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1 followed a diet suggested for patients with gastroparesis.
2 tinal motility disorders, including diabetic gastroparesis.
3 herapeutic option for patients with diabetic gastroparesis.
4 ebo, in patients with idiopathic or diabetic gastroparesis.
5 paresis, and 222 any of the 3 definitions of gastroparesis.
6 tained diabetic subjects without symptoms of gastroparesis.
7 es on the morbidity associated with diabetic gastroparesis.
8 e identified county residents with potential gastroparesis.
9 tcomes in diabetic patients with symptoms of gastroparesis.
10 n the gastric wall in patients with diabetic gastroparesis.
11 ts with refractory vomiting, with or without gastroparesis.
12 ost patients with diabetes have a history of gastroparesis.
13 f Kit expression and development of diabetic gastroparesis.
14 tics and other therapeutic interventions for gastroparesis.
15 is a viable option for medically refractory gastroparesis.
16 keted in many countries for the treatment of gastroparesis.
17 ed with a 15-year history of severe isolated gastroparesis.
18 motility disorders, especially patients with gastroparesis.
19 and (3) the pathophysiology and treatment of gastroparesis.
20 oxin A represents a novel technique to treat gastroparesis.
21 to be beneficial in idiopathic and diabetic gastroparesis.
22 /- mice, a well-established genetic model of gastroparesis.
23 ociation (AGA) on Diagnosis and Treatment of Gastroparesis.
24 oved quality of life in patients with severe gastroparesis.
25 ld contribute to the development of diabetic gastroparesis.
26 accelerate gastric emptying in patients with gastroparesis.
27 tric emptying, and symptoms in patients with gastroparesis.
28 of 4-hour testing in patients with suspected gastroparesis.
29 p gastrointestinal motor problems, including gastroparesis.
30 uded patients who had diabetic or idiopathic gastroparesis.
31 s could be utilized to predict patients with gastroparesis.
32 r potential role in the future management of gastroparesis.
33 nowledge gaps in their use for treatment for gastroparesis.
34 en compared in 177 patients with symptoms of gastroparesis.
35 a lesser extent in idiopathic than diabetic gastroparesis.
36 roparesis but is not described in idiopathic gastroparesis.
37 nship with the better-understood syndrome of gastroparesis.
38 ts with symptoms of diabetic or postsurgical gastroparesis.
39 n full-thickness biopsies from patients with gastroparesis.
40 ontrol, and pyloric dysfunction that lead to gastroparesis.
41 cells of Cajal (ICCs) is common in diabetic gastroparesis.
42 gastroparesis, and 7 (18.4%) had idiopathic gastroparesis.
43 patients with FD were reclassified as having gastroparesis.
44 clopramide and erythromycin in patients with gastroparesis.
45 considerable unmet needs in the treatment of gastroparesis.
46 an unmet need for efficacious therapies for gastroparesis.
47 f the underlying pathophysiology causing the gastroparesis.
48 ulceration, gastrointestinal perforation, or gastroparesis.
49 K1R, in patients with idiopathic or diabetic gastroparesis.
50 nts with diabetes) in patients with diabetic gastroparesis.
51 refractory vomiting, associated or not with gastroparesis.
52 etic dysfunction leading to constipation and gastroparesis.
53 hese findings indicate the chronic nature of gastroparesis.
54 port the use of nortriptyline for idiopathic gastroparesis.
55 placebo for symptomatic relief in idiopathic gastroparesis.
56 s, clinical presentations, and management of gastroparesis.
57 nitiated to delineate the natural history of gastroparesis.
58 n in 12 patients with diabetic or idiopathic gastroparesis.
59 astric dysrhythmias are each associated with gastroparesis.
60 vity could contribute to the pathogenesis of gastroparesis.
61 n in ICC may directly contribute to diabetic gastroparesis.
62 s are found in the majority of patients with gastroparesis.
63 mpare findings in idiopathic versus diabetic gastroparesis.
64 ies in patients with diabetic and idiopathic gastroparesis.
