Gastroparesis and Gastroparesis-like Syndrome: Response to Therapy and Its Predictors

Abstract

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 non-diabetic etiology. Out of 69 patients, 49 were responders (71%) and 20 were non responders (29%). The cause (diabetic vs. non-diabetic) 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 correlate 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 be a distinct syndrome with a greater proportion of males than classical gastroparesis.

Randomised clinical trial: ghrelin agonist TZP-101 relieves gastroparesis associated with severe nausea and vomiting - randomised clinical study subset data

“…Given the heterogeneous nature of gastroparesis, stratification of patients by symptom type and severity may provide useful information for predicting therapeutic responses. [30][31][32] In summary, TZP-101 was able to reduce severe nausea and vomiting as well as overall symptoms substantially and significantly in a subset of the most refractory diabetic gastroparesis patients. These observations support a future role of this GI motility agent as a potent therapy of gastroparesis.…”

Gastroparesis in pregnancy: case report and literature review

“…12 Tricyclic antidepressants have also been incorporated as a routine therapy and when combined with prokinetic agents, a response rate of 71% has been noted. 28 Surgical intervention (other than provision of a gastrostomy or jejunostomy) is usually reserved for patients with gastroparesis postvagotomy and involves completion or subtotal gastrectomy. 1 Regardless of the aetiology, up to one-third of patients showed no improvement on postsurgical intervention.…”

Understanding the Differences Between Gastroparesis and Gastroparesis-Like Syndrome: Filling a GaPing Hole?

“…Whether or not the degree of pylorus dysfunction in these states is related to these measures or others (i.e., antral contraction effect on pylorus or gastric dysrhythmias) remains to be seen. As the authors point out, GP and GLS may exist on a continuum; as an example, these diseases are frequently reclassified when assessed at time points from baseline-48 weeks after reimaging [2]. Further studies are needed to understand the pathophysiologic basis of GP and GLS since there is substantial morbidity in this patient cohort and since interventions may be invasive and potentially carry significant risk including postoperative mortality [11].…”

“…As such, the contribution of each of these physiologic derangements to the development of symptoms and, in some patients, delayed GE is unknown. A better understanding of the pathophysiologic mechanisms that lead to the unique clinical manifestations of GP and GLS is thus essential to developing novel therapies [2].…”