoxic T lymphocytes, leading to the in vivo expansion of a paroxysmal nocturnal haemoglobinuria clone.- - - - - - - - - - ranking = 1keywords = cell (Clic here for more details about this article) |
12/495. ticlopidine-induced aplastic anemia and quick recovery with G-CSF: case report and literature review.We report here a case of ticlopidine-induced aplastic anemia that responded to G-CSF and review the literature. An 83-year-old woman was started on ticlopidine for coronary artery disease after an episode of upper gastrointestinal bleeding secondary to aspirin. She developed aplastic anemia seven weeks after initiation of ticlopidine. She was hospitalised and received empiric antibiotic therapy and granulocyte colony stimulating factor (G-CSF). Her bone marrow started to recover quickly, and white blood cell and platelet counts returned to normal within three weeks. A review of medical literature revealed 20 similar cases of ticlopidine-induced aplastic anemia resulting in death in seven cases. G-CSF has been used previously with variable success. ticlopidine is associated with serious, sometimes fatal hematological side effects. This risk should be seriously taken into consideration when prescribing ticlopidine. G-CSF may be helpful in the treatment of ticlopidine-induced aplastic anemia.- - - - - - - - - - ranking = 0.052631578947368keywords = cell (Clic here for more details about this article) |
13/495. Clonal hematopoiesis in acquired aplastic anemia revealed by rearrangement of the immunoglobulin heavy chain gene-JH region.We report on a female patient with acquired aplastic anemia whose bone marrow cells showed DNA rearrangement of the immunoglobulin-JH region that disappeared after 1 month with recovery of hematopoiesis through treatment with granulocyte colony-stimulating factor (G-CSF) and immunosuppressive drugs. The patient is now 2 years and 6 months from onset, and her hematopoiesis is almost within normal limits without medication. This finding provides new data supporting clonal hematopoiesis in acquired aplastic anemia but does not imply that the disease is resistant to immunosuppressive therapy.- - - - - - - - - - ranking = 0.052631578947368keywords = cell (Clic here for more details about this article) |
14/495. Highly fluorescent reticulocyte count predicts haemopoietic recovery after immunosuppression for severe aplastic anaemia.Highly fluorescent reticulocyte (HFR) counts are the most reliable and sensitive index of haemopoietic recovery after bone marrow or peripheral blood stem cell transplantation. We report the behaviour of HFRs during haemopoietic recovery in two patients who were affected by severe aplastic anaemia (SAA) and treated with horse antithymocyte globulin (ATG), cyclosporin A (CsA) and granulocyte colony-stimulating factor (G-CSF). A HFR value > 5% of the total reticulocyte count, a reticulocyte count > 30 x 10(9)/l, and a polymorphonuclear (PMN) count > 0.5 x 10(9)/l were found after 9 and 8, 20 and 46, and 16 and 22 days, respectively, after the end of ATG. HFR recovery to > 5% anticipated the rise of PMN > 0.5 x 10(9)/l by at least 7 and 14 days, respectively. Thus, HFR evaluation could be used as a reliable and early marker of response to immunosuppression in severe aplastic anaemia.- - - - - - - - - - ranking = 0.052631578947368keywords = cell (Clic here for more details about this article) |
15/495. Syngeneic peripheral blood stem cell transplantation with brief immunosuppression for severe aplastic anemia.We report the cases of two severe aplastic anemia (SAA) patients who were successfully treated with syngeneic peripheral blood stem cell transplantation (PBSCT) using immunosuppression without high-dose chemotherapy or irradiation for conditioning. A 21-year-old woman with SAA of 6 years duration had been transfused heavily before transplantation and had developed refractory thrombocytopenia, chronic hepatitis and secondary hematochromatosis. Syngeneic PBSCT with immunosuppression using ATG, methylprednisolone, and cyclosporin-A was eventually performed without high-dose chemotherapy in September 1997. The second syngeneic PBSCT with the same immunosuppression was successfully performed in a 35-year-old male patient who had had SAA for 3 months in November 1998. Haemopoietic engraftment was rapid and sustained. There was no infection or mucositis during the syngeneic PBSCT. The patients are currently 9 to 22 months post-PBSCT without rejection. Our experience suggests that syngeneic PBSCT with brief immunosuppression is an effective alternative to pretransplant high-dose chemotherapy conditioning for SAA patients having syngeneic transplantation. bone marrow transplantation (2000) 25, 337-339.- - - - - - - - - - ranking = 0.26315789473684keywords = cell (Clic here for more details about this article) |
16/495. Indirect evidence of TTV replication in bone marrow cells, but not in hepatocytes, of a subacute hepatitis/aplastic anemia patient.The presence of a new DNA virus (TTV) has been reported in sera from patients with posttransfusion hepatitis of unknown etiology. The precise replication site of TTV, however, has not been established. In this study, the presence of TTV in liver autopsy material, and in bone marrow biopsy and autopsy samples taken from a subacute hepatitis/aplastic anemia patient was determined by PCR and Southern blot analyses. liver cells were found to contain only TTV DNA and not mRNA. Bone marrow material, especially that taken at biopsy, contained high levels of TTV DNA. It is suggested that the TTV replication site was in the bone marrow rather than in the liver, and that TTV infection was the cause of this patient's aplastic anemia. The precise etiological association of TTV with hepatitis remains to be established.- - - - - - - - - - ranking = 0.26315789473684keywords = cell (Clic here for more details about this article) |