65 sis, 83 met diagnostic criteria for definite gastroparesis, 127 definite plus probable gastroparesis,
69 (1) Determine prevalence of PN in idiopathic gastroparesis; (2) assess if patients with symptoms of g
72 s decreased in more patients with idiopathic gastroparesis (40%) compared with diabetic patients (20%
76 a symptomatic and premalignant disease, for gastroparesis, a less severe and often treatable disease
77 normal gastric retention of food is known as gastroparesis, a syndrome predominated by nausea (>90% o
79 sex and prevalence of symptoms suggestive of gastroparesis among patients with T2DM in Israel has not
80 this study is to evaluate the prevalence of gastroparesis among symptomatic patients and assess trea
82 clinical profiles in idiopathic and diabetic gastroparesis and are defining roles of gastric and extr
83 We identified a correlation between diabetic gastroparesis and cardiovascular disease, hypertension,
84 was to describe histologic abnormalities in gastroparesis and compare findings in idiopathic versus
85 gastrointestinal (GI) dysfunctions, such as gastroparesis and constipation, are prodromal to the car
87 red to be the gold standard for detection of gastroparesis and other disorders of gastric motility; S
88 sis; (2) assess if patients with symptoms of gastroparesis and PN differ in gastric emptying and symp
90 cing seems to be able to improve symptoms of gastroparesis and to accelerate gastric emptying in pati
91 in 70/250 (28%) of patients with symptoms of gastroparesis and was present to a lesser extent in idio
92 ta to help in predicting which categories of gastroparesis and which symptoms could benefit most from
93 underlying impairments in gastric emptying (gastroparesis) and receptive relaxation, but the specifi
94 te gastroparesis, 127 definite plus probable gastroparesis, and 222 any of the 3 definitions of gastr
95 3.2] years), of whom 31 (81.6%) had diabetic gastroparesis, and 7 (18.4%) had idiopathic gastroparesi
96 essary to comprehend derangements leading to gastroparesis, and additional research on human gastric
97 nal diseases including achalasia, refractory gastroparesis, and other esophageal motility disorders (
102 It is suggested that symptoms related to gastroparesis are more common in female than in male pat
105 initial classification, patients with FD and gastroparesis, as seen in tertiary referral centers at l
106 rmed a double-blind trial of 152 adults with gastroparesis at 47 sites in the United States from Nove
107 od of 2.1 years, 28% of patients treated for gastroparesis at centers of expertise had reductions in
108 initiation and propagation of slow waves in gastroparesis because research tools have lacked spatial
109 heral neuropathy (PN) is present in diabetic gastroparesis but is not described in idiopathic gastrop
111 nists were more efficacious than placebo for gastroparesis, but confidence in the evidence was low to
114 severity of gastroparesis symptoms using the Gastroparesis Cardinal Symptom Index (GCSI) and presence
116 oms, based on a decrease of 1 or more in the gastroparesis cardinal symptom index (GCSI) score after
121 toms were assessed by a daily symptom dairy, Gastroparesis Cardinal Symptom Index scores, and other p
122 normal, 85.75 minutes), recent vomiting, and gastroparesis cardinal symptom index-daily diary scores
124 pment for esophageal sensorimotor disorders, gastroparesis, chronic diarrhea, chronic constipation (i
125 f Diabetes and Digestive and Kidney Diseases Gastroparesis Clinical Research Consortium (GpCRC), comp
126 f Diabetes and Digestive and Kidney Diseases Gastroparesis Clinical Research Consortium Gastroparesis
127 f Diabetes and Digestive and Kidney Diseases Gastroparesis Clinical Research Consortium Registry.
128 ion in symptom severity (measured by the 0-5 Gastroparesis Clinical Symptom Index) for nausea (1.8 vs
133 nutritional consultation after the onset of gastroparesis; consultation was more likely among patien
135 ong 148 patients with symptoms of idiopathic gastroparesis, defined as non-diabetic, non-postsurgical
137 agnostic definitions were used: (1) definite gastroparesis, delayed gastric emptying by standard scin
139 Several conditions have been correlated to gastroparesis: diabetes, post-surgical sequelae, medicat
140 that Kit expression is lost during diabetic gastroparesis due to increased levels of oxidative stres
142 This review provides updated information on gastroparesis focusing on new findings from the past few
143 cidence per 100,000 person-years of definite gastroparesis for the years 1996-2006 was 2.4 (95% confi
154 ology, diagnostic evaluation, and therapy of gastroparesis in the past several years has offered insi
156 (type 1 and type 2) with classic symptoms of gastroparesis (including early satiety, postprandial ful
157 etiology, pathophysiology, and management of gastroparesis, including novel pharmacological agents, e
158 patient outcomes for trials of therapies for gastroparesis, including potential additional trials for
159 d it protect from PAN-PDE4 inhibitor-induced gastroparesis, indicating that gastric retention may res
160 CUNV were observed to be similar to those of gastroparesis, indicating that they could be spectra of
161 ts associated with colonic aganglionosis and gastroparesis, indicating their therapeutic potential as
162 fficacy of drugs based on global symptoms of gastroparesis; individual symptoms, including nausea, vo
163 US adults, whereas prevalence of "definite" gastroparesis (individuals diagnosed within 3 months of
164 death, and adverse gastrointestinal events (gastroparesis, intestinal obstruction, gallstones, acute
165 d to severe conditions, including achalasia, gastroparesis, intestinal pseudo-obstruction and chronic
166 gic disorders include sialorrhea, dysphagia, gastroparesis, intestinal pseudo-obstruction, constipati
167 ge was associated with a higher incidence of gastroparesis, intra-abdominal fluid collection, intra-a
184 ed to reduce the aspiration risk of diabetic gastroparesis is likely over-utilized and may only be in
185 lence and severity of symptoms suggestive of gastroparesis is particularly high among obese females w
186 The pathophysiological basis of diabetic gastroparesis is poorly understood, in large part due to
188 date, the definition of clinical success in gastroparesis is still not standardized, the correlation
191 usea and vomiting caused by gastroparesis or gastroparesis-like syndrome, aprepitant did not reduce t
194 ted in patients with CUNV than in those with gastroparesis (mean, 3.5 vs 2.3 bodies/field, respective
196 slow-wave initiation and conduction occur in gastroparesis, often at normal frequency, which could be
198 ently cross the blood-brain barrier, induced gastroparesis only at significantly higher doses (>=1 mg
199 l interventions for patients with idiopathic gastroparesis or gastroparesis related to diabetes.
