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1 en compared in 177 patients with symptoms of gastroparesis.
2 tained diabetic subjects without symptoms of gastroparesis.
3 es on the morbidity associated with diabetic gastroparesis.
4 e identified county residents with potential gastroparesis.
5 tcomes in diabetic patients with symptoms of gastroparesis.
6 n the gastric wall in patients with diabetic gastroparesis.
7 ost patients with diabetes have a history of gastroparesis.
8 f Kit expression and development of diabetic gastroparesis.
9 tics and other therapeutic interventions for gastroparesis.
10 is a viable option for medically refractory gastroparesis.
11 keted in many countries for the treatment of gastroparesis.
12 ed with a 15-year history of severe isolated gastroparesis.
13 motility disorders, especially patients with gastroparesis.
14 and (3) the pathophysiology and treatment of gastroparesis.
15 oxin A represents a novel technique to treat gastroparesis.
16 to be beneficial in idiopathic and diabetic gastroparesis.
17 /- mice, a well-established genetic model of gastroparesis.
18 ociation (AGA) on Diagnosis and Treatment of Gastroparesis.
19 oved quality of life in patients with severe gastroparesis.
20 ld contribute to the development of diabetic gastroparesis.
21 accelerate gastric emptying in patients with gastroparesis.
22 tric emptying, and symptoms in patients with gastroparesis.
23 nts with diabetes) in patients with diabetic gastroparesis.
24 etic dysfunction leading to constipation and gastroparesis.
25 hese findings indicate the chronic nature of gastroparesis.
26 cells of Cajal (ICCs) is common in diabetic gastroparesis.
27 port the use of nortriptyline for idiopathic gastroparesis.
28 placebo for symptomatic relief in idiopathic gastroparesis.
29 s, clinical presentations, and management of gastroparesis.
30 nitiated to delineate the natural history of gastroparesis.
31 n in 12 patients with diabetic or idiopathic gastroparesis.
32 astric dysrhythmias are each associated with gastroparesis.
33 vity could contribute to the pathogenesis of gastroparesis.
34 n in ICC may directly contribute to diabetic gastroparesis.
35 s are found in the majority of patients with gastroparesis.
36 mpare findings in idiopathic versus diabetic gastroparesis.
37 ies in patients with diabetic and idiopathic gastroparesis.
38 followed a diet suggested for patients with gastroparesis.
39 tinal motility disorders, including diabetic gastroparesis.
40 herapeutic option for patients with diabetic gastroparesis.
41 paresis, and 222 any of the 3 definitions of gastroparesis.
42 sis, 83 met diagnostic criteria for definite gastroparesis, 127 definite plus probable gastroparesis,
47 s decreased in more patients with idiopathic gastroparesis (40%) compared with diabetic patients (20%
50 a symptomatic and premalignant disease, for gastroparesis, a less severe and often treatable disease
51 sex and prevalence of symptoms suggestive of gastroparesis among patients with T2DM in Israel has not
53 clinical profiles in idiopathic and diabetic gastroparesis and are defining roles of gastric and extr
54 We identified a correlation between diabetic gastroparesis and cardiovascular disease, hypertension,
55 was to describe histologic abnormalities in gastroparesis and compare findings in idiopathic versus
56 gastrointestinal (GI) dysfunctions, such as gastroparesis and constipation, are prodromal to the car
58 red to be the gold standard for detection of gastroparesis and other disorders of gastric motility; S
60 cing seems to be able to improve symptoms of gastroparesis and to accelerate gastric emptying in pati
61 underlying impairments in gastric emptying (gastroparesis) and receptive relaxation, but the specifi
62 te gastroparesis, 127 definite plus probable gastroparesis, and 222 any of the 3 definitions of gastr
65 It is suggested that symptoms related to gastroparesis are more common in female than in male pat
67 od of 2.1 years, 28% of patients treated for gastroparesis at centers of expertise had reductions in
68 initiation and propagation of slow waves in gastroparesis because research tools have lacked spatial
72 oms, based on a decrease of 1 or more in the gastroparesis cardinal symptom index (GCSI) score after
75 normal, 85.75 minutes), recent vomiting, and gastroparesis cardinal symptom index-daily diary scores
76 pment for esophageal sensorimotor disorders, gastroparesis, chronic diarrhea, chronic constipation (i
77 f Diabetes and Digestive and Kidney Diseases Gastroparesis Clinical Research Consortium (GpCRC), comp
78 f Diabetes and Digestive and Kidney Diseases Gastroparesis Clinical Research Consortium Gastroparesis
79 f Diabetes and Digestive and Kidney Diseases Gastroparesis Clinical Research Consortium Registry.
