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OBJECTIVE
To explore the possible risk factors for the occurrence and mortality of thrombotic microangiopathy (TMA) with concomitant acute graft-vs-host disease (aGVHD) and to investigate outcomes and treatments of this disorder after allo-HSCT.
METHODS
Fifty cases diagnosed with TMA with
Thrombotic microangiopathies (TMA) encompass various diseases characterized by a microangiopathic hemolytic anemia, platelet clumping, and organ failure of variable severity. Thrombotic thrombocytopenic purpura (TTP) is a particularly severe form of TMA characterized by systemic organ failure which
The classification of thrombotic microangiopathy has evolved and expanded due to treatment and mechanistic advances. The two basic clinical forms of thrombotic microangiopathy (excluding disseminated intravascular coagulation [DIC]), thrombotic thrombocytopenic purpura (TTP), and hemolytic uremic
Thrombotic microangiopathy (TMA) is a microvascular disorder characterized by platelet aggregation and hemolytic anemia. In the setting of bone marrow transplantation (BMT), ischemic colitis due to TMA is difficult to differentiate from acute graft-versus-host disease. We report a 32-year-old man
Thrombotic microangiopathy (TMA) is a significant complication after hematopoietic stem-cell transplantation (HSCT); however, there is little information on it following reduced-intensity cord blood transplantation (RI-CBT). We reviewed the medical records of 123 adult patients who received RI-CBT
We report on a 19-month-old boy with refractory T-cell acute lymphoblastic leukemia who underwent allogeneic peripheral blood stem cell transplantation using positively selected CD34 cells from his HLA two-loci mismatched mother. The conditioning regimen consisted of busulfan (140 mg/m2/d for 2
BACKGROUND
Thrombotic microangiopathy (TMA) is characterized by microvascular thrombosis, thrombocytopenia, and microangiopathic hemolytic anemia. Previous studies have shown that cyclosporine (CsA) is associated with TMA but the number of reported cases is very limited. We describe a 13-year-old
BACKGROUND
Thrombotic microangiopathy (TM) is a disorder characterized by fibrin formation and platelet aggregation in the small arteries and capillaries. Two main clinical settings are reported in association with this disorder: hemolitic uremic syndrome (HUS) and thrombotic thrombocytopenic
Hemolytic-uremic syndrome (HUS) is an important cause of acute kidney injury in children often caused by Shiga toxin-producing Escherichia coli (STEC) enterocolitis. In a screening program for STEC infection in children with bloody diarrhea in northern Italy for early diagnosis of HUS, co-infection
We report four cases of adult thrombotic microangiopathy associating diarrhea with severe ischemic colitis. In one case, the intestinal complications was severe and diffuse ischemic colitis, in two cases an inaugural colonic perforation requiring colectomy and in the last case a massive mesenteric
Thrombotic microangiopathy after bone marrow transplantation (post-BMT TMA) is a serious transplant-related complication. We identified 16 patients with TMA after allogeneic BMT who showed histopathological evidence of intestinal TMA in their gut specimens (six autopsies, 10 biopsies). In all, 14
A 52-year-old man with an end stage renal failure of undetermined aetiology was hemodialysed in 2002. He received a cadaveric kidney transplantation in 2004. After an episode of diarrhea, a thrombotic microangiopathy was diagnosed in July 2009 and during this episode, a low C3 serum level was
Hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) are syndromes of microangiopathic hemolytic anemia, and thrombocytopenia in which endothelial dysfunction appears to be an important factor in the sequence of events leading to microvascular thrombosis. They are termed
BACKGROUND
Thrombotic microangiopathy (TMA) is a rare but potentially lethal complication encountered in solid organ and bone marrow transplant recipients, requiring rapid recognition, diagnosis, and initiation of therapy. Several potential causes have been identified in this setting, including
BACKGROUND
Castleman's disease (CD) is an uncommon, heterogeneous lympho-proliferative disorder leading to high circulating levels of interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF). Renal involvement has been only described in a limited number of small studies. Herein, we report