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

Excerpt

The terms gastroparesis (GP) and gastroparesis-like syndrome (GLS) are used to diagnose patients experiencing similar symptoms of nausea, vomiting, and postprandial abdominal pain with GP defined as this symptom complex accompanied by delayed gastric emptying (GE). A current conundrum is why similar symptoms are present in these two groups despite differing gastric motor function. Historically, studies have focused on interstitial cells of Cajal (ICC) networks and collagen fibrosis in the gastric antrum, although their results do not explain the development of delayed gastric emptying (GE) in some patients and not in others. Growing interest in the pylorus stems from attempts to determine whether aberrant pyloric function is the mechanism that delays GE in GP and not in GLS patients, despite both groups experiencing similar symptoms. Previously, authors have suggested that GP and GLS exist along a continuum of the same pathophysiologic process of a complex interplay of inflammation, fibrosis, and neural network changes that alter gastric motility and eventually lead to delayed GE [1]. 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]. …