As the Stomach Churns—or Not!

Abstract

Gastroparesis is defined as a disorder characterized by delayed gastric emptying in the absence of mechanical obstruction. However, symptom presentation and severity can be extremely variable and rather broad, and may include any of the following: nausea, vomiting, retching, bloating, early satiety, loss of appetite, weight loss, and/or abdominal pain.1 Associated conditions including irritable bowel syndrome, autonomic dysfunction, increased risk of thromboembolic phenomenon, and depression have also been described. The prevalence of a history of abuse seems to be high in female patients with an idiopathic etiology, which is of interest.2–5 Although not considered a fatal condition, the severity of gastroparesis ranges from being an inconvenience that minimally impairs quality of life in patients who are able to maintain their weight or even paradoxically gain weight to a major impairment with significant weight loss and malnutrition that may lead to hospitalization and require enteral and/or parenteral feeding with their inherent risks and complications.6 As there is no mechanical cause for obstruction, this condition is considered a functional disorder by many. However, significant evidence has now implicated a malfunctioning of vagal neurons, enteric neurons, interstitial cell of Cajal (ICC), smooth muscle cells, and/or humoral factors.7,8 Etiology of most functional disorders is multifactorial, but yet they are often classified according to their dominant symptoms, like irritable bowel syndrome with constipation-predominant versus diarrhea-predominant. In this issue, Harrell and colleagues9 report on “A novel classification scheme for gastroparesis based on predominant-symptom presentation.” The authors have made a bold attempt to classify gastroparesis according to the dominant symptom at presentation. This is novel because there has not been an accepted official classification for gastroparesis thus far. Previously, patient assessment of upper gastrointestinal disorders-symptom severity index (PAGI-SYM) was developed and evaluated in 2004 by Revicki and coworkers10 as a new self-report instrument based on subjects recruited from multiple centers from 7 different countries with gastroesophageal reflux disease, dyspepsia, or gastroparesis. This was a 20-item scoring system with 6 subscales that proved to have a good reliability and construct validity.11 Subsequently, the same group developed another instrument called the Gastroparesis Cardinal Symptom Index specifically for gastroparesis.10 Gastroparesis Cardinal Symptom Index was derived from the longer PAGI-SYM based on 3 subscales: postprandial fullness/early satiety, nausea/vomiting, and bloating. Existence of such a measure could help clinicians objectively document patient disease severity at each visit and gauge response to therapy. This instrument has proven very useful especially with the availability of newer therapeutic options like the gastric electrical stimulator. As previously mentioned, Harrell et al9 have attempted to classify gastroparesis based on dominant symptom of presentation to guide and improve the management strategy for this group of patients. Although 2 of the subgroups, vomiting-predominant and regurgitation-predominant, are self explanatory, the other dyspepsia-predominant group pools together all the other symptomatology including discomfort, pain, fullness, bloating, and nausea. No particular subgroup has been designated for patients with refractory heartburn associated with impaired gastric emptying or those with profound weight loss and/or malnutrition with a need for specialized nutrition support. Each of the above symptoms could be attributed to a number of pathophysiologic causes such as impaired gastric accommodation reflex, bacterial overgrowth in the small bowel as a result of pangut dysmotility, autonomic dysfunction, or visceral hypersensitivity. Thus, grouping them together is rather arbitrary and not surprisingly the results indicate the same. The authors did not find a correlation between the patient and physician scoring in this subset described as dyspepsia-predominant gastroparesis. Additionally, this subset did not correlate well with the PAGI-SYM. Moreover, gastroparesis could also be classified based on etiology or clinically on the basis of the presence of weight loss and/or need for supplemental nutrition, presence of cyclical symptoms, features of autonomic dysfunction, and pangut dysmotility. Alternatively, the classification could be based on responsiveness to medication, electrical stimulation therapy, or even on histologic criteria on the basis of the density of the interstitial cell of Cajal. All of these options would potentially have therapeutic implications. Although we agree with the authors on the need for better identification of the different subgroups of gastroparesis, the proposed system is rather simplistic and inherently flawed. A better understanding of the natural history, pathophysiology, and response to therapy of each subset is required on a prospective basis. The authors are to be complimented for attempting to get a better understanding of gastroparesis, but much more work in this seemingly ignored area must be done. For most clinicians and patients alike, gastric motility issues continue to be a confusing “black box.”