PURPOSE: The natural history and outcome of patients with gastroparesis is not well known. The aim of this study was to identify the clinical or pathophysiological characteristics, if any, that may be helpful in predicting therapeutic response in this condition. METHODS: This is a retrospective study of a cohort of patients who presented to a tertiary referral center with symptoms suggestive of gastroparesis. All patients were evaluated by scintigraphic measurement of gastric emptying and symptoms were scored using a modification of the Gastroparesis Cardinal Symptom Index (GCSI). Treatment generally included conservative measures such as antiemetics, prokinetics, tricyclic antidepressants, and analgesics as well as various more invasive interventions in selected patients. Response to treatment was defined as a change in the overall GCSI score of two-thirds or more as compared with baseline. RESULTS: Out of a total of 93 patients, 69 patients met the eligibility criteria. Of these, 29 patients had diabetes mellitus and 40 patients had gastroparesis of nondiabetic etiology. Out of 69 patients, 49 were responders (71%) and 20 were nonresponders (29%). The cause (diabetic versus nondiabetic) of gastroparesis or the presence of delayed emptying did not correlate with response. However, the severity of stomach distension, bloating subscale score, and the global GCSI score at baseline presentation were predictive of response by multivariate analysis. CONCLUSION: Higher global GCSI score, bloating subscale score, and severity of stomach distension at baseline presentation correlated with an unfavorable response in gastroparetic patients. On the other hand, neither the etiology of gastroparesis nor associated delay in gastric emptying appeared to be important in the clinical response. Patients with symptoms of typical gastroparesis but without delays in gastric emptying may have a distinct syndrome with a greater proportion of males than classical gastroparesis.
PURPOSE: The natural history and outcome of patients with gastroparesis is not well known. The aim of this study was to identify the clinical or pathophysiological characteristics, if any, that may be helpful in predicting therapeutic response in this condition. METHODS: This is a retrospective study of a cohort of patients who presented to a tertiary referral center with symptoms suggestive of gastroparesis. All patients were evaluated by scintigraphic measurement of gastric emptying and symptoms were scored using a modification of the Gastroparesis Cardinal Symptom Index (GCSI). Treatment generally included conservative measures such as antiemetics, prokinetics, tricyclic antidepressants, and analgesics as well as various more invasive interventions in selected patients. Response to treatment was defined as a change in the overall GCSI score of two-thirds or more as compared with baseline. RESULTS: Out of a total of 93 patients, 69 patients met the eligibility criteria. Of these, 29 patients had diabetes mellitus and 40 patients had gastroparesis of nondiabetic etiology. Out of 69 patients, 49 were responders (71%) and 20 were nonresponders (29%). The cause (diabetic versus nondiabetic) of gastroparesis or the presence of delayed emptying did not correlate with response. However, the severity of stomach distension, bloating subscale score, and the global GCSI score at baseline presentation were predictive of response by multivariate analysis. CONCLUSION: Higher global GCSI score, bloating subscale score, and severity of stomach distension at baseline presentation correlated with an unfavorable response in gastroparetic patients. On the other hand, neither the etiology of gastroparesis nor associated delay in gastric emptying appeared to be important in the clinical response. Patients with symptoms of typical gastroparesis but without delays in gastric emptying may have a distinct syndrome with a greater proportion of males than classical gastroparesis.
Authors: V Stanghellini; C Tosetti; A Paternicò; R De Giorgio; G Barbara; B Salvioli; R Corinaldesi Journal: Am J Gastroenterol Date: 1999-08 Impact factor: 10.864
Authors: G Tougas; E Y Eaker; T L Abell; H Abrahamsson; M Boivin; J Chen; M P Hocking; E M Quigley; K L Koch; A Z Tokayer; V Stanghellini; Y Chen; J D Huizinga; J Rydén; I Bourgeois; R W McCallum Journal: Am J Gastroenterol Date: 2000-06 Impact factor: 10.864
Authors: D A Revicki; A M Rentz; D Dubois; P Kahrilas; V Stanghellini; N J Talley; J Tack Journal: Aliment Pharmacol Ther Date: 2003-07-01 Impact factor: 8.171
Authors: Pankaj J Pasricha; Katherine P Yates; Linda Nguyen; John Clarke; Thomas L Abell; Gianrico Farrugia; William L Hasler; Kenneth L Koch; William J Snape; Richard W McCallum; Irene Sarosiek; James Tonascia; Laura A Miriel; Linda Lee; Frank Hamilton; Henry P Parkman Journal: Gastroenterology Date: 2015-08-21 Impact factor: 22.682
Authors: Pankaj J Pasricha; Ryan Colvin; Katherine Yates; William L Hasler; Thomas L Abell; Aynur Unalp-Arida; Linda Nguyen; Gianrico Farrugia; Kenneth L Koch; Henry P Parkman; William J Snape; Linda Lee; James Tonascia; Frank Hamilton Journal: Clin Gastroenterol Hepatol Date: 2011-03-11 Impact factor: 11.382
Authors: William L Hasler; Laura A Wilson; Henry P Parkman; Linda Nguyen; Thomas L Abell; Kenneth L Koch; Pankaj J Pasricha; William J Snape; Gianrico Farrugia; Linda Lee; James Tonascia; Aynur Unalp-Arida; Frank Hamilton Journal: Am J Gastroenterol Date: 2011-04-12 Impact factor: 10.864
Authors: W L Hasler; L A Wilson; H P Parkman; K L Koch; T L Abell; L Nguyen; P J Pasricha; W J Snape; R W McCallum; I Sarosiek; G Farrugia; J Calles; L Lee; J Tonascia; A Unalp-Arida; F Hamilton Journal: Neurogastroenterol Motil Date: 2013-02-17 Impact factor: 3.598