Domination of gastric Complications Among Diabetic Patients

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Domination of gastric Complications Among Diabetic Patients

Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2018, Vol 19, Issue 4

Abstract

Up to 50% of patients with type 1 and 2 diabetes mellitus (DM) and suboptimal glycemic control have delayed gastric emptying (GE), which can be documented with scintigraphy, 13 C-breath tests, or a wireless motility capsule; the remainder have normal or rapid GE [1-3]. Also, it has been determined that 29% of patients with gastroparesis had diabetes mellitus [4], 13% developed symptoms after gastric surgery and 36% were idiopathic. About 12% of global health care expenditure (727 billion USD) is spent on diabetes. When expanded to the age group between 18 and 99 years, the cost would total to 850 billion USD. In conjunction with the rising prevalence, the cost is expected to rise to a staggering 958 billion USD by 2045. In the USA, an estimated 5 million patients suffer from some form of gastroparesis, and the female: male ratio is 4:1. Many patients with delayed GE are asymptomatic; others have dyspepsia (i.e., mild-moderate indigestion, with or without a mild delay in GE) or gastroparesis (GP), which is a syndrome characterized by moderate-severe upper gastrointestinal symptoms and delayed GE that suggest, but are not accompanied by, gastric outlet obstruction [5]. GP can markedly impair quality of life and up to 50% of patients have significant anxiety and/or depression [1], [6-8]. In diabetic patients (without neuropathy) and healthy controls, acute hyperglycemia will instead relax the proximal stomach, and suppress gastric electrical activity (e.g., reduced the frequency, propagation, and contraction of the antrum) in both fasting and post-prandial conditions, thereby slowing gastric emptying [9]. Abdominal pain is often epigastric (43%), postprandial (72%), nocturnal (74%), and frequently associated with interference with sleep (66%) [7]. Early satiety (88%), and bloating (64%) were the most common symptoms, however 94% of patients had resolution of their symptoms a year after their operation [10]. Severe/very severe upper abdominal pain occurred in 34% of GP patients and associated with other gastroparesis symptoms, somatization, and opiate medication use [11]. Nausea and vomiting are more common in diabetic gastroparesis (DGP) whereas abdominal pain and early satiety are more frequent in idiopathic gastroparesis. The 3 main causes of gastroparesis are diabetic, postsurgical, and idiopathic [12]. In diabetes, measuring gastric emptying has an additional justification in determining the absorption of orally administered drugs and nutrients, and thus post-prandial glucose regulation. Indeed, new onset or worsening of existing difficulties in blood glucose regulation may be the first symptom of diabetic gastroparesis [2]. Growing clinical evidence shows that delayed GE (in GP patients) may be a factor associated with severe reflux, dyspepsia, or both. Gastroparesis, concomitant in 25% of patients with gastroesophageal reflux disease (GERD), has been shown to improve after Nissen fundoplication [13]. If a doctor suspects a person with diabetes has gastroparesis, he will typically order one or more of the following tests to confirm the diagnosis: Barium X-ray; Barium beefsteak test; Radioisotope gastric-emptying scan; Gastric manometry Blood tests to check for nutritional deficiencies and electrolyte imbalances that are common with gastroparesis; Imaging of the gallbladder, kidneys, and pancreas to rule out gallbladder problems, kidney disease, or pancreatitis as causes; An upper endoscopy to check for abnormalities in the structure of the stomach [14]. It is critical to clearly distinguish patients with functional dyspepsia (FD) from those with GP and to better understand the relationship among alterations in specific symptoms, GE, and altered peripheral and central sensory responses to gastric stimuli [15]. A similar situation may occur in a misguided attempt to improve gastric health by using the ubiquitously prescribed proton pump inhibitors, H2 receptor antagonists, and sucralfate or aluminum hydroxide-based antacids. These drugs are a cause of delayed gastric emptying. Such “therapeutic adventures”, akin to a pyromaniac leading a firefighting operation, may harm rather than improve diabetic gastroparesis. A combination of acid-suppressing and prokinetic drugs is indicated only if dyspepsia and gastroparesis co-exist with each other [16]. Vagal dysfunction has also been postulated to play a role in DGP. When food is ingested and gastric accommodation is impaired, patients may experience symptoms such as early satiation, fullness and discomfort. Animal and human data suggest that vagal neuropathy can lead to reduction in pyloric relaxation, impaired antral contraction and disturbed antro-pyloric coordination [17]. GP has also been associated with bronchiectasis, aspiration and chronic rejection. GI bleeding secondary to severe refractory esophagitis with an eventual necessity for surgery has also been reported [18]. Most patients respond to conservative treatment with frequent small meals and an upright eating position, in combination with motility agents, such as oral erythromycin analogs, metoclopramide, and domperidone (the last of these is not FDA approved in the US) [19]. Metoclopramide and domperidone, a D2 dopamine receptor antagonist, are the most widely used but only metoclopramide is FDA approved in the US while domperidone is available in Europe, Canada, Mexico, and New Zealand. Metoclopramide also carries a significant risk of extrapyramidal adverse effects, including tardive dyskinesia when taken longer than 12 wk. Other groups of medication, such as 5-HT3 receptor antagonists, phenothiazines, and muscarinic cholinergic receptor antagonist, have been used off-label for symptomatic relieve but they do not have effect of gastric motility. While medications and dietary modification are the first line treatment, approximately 30% of patients do not respond to conservative management.

Authors and Affiliations

Abdul Kader Mohiuddin

Keywords

EP ID EP622328
DOI 10.26717/BJSTR.2019.19.003331
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