Diabetic Gastroparesis: A Review.

Abstract

Gastroparesis is characterized by delayed gastric emptying in the absence of mechanical obstruction. This complication is associated with uncontrolled diabetes, contributing to approximately one-third of all gastroparesis cases (1–3). Gastroparesis is more prevalent in patients with type 1 diabetes than in those with type 2 diabetes (4). The 10-year cumulative incidence of diabetic gastroparesis has been estimated to be 5.2% in patients with type 1 diabetes and 1% in those with type 2 diabetes (5,6). The prevalence of diabetes-associated gastrointestinal symptoms is 5–12% (7,8). In a study by Jung et al. (9) conducted in Olmsted County, MN, the prevalence of gastroparesis was about 5% in patients with type 1 diabetes and 1% in type 2 diabetes (9). In the same study, the age-adjusted incidence rate of gastroparesis was 2.4/100,000 person-years in men and 9.8/100,000 person-years in women (9). Gastroparesis, a form of autonomic neuropathy, is most commonly seen in people who have had diabetes for >10 years and who have already developed other microvascular complications (10). Once the symptoms from gastroparesis begin, they typically persist and are stable over 12–25 years; this is true even when blood glucose levels have been controlled (11). The most common symptoms are early satiety, nausea, bloating, abdominal pain, and vomiting. In terms of prognosis, a recent study published by Chang et al. (12) found no association between delayed gastric emptying and increased mortality over a 25-year period. Although there is no evidence to date that diabetic gastroparesis increases mortality, this complication substantially impairs all aspects of life (13). Although still not fully elucidated, the suggested pathophysiology of diabetic gastroparesis includes poor glycemic control, sympathetic vagal neuropathy, Cajal interstitial cell abnormalities, and loss of neuronal nitric oxide synthase (nNOS) (3,14). The loss of interstitial cells …