17/495. HLA-mismatched CD34-selected stem cell transplant complicated by HHV-6 reactivation in the central nervous system.We report here a patient who suffered from PCR- confirmed human herpesvirus type 6 (HHV-6) meningoencephalitis after allogeneic purified CD34 cell transplantation from his HLA-mismatched sibling donor, even though he had been on intense prophylaxis with i.v. ganciclovir (GCV), acyclovir (ACV) and gamma-globulin containing a specific antibody against HHV-6. Serological evaluation disclosed that both the donor and recipient had IgG antibody against HHV-6 before transplantation. His blood WBC count started to transiently increase on day 10, and all blood components had decreased by day 20. He then developed a severe headache and high blood pressure, and sporadic abnormal neurological findings including nystagmus and delirium. An analysis of cerebrospinal fluid (CSF) revealed 8 cells/microl, a glucose level of 130 mg/dl and a protein level of 201 mg/dl (normal, 50 mg/dl) on day 26. At the time, HHV-6 was detected only in CSF by a PCR-based method and he was diagnosed as having meningoencephalitis due to the local reactivation of HHV-6. Although he failed to respond to high-dose therapy with ACV (60 mg/kg/day) and gamma-globulin, the DNA of this virus disappeared from the CNS upon treatment with GCV (30 mg/kg/day) combined with the intraventricular infusion of alpha-interferon. His clinical course was further complicated with meningoencephalitis due to staphylococcus epidermidis, and he died of tentorial herniation on day 79 without the recovery of blood components. This experience may indicate that intense prophylaxis to prevent reactivation of HHV-6 in the CNS is essential for the management of such profoundly immunosuppressed patients.- - - - - - - - - - ranking = 0.31578947368421keywords = cell (Clic here for more details about this article) |
18/495. colchicine-induced bone marrow suppression: treatment with granulocyte colony-stimulating factor.Bone marrow aplasia is a frequent complication of colchicine poisoning. This typically occurs on day 3 to 5 postexposure, and the blood cell counts remain depressed for a week or more. Unfortunately, because patients suffering from colchicine toxicity develop multiple organ complications and sepsis, the morbidity and mortality associated with bone marrow depression is high. In this article, we present three cases of colchicine toxicity in which granulocyte colony-stimulating factor (G-CSF) was used to treat bone marrow depression. In all three cases, there was a dramatic increase in the white cell count and, to a lesser extent, the platelet count. In view of the critical nature of the bone marrow depression and multi-organ toxicity induced by colchicine, we believe that consideration of the use of G-CSF to shorten the duration of neutropenia is warranted.- - - - - - - - - - ranking = 0.10526315789474keywords = cell (Clic here for more details about this article) |
19/495. Aplastic anemia: presence in human bone marrow of cells that suppress myelopoiesis.Bone marrow from a patient with aplastic anemia was shown by multiple criteria to have a block in early myeloid differentiation. This block was overcome in vitro by elimination of marrow lymphocytes. Furthermore, this differentiation block was transferred in vitro to normal marrow by coculturing with the patient's marrow. We suggest that some cases of aplastic anemia may be due to an immunologically based suppression of marrow cell differentiation rather than to a defect in stem cells or their necessary inductive environment.- - - - - - - - - - ranking = 0.31578947368421keywords = cell (Clic here for more details about this article) |
20/495. Abnormal lymphocyte populations in pure red cell aplasia.Studies of blood lymphocytes from 4 patients with pure red cell aplasia were performed with lymphocyte surface markers, and with various in vitro tests for lymphocyte functions. Pathologically low B-lymphocyte values were found. In contrast, no marked deviation from normals were seen for t-lymphocytes and Fc-receptor-bearing lymphocytes thought largely to represent non-B, non-t-lymphocytes. In 3 patients normal lymphocyte transformation was found with unspecific and specific mitogens, while the DNA-synthesis induced by unspecific mitogens was subnormal in the fourth patients. The lymphocyte-mediated PHA-induced cytotoxicity against target cells in vitro was subnormal in 2 patients, while no depression was seen in antibody-dependent cytotoxicity mediated in vitro by lymphocytes (K-cells). It is concluded that considerable immunological abnormalities are associated with pure red cell aplasia, and the possible significance of this is discussed.- - - - - - - - - - ranking = 0.42105263157895keywords = cell (Clic here for more details about this article) |
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