80 ion in symptom severity (measured by the 0-5 Gastroparesis Clinical Symptom Index) for nausea (1.8 vs
82 nutritional consultation after the onset of gastroparesis; consultation was more likely among patien
84 agnostic definitions were used: (1) definite gastroparesis, delayed gastric emptying by standard scin
85 that Kit expression is lost during diabetic gastroparesis due to increased levels of oxidative stres
87 This review provides updated information on gastroparesis focusing on new findings from the past few
88 cidence per 100,000 person-years of definite gastroparesis for the years 1996-2006 was 2.4 (95% confi
94 ology, diagnostic evaluation, and therapy of gastroparesis in the past several years has offered insi
95 (type 1 and type 2) with classic symptoms of gastroparesis (including early satiety, postprandial ful
96 patient outcomes for trials of therapies for gastroparesis, including potential additional trials for
97 CUNV were observed to be similar to those of gastroparesis, indicating that they could be spectra of
98 ge was associated with a higher incidence of gastroparesis, intra-abdominal fluid collection, intra-a
108 ed to reduce the aspiration risk of diabetic gastroparesis is likely over-utilized and may only be in
109 lence and severity of symptoms suggestive of gastroparesis is particularly high among obese females w
110 The pathophysiological basis of diabetic gastroparesis is poorly understood, in large part due to
113 usea and vomiting caused by gastroparesis or gastroparesis-like syndrome, aprepitant did not reduce t
116 ted in patients with CUNV than in those with gastroparesis (mean, 3.5 vs 2.3 bodies/field, respective
118 slow-wave initiation and conduction occur in gastroparesis, often at normal frequency, which could be
120 s with chronic nausea and vomiting caused by gastroparesis or gastroparesis-like syndrome, aprepitant
122 mptying has added value for the diagnosis of gastroparesis over a study of solid emptying alone.
124 The age-adjusted prevalence of definite gastroparesis per 100,000 persons on January 1, 2007, wa
125 hilic esophagitis, functional dyspepsia, and gastroparesis, posing a challenge for patient management
126 strointestinal tract that include dysphagia, gastroparesis, prolonged gastrointestinal transit time,
127 ive treatment is available for patients with gastroparesis refractory to standard medical therapy.
128 f Diabetes and Digestive and Kidney Diseases Gastroparesis Registry and completed diet questionnaires
129 s Gastroparesis Clinical Research Consortium Gastroparesis Registry, seen every 16 weeks and treated
130 n a clinical trial of patients with diabetic gastroparesis, relamorelin (10 mug twice daily) signific
132 y of full thickness gastric tissue in severe gastroparesis shows heterogeneous enteric neuronal, smoo
133 electrical mapping to quantify and classify gastroparesis slow-wave abnormalities in spatiotemporal
138 dies are more sensitive for the detection of gastroparesis than are liquid studies; thus, liquid stud
139 d splicing of Ano1 in patients with diabetic gastroparesis that alter the electrophysiological proper
141 of CUNV substantially overlap with those of gastroparesis, therefore the diseases may share pathophy
142 NTS: The NORIG (Nortriptyline for Idiopathic Gastroparesis) trial, a 15-week multicenter, parallel-gr
143 r upper gastrointestinal study; (3) possible gastroparesis, typical symptoms alone or delayed gastric
144 ymptoms for more than 3 months; (2) probable gastroparesis, typical symptoms and food retention on en
145 stimulation for the treatment of symptomatic gastroparesis unresponsive to standard medical therapy.
146 disorders such as irritable bowel syndrome, gastroparesis, urinary incontinence and cardiac arrhythm
147 One hundred thirty patients with idiopathic gastroparesis were enrolled between March 2009 and June
149 h those of controls as well as patients with gastroparesis who were studied previously by identical m
151 5 y; 88% with type 2 diabetes) with diabetic gastroparesis with moderate to severe symptoms and delay
152 s were found between diabetic and idiopathic gastroparesis with the exception of nNOS expression, whi
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