Allogenic Bone Marrow Transplantation (allogenic + bone_marrow_transplantation)

Distribution by Scientific Domains


Selected Abstracts


Fulminant hepatitis after allogenic bone marrow transplantation caused by reactivation of hepatitis B virus with gene mutations in the core promotor region

EUROPEAN JOURNAL OF HAEMATOLOGY, Issue 3 2006
Kiyoshi Kitano
Abstract:, Under immunosuppressive conditions after hematopoietic stem cell transplantation (HSCT), even if hepatitis B virus (HBV) antigen is negative but hepatitis B surface antibody (HBsAb) or hepatitis B core antibody (HBcAb) is presented, HBV reactivates and sometimes causes fulminant hepatitis. However, it remains unclear which patients will develop fulminant hepatitis, or whether fulminant hepatitis is caused by host-related factors or by virus-related factors. A 30-yr-old man with a history of aplastic anemia since 3 yr of age underwent allogenic BMT, when HBsAb and HBcAb were positive but HBs antigen (HBsAg) was negative. The donor was negative for HBsAg, HBsAb and HBcAb. After transplantation, the patient was complicated by acute graft-vs.-host disease (GVHD), cytomegalovirus infection, intestinal thrombotic microangiopathy and aspergillus colitis. Chronic GVHD was well controlled by FK506 and prednisolone. Twenty months after transplantation, the patient was admitted with general fatigue and liver dysfunction and was found to be positive for HBsAg and HBeAg. His serum HBV-DNA level was >8.8 log of the genome equivalent (LGE)/mL. Therefore, he was diagnosed as having hepatitis B caused by HBV reactivation and 100 mg/d lamivudine treatment was started. However, jaundice and hepatic failure deteriorated and became fatal. On analysis of the HBV-DNA, two adjacent gene mutations in the core promoter region (T1762/A1764) were detected. Increased replication of the mutated HBV might have caused HBV reactivation which progressed to fulminant hepatitis. [source]


Linear IgA dermatosis in an immunosuppressed patient after allogenic bone marrow transplantation

JOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 6 2004
T Schultewolter
ABSTRACT Linear IgA dermatosis (LAD) is a well-recognized acquired subepidermal bullous autoimmune disease. LAD is characterized by clinical, histopathological and immunopathological findings. We report the case of a 38-year-old man who suffered from a chronic myeloic leukaemia. Although he received immunosuppressive therapy he developed LAD after an allogenic bone marrow transplantation. After diagnosis of LAD was established we started a successful systemic therapy with dapsone, while continuing the preliminary medication. Here we report for the first time on a possible relationship between LAD and bone marrow transplantation in an immunosuppressed patient. [source]


Successful treatment of cyclophosphamide induced intractable hemorrhagic cystitis with recombinant FVIIa (NovoSeven®) after allogenic bone marrow transplantation

JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 10 2004
M. Karimi
[source]


Effects of sarpogrelate hydrochloride in a patient with chronic graft-versus-host disease: a case report

AMERICAN JOURNAL OF HEMATOLOGY, Issue 2 2006
Tomoe Hayashi
Abstract Chronic graft-versus-host disease (cGVHD) is a frequent complication of allogenic bone marrow transplantation. Even with aggressive treatment, cGVHD is associated with a significant degree of morbidity and mortality. cGVHD resembles autoimmune disorder, particularly systemic sclerosis (SSc). Sarpogrelate hydrochloride (SH) is an antagonist of the 5-hydroxytryptamine2A (5HT2A) receptor and has been reported to be effective in the treatment of systemic sclerosis (SSc) patients with Raynaud phenomenon. We used SH to treat a cGVHD patient, and we measured plasma PDGF and total TGF-, levels. After SH treatment, his plasma PDGF and total TGF-, levels decreased, and he noticed improvement in his skin pigmentation. In the present case, SH may have improved the skin lesion by inhibiting the synthesis of PDGF and TGF-,. Am. J. Hematol. 81:121,123, 2006. © 2006 Wiley-Liss, Inc. [source]