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1 hes and may clarify the etiology of diabetic gastropathy.
2 y a key role in the pathogenesis of diabetic gastropathy.
3 idal anti-inflammatory drug [NSAID])-induced gastropathy.
4 s evaluated for efficacy in preventing NSAID gastropathy.
5 cally different lactacystin, prevented NSAID gastropathy.
6 sing enteropathy secondary to a hypertrophic gastropathy.
7 gastroprotective agent against NSAID-induced gastropathy.
8 ls, which play a pathogenic role in inducing gastropathy.
9 coxib for reducing the risk of NSAID-induced gastropathy.
10 up and 8 in the sclerotherapy group), portal gastropathy (1 patient in each group), and gastric lipom
11 diatric endoscopists are alerted to prolapse gastropathy, a more accurate description of an old and p
12 new molecular and mechanistic basis for PHT gastropathy and provide a new therapeutic modality for p
13 ally believed to be responsible for diabetic gastropathy and the underlying impairments in gastric em
14 of proteasome inhibitors in preventing NSAID gastropathy and their potency in inhibiting intracellula
15 sly used to establish the incidence of NSAID gastropathy, and also information on patient risk factor
16 sociated with a declining incidence of NSAID gastropathy, and, if so, what measures may have caused t
17 ed for treatment failures due to symptomatic gastropathy; and Strategy 2-safer, more expensive NSAID
19 secondary prophylaxis), portal hypertensive gastropathy, ascites, hepatorenal syndrome, spontaneous
20 pful in the treatment of hypertensive portal gastropathy but not gastric vascular ectasias.In the are
21 ary strategies to reduce the risk of serious gastropathy caused by traditional nonsteroidal anti-infl
22 ffer from gastric neuromuscular dysfunction (gastropathy) causing symptoms ranging from postprandial
23 H signalling that might be associated with a gastropathy clinically overlapping with Menetrier diseas
30 dal antiinflammatory drug (NSAID)-associated gastropathy is a major cause of hospitalization and deat
34 al hypertension, namely, portal hypertensive gastropathy (PHG) and gastric vascular ectasia (GVE), to
35 as well as hyperplastic polyps, hyperplastic gastropathy, postendoscopic resection for gastric malign
36 iduals from a family with autosomal dominant gastropathy resembling Menetrier disease, a premalignant
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