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1 17 patients (3%) had hepatic veno-occlusive disease.
2 is crucial for the development of pulmonary veno-occlusive disease.
3 transaminase and bilirubin without signs of veno-occlusive disease.
4 dysfunction, and a high frequency of hepatic veno-occlusive disease.
5 eveloped severe hepatotoxicity suggestive of veno-occlusive disease.
6 Two patients had reversible hepatic veno-occlusive disease.
7 used as therapy for Budd-Chiari syndrome and veno-occlusive disease.
8 or of 100-day mortality was the diagnosis of veno-occlusive disease.
9 acteristic that predicted the development of veno-occlusive disease.
10 ty, any infection, organ failure, or hepatic veno-occlusive disease (1-year cumulative incidence, 71%
11 d $20,500, respectively), whereas infection, veno-occlusive disease, acute graft-versus-host disease,
12 nary capillary hemangiomatosis and pulmonary veno-occlusive disease, an autosomal recessively inherit
14 tioned well initially, the patient developed veno-occlusive disease and required repeat transplantati
15 irected deletion of Aplnr manifest pulmonary veno-occlusive disease and right heart failure, detectab
16 elopment of sinusoidal obstruction syndrome (veno-occlusive disease) and by total serum bilirubin lev
17 erapy; (2) posttransplant fever; (3) hepatic veno-occlusive disease; and (4) use of posttransplant gr
18 ction (presenting as the syndrome of hepatic veno-occlusive disease) are all associated with signific
20 and 3 months of age as a result of pulmonary veno-occlusive disease, capillary hemorrhage, and pancyt
21 ary hypertension and differentiate pulmonary veno-occlusive disease from pulmonary arterial hypertens
23 was also a trend toward an increased risk of veno-occlusive disease in patients with high ferritin.
24 nusoidal obstruction syndrome (also known as veno-occlusive disease) in patients during study treatme
31 the initiation of pulmonary vasodilators in veno-occlusive disease often leads to increased mortalit
33 lantation-related mortality; acute toxicity (veno-occlusive disease or acute graft versus-host diseas
36 ients with a clinical diagnosis of pulmonary veno-occlusive disease/pulmonary capillary hemangiomatos
37 4 gene (EIF2AK4) are described in pulmonary veno-occlusive disease/pulmonary capillary hemangiomatos
38 opathic and heritable PAH and with pulmonary veno-occlusive disease/pulmonary capillary hemangiomatos
39 athic or heritable PAH and 16 with pulmonary veno-occlusive disease/pulmonary capillary hemangiomatos
44 en successfully used to treat severe hepatic veno-occlusive disease (sVOD) with multiorgan failure (M
46 vely evaluated for the clinical diagnosis of veno-occlusive disease, the occurrence of acute graft-ve
47 ary ERG and APLNR in patients with pulmonary veno-occlusive disease undergoing lung transplantation w
48 n and melphalan group had Bearman grades 1-3 veno-occlusive disease versus 21 (9%) of 239 in the carb
50 bstruction syndrome (SOS), previously called veno-occlusive disease (VOD) can be a difficult problem
58 One patient treated at 9 mg/m2 developed veno-occlusive disease (VOD) of the liver and defined th
61 ibrotide for the treatment of severe hepatic veno-occlusive disease (VOD), showing a 23% improvement
65 l recessive primary immunodeficiency disease veno-occlusive disease with immunodeficiency syndrome (V
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