![]() In the 20th century, that is before the routine use of intensive insulin therapy for type 1 DM, up to 60% of patients with long-standing type 1 DM and GI symptoms had diabetic gastroparesis ( 5). A smaller proportion of DM patients have rapid GE. A few studies also considered the presence of retained food in the stomach at endoscopy or during an upper GI radiograph to suggest delayed GE ( 4).Īlthough GE is the primary and most widely used objective assessment in patients with diabetic gastroenteropathy, the condition is also associated with impaired gastric accommodation and increased or reduced visceral sensation, which may coexist with delayed GE. Among these, scintigraphy is the criterion standard and the most widely used. In some patients, discriminating between dyspepsia and gastroparesis can be challenging because the symptom- and emptying-based boundaries are poorly defined ( 3).Ĭonsistent with clinical practice and research studies, the studies cited in this review defined delayed GE by an objective assessment of GE with scintigraphy, a capsule, or a gastric emptying breath test (GEBT). The latter comprises up to 40% of patients with DM and delayed GE ( 2). In addition to gastroparesis, diabetic gastroenteropathy also includes diabetic dyspepsia ( i.e., indigestion), which is characterized by upper GI symptoms and normal, rapid, or slightly delayed GE and paucisymptomatic or asymptomatic delayed GE. Hence, diabetic gastroenteropathy is a more inclusive term to describe the GI manifestations of DM. Also, these GI symptoms may originate not only from the stomach but also from the small intestine ( 1). However, other patients with DM have GI symptoms with normal GE or abnormal GE with no or mild symptoms. Gastroparesis is a syndrome characterized by delayed gastric emptying (GE) and upper GI symptoms that suggest, but are not associated with, gastric outlet obstruction. Promising newer therapeutic approaches include ghrelin receptor agonists and selective 5-hydroxytryptamine receptor agonistsīy tradition, diabetic gastroparesis has been used to describe the upper gastrointestinal (GI) manifestations of diabetes mellitus (DM). Promising newer therapeutic approaches include ghrelin receptor agonists and selective 5-hydroxytryptamine receptor agonists. Patients with more severe symptoms may require a venting gastrostomy or jejunostomy and/or gastric electrical stimulation. Initial options include dietary modifications, supplemental oral nutrition, and antiemetic and prokinetic medications. The management of diabetic gastroparesis is guided by the severity of symptoms, the magnitude of delayed GE, and the nutritional status. Alternatively, there are limited data to suggest that delayed GE may affect glycemic control. Hyperglycemia, autonomic neuropathy, and enteric neuromuscular inflammation and injury are implicated in the pathogenesis of delayed GE. Often the distinction between dyspepsia and gastroparesis is based on clinical judgement rather than established criteria. Gastroparesis can markedly impair quality of life, and up to 50% of patients have significant anxiety and/or depression. ![]() Many patients with delayed GE are asymptomatic others have dyspepsia ( i.e., mild to moderate indigestion, with or without a mild delay in GE) or gastroparesis, which is a syndrome characterized by moderate to severe upper gastrointestinal symptoms and delayed GE that suggest, but are not accompanied by, gastric outlet obstruction. Up to 50% of patients with type 1 and type 2 DM and suboptimal glycemic control have delayed gastric emptying (GE), which can be documented with scintigraphy, 13C breath tests, or a wireless motility capsule the remainder have normal or rapid GE. This review covers the epidemiology, pathophysiology, clinical features, diagnosis, and management of diabetic gastroparesis, and more broadly diabetic gastroenteropathy, which encompasses all the gastrointestinal manifestations of diabetes mellitus.
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