Cases reported "Anemia, Aplastic"

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1/221. Late graft rejection and second infusion of bone marrow in children with aplastic anaemia.

    Late graft rejection following allogeneic bone marrow transplantation (BMT) for aplastic anaemia is a significant clinical problem and is associated with a high risk of mortality. We report two children with severe aplastic anaemia (SAA) who developed very late graft rejection 2 years and 4 months and 10 years respectively after allogeneic BMT from HLA-identical siblings. Following a second BMT from their initial donors, engraftment has been sustained in both cases. The patients are alive with full donor chimaerism, 18 and 19 years from initial transplant. These cases illustrate that graft failure can be an extremely late event after allogeneic BMT for SAA, and that long-term sustained engraftment can be achieved in these patients with second BMT from the original donors.
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2/221. A case of aplastic anaemia in pregnancy.

    Aplastic anaemia in pregnancy is an extremely rare condition with high maternal morbidity and mortality rates. Intensive haematological support remains the mainstay of therapy and a successful obstetric outcome can be best accomplished with the close clinical collaboration of the haematologist and the obstetrician as occurred with our patient reported here.
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3/221. Graves' disease following successful treatment of severe aplastic anaemia with antilymphocyte globulin.

    This case report is only the third report of thyroid dysfunction following the administration of anti-lymphocyte globulin for severe aplastic anaemia. It is the first report of the development of Grave's disease. We discuss a possible mechanism by which this may occur and highlight instances of other immune-mediated diseases occurring in ALG treated patients.
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4/221. Abnormal tryptopham metabolism in congenital erythroid hypoplastic (diamond-Blackfan) anaemia.

    tryptophan loading was performed in a child with diamond-Blackfan anaemia as well as in his parents and two control persons. There was a fivefold increase of anthranilic acid and kynurenine excretion beside a marked generalized aminoaciduria in the proband; in the parents and the controls no such phenomenon could be demonstrated. The importance of the finding is discussed and investigation of tryptophan metabolism before the first blood transfusion is recommended. The finding cannot be used as a heterozygote test.
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5/221. Epstein-Barr virus (EBV) associated B-cell lymphoproliferative disease following HLA identical sibling marrow transplantation for aplastic anaemia in a patient with an EBV seronegative donor.

    BACKGROUND: B-cell lymphoproliferative disorders (BLPD*) caused by Epstein-Barr virus (EBV) occurring after allogeneic bone marrow transplantation (BMT) are usually of donor origin. Treatment such as discontinuation of immunosuppression may be successful in some cases, but infusion of donor T cells results in successful eradication of EBV BLPD in most cases. methods AND RESULTS: We report a case of EBV positive aggressive BLPD after HLA matched sibling BMT for aplastic anaemia. The tumour completely regressed after withdrawal of cyclosporin and donor lymphocyte infusion. However, although the tumor was of donor origin, the donor serum was negative for antibodies to EBV antigens and no EBV-specific cytotoxicity was detected in donor peripheral blood mononuclear cells. The recipient was seropositive for EBV before BMT. CONCLUSIONS: We speculate that a 'second primary' EBV infection occurred involving donor cells in the recipient during BMT immunosuppression, with subsequent outgrowth of donor-derived BLPD. EBV infection may have been by an endogenous EBV isolate, from external sources, or from third party transfusions.
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6/221. Apparent cure of Graves-Basedow disease after sibling allogeneic bone marrow transplantation.

    Evidence that allogeneic bone marrow transplantation (BMT) can cure or alter the course of intractable autoimmune diseases comes from both extensive experimental work in animal models and anecdotal case reports in humans. We describe a female patient diagnosed as having severe aplastic anaemia (SAA), hyperthyroidism and ophthalmopathy of Graves-Basedow disease who received a BMT from her histocompatible sister. Fifty-three months after BMT, complete remission of hyperthyroidism and ocular signs persists. The SAA is cured and she is free of any chronic graft-versus-host disease (GVHD). In the early post-BMT period, PCR analysis of bone marrow and peripheral blood cells confirmed a complete chimerism of donor origin. Thus, it is plausible to attribute the resolution of the patient's thyroid hyperfunction and opththalmopathy to the replacement of the host immune system.
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7/221. Syngeneic blood stem cell transplantation for infectious mononucleosis-related aplastic anaemia.

    A 17-year-old girl developed severe aplastic anaemia following an episode of infectious mononucleosis. Her identical twin sister underwent mobilization with filgrastim and subsequent leukapheresis for blood stem cell collection. The cells were freshly infused without prior immunosuppression. The patient became transfusion-independent and achieved a trilineage complete haematological response. Her engraftment lasted 6 months, but subsequently she relapsed with pancytopenia. The patient then received a second infusion of syngeneic blood stem cells, preceded by conditioning with cyclophosphamide and antithymocyte globulin. This led to durable trilineage haematological recovery still ongoing at 16 months after her second transplant.
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8/221. hepatitis G virus infection as a possible causative agent of community-acquired hepatitis and associated aplastic anaemia.

    Aplastic anaemia complicating hepatitis is a rare but well-documented phenomenon; however in many patients the cause remains unknown. We present a 24-year-old man with a well-defined community-acquired hepatitis, probably due to hepatitis G virus (HGV), who developed severe aplastic anaemia. In this case, the absence of other agents likely to cause the clinical manifestations, and the detection of HGV rna at the time of illness, clearly point to this agent as being responsible for both the hepatitis and the aplastic anaemia. Further studies in serial serum samples and meticulous evaluation of the disorders associated with the infection will be needed to prove or dispute a causal association of HGV and aplastic anaemia.
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9/221. High-dose peripheral blood stem cell transplant for multitransfused severe aplastic anaemia patients without antithymocyte globulin in the conditioning regimen.

    Four multitransfused patients with severe aplastic anaemia (SAA) are described. Two received a BMT after conditioning with cyclophosphamide (Cy) plus antithymocyte globulin (ATG). Both suffered a graft failure (GF) and had a second transplant with PBSC from the original donor. Two other patients received a PBSCT as a first option, with Cy as the only conditioning drug. The four patients received methotrexate (MTX) and cyclosporine (CYA) as post-grafting immunosuppression. The two BMT patients with GF were successfully rescued with a PBSC second transplant. In the two cases where a PBSCT was done as a first option no GF was observed and a successful and complete haematological recovery was achieved. In conclusion, PBSCT rescued two SAA patients with GF after BMT. PBSCT without ATG as a first option produced a quick and complete haematological recovery in two additional patients, suggesting that PBSCT without ATG can be an alternative to BMT plus ATG in SAA as a first transplant option.
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10/221. 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.
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