200 s with chronic nausea and vomiting caused by gastroparesis or gastroparesis-like syndrome, aprepitant
202 ish it from its offshoots such as G-POEM for gastroparesis or Z-POEM for Zenker's diverticula) is the
204 mptying has added value for the diagnosis of gastroparesis over a study of solid emptying alone.
206 role of the GCSI in assessing and monitoring gastroparesis, particularly in resource-limited settings
207 The age-adjusted prevalence of definite gastroparesis per 100,000 persons on January 1, 2007, wa
208 any of these subtypes in mice did not induce gastroparesis per se, nor did it protect from PAN-PDE4 i
210 hilic esophagitis, functional dyspepsia, and gastroparesis, posing a challenge for patient management
211 strointestinal tract that include dysphagia, gastroparesis, prolonged gastrointestinal transit time,
212 determine how often pediatric patients with gastroparesis receive dietary education (from a gastroen
213 Only a little over half of children with gastroparesis receive dietary education and use of a die
214 ive treatment is available for patients with gastroparesis refractory to standard medical therapy.
215 f Diabetes and Digestive and Kidney Diseases Gastroparesis Registry and completed diet questionnaires
216 s Gastroparesis Clinical Research Consortium Gastroparesis Registry, seen every 16 weeks and treated
217 n a clinical trial of patients with diabetic gastroparesis, relamorelin (10 mug twice daily) signific
222 tric electrical stimulation in patients with gastroparesis, reserving these treatments for select pat
223 y of full thickness gastric tissue in severe gastroparesis shows heterogeneous enteric neuronal, smoo
224 electrical mapping to quantify and classify gastroparesis slow-wave abnormalities in spatiotemporal
225 d include gastro-oesophageal reflux disease, gastroparesis, small intestinal bacterial overgrowth, in
227 P alone, resulting in greater alleviation of gastroparesis symptoms and a reduction in hospitalizatio
228 nswered questionnaires including severity of gastroparesis symptoms using the Gastroparesis Cardinal
232 dies are more sensitive for the detection of gastroparesis than are liquid studies; thus, liquid stud
233 d splicing of Ano1 in patients with diabetic gastroparesis that alter the electrophysiological proper
235 ugh there have been multiple drugs tested in gastroparesis, their relative efficacy and safety are un
236 of CUNV substantially overlap with those of gastroparesis, therefore the diseases may share pathophy
237 NTS: The NORIG (Nortriptyline for Idiopathic Gastroparesis) trial, a 15-week multicenter, parallel-gr
238 r upper gastrointestinal study; (3) possible gastroparesis, typical symptoms alone or delayed gastric
239 ymptoms for more than 3 months; (2) probable gastroparesis, typical symptoms and food retention on en
242 stimulation for the treatment of symptomatic gastroparesis unresponsive to standard medical therapy.
243 disorders such as irritable bowel syndrome, gastroparesis, urinary incontinence and cardiac arrhythm
244 for any reason were screened for symptoms of gastroparesis using the gastroparesis cardinal symptom i
245 ere is a consensus for standards to diagnose gastroparesis utilizing a gastric emptying study as the
248 One hundred thirty patients with idiopathic gastroparesis were enrolled between March 2009 and June
249 's or connective tissue disease, symptoms of gastroparesis were more severe in PN than nPN: bloating
250 42% of patients with an initial diagnosis of gastroparesis were reclassified as FD based on gastric-e
253 the most frequent condition associated with gastroparesis, which has been reported in up to 50% of p
255 h those of controls as well as patients with gastroparesis who were studied previously by identical m
257 5 y; 88% with type 2 diabetes) with diabetic gastroparesis with moderate to severe symptoms and delay
258 s were found between diabetic and idiopathic gastroparesis with the exception of nNOS expression, whi
259 tandard deviation, 45 +/- 12 years; 133 with gastroparesis) with chronic (>12 months) of refractory v
260 professionals in recognizing and diagnosing gastroparesis would benefit future studies and improve u