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1 as acquired von Willebrand factor defect and angiodysplasia).
2 ulcers and erosions; 8.3%, masses; and 3.4%, angiodysplasia.
3 rsus 1.1 +/- 0.1, P < 0.001) than those with angiodysplasia.
4 peculated that LVAD support itself may cause angiodysplasia.
5 t gastrointestinal blood loss resulting from angiodysplasia.
6  an autosomal dominant disorder of localized angiodysplasia.
7 ce that LVAD support causes gastrointestinal angiodysplasia.
8  reported 17 polyps (largest size 10 mm) and angiodysplasia.
9 strointestinal bleeding and gastrointestinal angiodysplasia.
10 s and gastrointestinal bleeding secondary to angiodysplasias.
11 ing secondary to vascular lesions, including angiodysplasias.
12 6 patients (54.5%) who no longer had typical angiodysplasias.
13  an autosomal dominant disorder of localized angiodysplasia, although it is sometimes mistakenly iden
14 ectasia hemorrhage included 27 patients with angiodysplasia and 19 with GAVE.
15            Vascular malformations, including angiodysplasia and Dieulafoy's lesions, have been implic
16 of treatment of upper gastrointestinal (UGI) angiodysplasia and GAVE hemorrhage by endoscopic argon p
17 th APC is a safe treatment modality for both angiodysplasia and vascular ectasia bleeding.
18  re-bleeding etiologies were the small bowel angiodysplasias and abnormal vascular lesions.
19 ort, abnormal angiogenesis, gastrointestinal angiodysplasia, and bleeding.
20                             Gastrointestinal angiodysplasias are vascular anomalies that may result i
21 g gastric antral vascular ectasia (GAVE) and angiodysplasia, are increasingly recognized as important
22 tor (vWF) and bleeding from gastrointestinal angiodysplasia at an alarming rate.
23                                Patients with angiodysplasia bleeding were required to have had at lea
24                                              Angiodysplasia can be associated with von Willebrand dis
25  versus 5%; P=0.02) and greater frequency of angiodysplasia confirmed during endoscopy (58% versus 23
26 dy was to determine whether gastrointestinal angiodysplasia develops during continuous-flow left vent
27 s associated with reduced size and number of angiodysplasias in these patients.
28 s diagnosed with upper GI bleeding caused by angiodysplasia or GAVE at a tertiary hospital were recru
29                      More GAVE patients than angiodysplasia patients had co-existing liver cirrhosis
30 he transfusion requirements of patients with angiodysplasia-related anemia in a clinical trial settin
31 need for endoscopic therapy in patients with angiodysplasia-related anemia.
32 The efficacy of APC treatment is greater for angiodysplasia than for vascular ectasia bleeding.
33 anifestation of pathological angiogenesis is angiodysplasia, vascular malformations that cause severe
34                             Gastrointestinal angiodysplasia was noted in 5 of 6 bleeding patients wit
35                                Resolution of angiodysplasias was less frequent in patients who had mu
36                            The patients with angiodysplasia were older than those with GAVE (71.6 +/-
37 eficiency anemia and severe aortic stenosis, angiodysplasias were present in 75.0% of patients.