Diagnosis, Differential ; Humans ; Thrombotic Microangiopathies

Child ; Humans ; Plasma Exchange ; Thrombotic Microangiopathies ; therapy

China ; Consensus ; Humans ; Purpura, Thrombotic Thrombocytopenic ; Thrombotic Microangiopathies/therapy*

No abstract available.
Breast Neoplasms* ; Breast* ; Humans ; Pulmonary Heart Disease* ; Thrombotic Microangiopathies*

Pulmonary tumor thrombotic microangiopathy (PTTM) is a rare, malignancy-related complication that causes marked pulmonary hypertension, right heart failure, and death. We report on a patient with locally advanced breast cancer whose course was complicated by fatal PTTM based on clinical and laboratory findings.
Breast ; Breast Neoplasms ; Heart Failure ; Humans ; Hypertension, Pulmonary ; Thrombotic Microangiopathies

Mitomycin (MMC) is a naturally ocurring alkylating agent, introduced for clinical use as early as 1958. This drug is useful in the therapy of gastrointestinal carcinomas when used in combination with 5-fluorouracil. Nephrotoxicity among toxicities from MMC is unusual with cumulative doses less than 30 mg/m2. In large studies in which the incidence of MMC nephrotoxicity were assessed, 3-15% of patients developed total dose related renal dysfunction. Three patients in our clinical practice have developed thrombotic microangiopathy clearly related to MMC. We report the clinical and pathologic features of our cases. In view of the probable dose-related and delayed toxicity of MMC, it seems necessary to monitor regularly after initiation of chemotherapy. Early detection of the renal impairment and withdrawal of MMC might halt further progression of renal failure.
Drug Therapy ; Fluorouracil ; Humans ; Incidence ; Mitomycin* ; Renal Insufficiency ; Thrombotic Microangiopathies*

No abstract available.
Catheters* ; Humans ; Oxygen Inhalation Therapy ; Oxygen* ; Thrombotic Microangiopathies*

No abstract available.
Catheters* ; Humans ; Oxygen Inhalation Therapy ; Oxygen* ; Thrombotic Microangiopathies*

Hematopoietic Stem Cell Transplantation ; adverse effects ; Humans ; Thrombotic Microangiopathies ; etiology

OBJECTIVETo illustrate the early alteration of plasminogen activator inhibitor-1 (PAI-1) in the recipients of hematopoietic stem cell transplantation (HSCT) and explore its clinical significance in transplantation-associated thrombotic complications.

METHODSNinety-five patients undergoing HSCT were enrolled in this study. PAI-1 level and other hemostatic parameters were measured by enzyme linked immunosorbent assay (ELISA) in platelet poor plasma samples from patients on conditioning therapy and then weekly until four weeks after HSCT.

RESULTSSignificant increase in PAI-1 was detected after conditioning treatment, followed by a diminution in the very week on transplantation (week 0), then increased with in time after transplantation. According to the occurrence of transplant-associated complications, patients were classified into four groups: thrombus group \[veno-occlusive disease (VOD) (n = 5), thrombotic microangiopathy (TMA) n = 1\], aGVHD group (n = 29), infection group (n = 19) and non-complication group (n = 41). One of 30 patients (3.3%) was diagnosed as thrombus in the auto-HSCT group, while five of 65 patients (7.7%) did in the allo-HSCT group. PAI-1 level of thrombotic patients was significantly increased compared with non-thrombotic subjects, and the patients without thrombotic complications have higher PAI-1 level in the allo-HSCT group than in auto-HSCT group. All the patients with complications presented with significantly increased PAI-1 compared with those with no complications (P < 0.05). The six patients with thrombotic complications showed extremely elevated PAI-1 \[(62.8 +/- 7.5) microg/L\] compared with that of aGVHD patients \[(45.1 +/- 9.1) microg/L\] or infection patients \[(50.0 +/- 11.2) microg/L\] post-HSCT (P < 0.05).

CONCLUSIONThe increase in plasma PAI-1 may be a specific mark for transplantation-associated thrombotic complications. Increased PAI-1 reflects the development of thrombotic complications. Extreme elevation of PAI-1 contributes to the early diagonsis of VOD and TMA after HSCT.