In an editorial published by the American Journal of Gastroenterology, authors Brian E. Lacy, MD, PhD and David J. Cangemi, MD addressed common misconceptions regarding the diagnosis and treatment of gastroparesis (GP). The prevalence, etiology, and pathogenesis of GP were described, along with diagnostic techniques and prognosis.
The first “controversy” authors challenged is the conception that gastroparesis is rare and primarily affects patients with diabetes. In actuality, authors wrote, prior studies suggest that 2 to 3 million adults in the United States (US) have GP, making it one of the most common sensorimotor disorders of the stomach.
Up to 50% of GP cases are categorized as “idiopathic”, or having no precise cause. Many of these patients are hypothesized to have had a prior infection or inflammatory “insult”. The next most common etiologies are diabetes (30%), medications (20%), bariatric surgery (7%), and connective tissue disorders (5%).
Authors also noted that while chronic nausea and vomiting are frequently attributed to GP, many differential diagnoses can cause these symptoms. Instead, authors described abdominal pain as the “cardinal symptom” of GP. Other common symptoms include nausea, early satiety, and bloating. A full medical history, panel of laboratory tests, and thorough symptom assessment is the best approach to distinguishing GP from diseases and disorders that mimic it. Authors also noted that degree of gastric emptying (GE) is not necessarily associated with symptom severity, suggesting that the pathophysiology of GP is more “complex [and] heterogeneous” than a delay in GE.
Regarding diagnosis of GP, a GE scan is typically considered the gold standard test. However, many centers perform GE scans incorrectly, leading to misdiagnosis and inappropriate treatment. To improve GE scan performance, authors recommend stopping medications that affect GE prior to the scan, measuring blood glucose levels, using a standardized meal, and performing a 4-hour scan.
Mild delays in emptying are more common in functional dyspepsia than in GP; authors advised against “over-interpreting” a mild delay as evidence of GP. Further, GE alone is not diagnostic of GP. In addition to scans, practitioners should investigate medical history and current symptoms.
Most GP therapies to date have focused on accelerating GE. While important, improved emptying does not necessarily induce global symptom improvement. Recent research has demonstrated that prucalopride, a 5-HT4 agonist, improved many GP symptoms, while GE accelerating agents failed to demonstrate efficacy.
Currently, metoclopramide is the only US Food and Drug Administration (FDA)-approved medication for the treatment of GP. The effects of this drug are modest, and adverse events occur in 30 to 40% of users. However, the risk for tardive dyskinesia, a severe side effect, has been reported in some studies at just 1%, a rate significantly lower than generally assumed.
As another treatment modality, authors described endoscopic pyloric therapy, which has shown promise in preliminary studies. However, large-scale, sham-controlled trials are necessary to confirm its efficacy in GP treatment.
Gastric peroral endoscopic myotomy is another novel method showing promise. Other suggested treatment methods include diet alterations, prokinetic agents, antiemetic agents, neuromodulators, complementary and alternative medications, and surgical interventions.
Taken together, these points are meant to guide practitioners in the diagnosis and treatment of GP. Authors advocated for further research into the condition to improve understanding and introduce novel treatment options.
Lacy BE, Cangemi DJ. Controversies in gastroparesis: discussing the sticky points. Am J Gastroenterol. 2021;116(8):1572–1576. doi: 10.14309/ajg.0000000000001243
This article originally appeared on Gastroenterology Advisor