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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review briefly outlines the gastrointestinal manifestations of diabetes mellitus. Usually, gastrointestinal abnormalities are asymptomatic. Severe gastrointestinal dysfunction may be quite debilitating, however. Gastrointestinal symptoms that are a consequence of diabetes may be confused with other primary gastrointestinal disorders. We attempt to provide a clinical approach to differentiating the basis of symptoms and outline the therapeutic plan that we generally employ. Much additional research is necessary to clarify our understanding of the pathophysiology of the gastrointestinal complications of diabetes and to develop improved therapeutic strategies.
Diabetes Care
PMID:Gastrointestinal manifestations of diabetes mellitus. 38 88

Gastroparesis causes gastric emptying disorders in patients with chronic diabetes mellitus and it results from reduced smooth muscle contractility secondary to autonomic dysfunction. Today there has been little objective evidence of improvement in gastric emptying following correction of both uremia and diabetes by combined kidney-pancreas transplantation. We used gastrointestinal symptom scores, solid gastric emptying tests and electrogastrography to evaluate the effect of combined kidney-pancreas transplantation on gastric emptying in 8 uremic diabetic patients. The mean age of the patients was 40 years (range: 30-51 years) and the mean duration of diabetes was 24 years (range: 16-30 years). The patients had been on dialysis up to 24 months. The pretransplant A1 mean was 6.5 before improving to 4.3 after transplantation. All patients were receiving exogenous insulin. Our study data indicate that uremic diabetics have a high prevalence of symptomatic gastrointestinal dysfunction including abnormalities of gastric emptying and gastric electrical activity. Following transplantation, the gastrointestinal symptomatology improved significantly. Significant improvement in the rate of gastric emptying also correlated with improvement in the symptom complex. Gastric electrical activity also improved during the follow-up period.
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PMID:Changes in gastric emptying in recipients of successful combined pancreas-kidney transplants. 180 83

In 87 randomly selected diabetic patients (67 type 1, 20 type 2) and 25 control subjects, gastric emptying of digestible solid and liquid meals and oesophageal transit of a solid bolus were measured with scintigraphic techniques. Gastrointestinal symptoms, autonomic nerve function and glycaemic control were evaluated in the diabetic patients. Gastric emptying and oesophageal transit were slower (P less than 0.001) in the diabetic patients compared with the control subjects, and each was delayed in about 40% of them. There was a relatively weak (r = 0.32; P less than 0.01) relationship between solid and liquid gastric emptying, and no significant correlation (r = 0.11, NS) between oesophageal transit and gastric emptying of the solid meal. Scores for upper gastrointestinal symptoms and autonomic nerve function correlated weakly (r = 0.21; P less than 0.05) with both oesophageal transit and gastric emptying. Gastric emptying of the liquid meal was slower (P less than 0.05) in patients with blood glucose concentrations greater than 15 mmol/l. These results indicate that gastric emptying in patients with diabetes mellitus should be assessed by liquid as well as by solid test meals and that oesophageal transit should not be used as a predictor of generalised diabetic gastroenteropathy.
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PMID:Relationships between oesophageal transit and solid and liquid gastric emptying in diabetes mellitus. 207 Aug 1

Esophageal function was prospectively studied in 50 consecutive insulin-requiring diabetes mellitus patients. The patients were stratified in three groups: A) 18 without peripheral neuropathy (PN); B) 20 with PN but no autonomic neuropathy; C) 12 with PN and autonomic neuropathy. Twelve patients (four B, eight C) had gastrointestinal symptoms including six with dysphagia. Radionuclide esophageal emptying was abnormal in 55, 70, and 83% of patients in groups A, B, and C, respectively. Eleven of the 12 (92%) symptomatic and 23 of the 38 (60%) asymptomatic diabetes mellitus patients had abnormal emptying. Five of six patients with dysphagia had abnormal emptying. Esophageal manometry was also performed in 15 patients. Twelve patients had abnormal manometry. These included nutcracker esophagus in two, achalasia in one, and increased percentage of multipeaked and simultaneous contractions in nine. There were no significant correlations between radionuclide esophageal emptying, manometric changes and symptoms. Gastrointestinal symptoms were more common in the presence of autonomic neuropathy. Delayed esophageal emptying was more profound in the presence of PN, but abnormal esophageal emptying was present in patients with neuropathy as commonly as patients without. Furthermore, the presence of diabetic retinopathy, duration or control of diabetics, and fasting blood sugar did not influence the frequency of abnormal esophageal emptying. Our data indicate that esophageal dysfunction is common in male diabetics even in the absence of clinical PN and retinopathy, suggesting that diabetic gastroenteropathy can occur in the absence of significant diabetic complications. Commonly observed abnormal esophageal manometry in diabetics is not necessarily accompanied by significant functional disturbances or symptoms.
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PMID:Radionuclide esophageal emptying and manometric studies in diabetes mellitus. 360 23

Gastrointestinal symptoms such as vomiting, constipation, diarrhea, and fecal incontinence occur frequently in patients with diabetes mellitus. In a survey of 136 diabetic outpatients, 76% had one or more gastrointestinal symptoms, the commonest symptom being constipation (found in 60%). In many cases these symptoms are thought to be due to abnormal gastrointestinal motility that, in turn, may be a manifestation of diabetic autonomic neuropathy involving the gastrointestinal tract. The pathophysiology of these gastrointestinal symptoms, clarified in recent studies, and the clinical features and treatment of these problems in diabetic patients are reviewed.
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PMID:Disorders of gastrointestinal motility associated with diabetes mellitus. 640 69

Using a scintigraphic technique, we investigated gastric emptying of a semisolid meal in 20 patients with liver cirrhosis and in 10 control subjects and correlated gastric emptying with gastrointestinal symptoms and with autonomic nervous function as determined by R-R interval variation on the electrocardiogram. All subjects lacked endoscopic abnormalities that might explain their gastrointestinal symptoms. None had alcoholic liver disease, diabetes, or other diseases known to affect gastric emptying. The half-time for gastric emptying was significantly prolonged in the cirrhotic patients (51.3 +/- 16.6 minutes) as compared with control subjects (29.9 +/- 8.4) (P < 0.01). There was a significant correlation between the gastrointestinal symptom score and the half-time for gastric emptying (r = 0.46, P < 0.05) in the cirrhotic patients. However, the decreases in R-R interval variation and gastric emptying were not significantly correlated. These observations indicate that delayed gastric emptying is frequently present in patients with liver cirrhosis and may produce their gastrointestinal symptoms.
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PMID:Delayed gastric emptying in patients with liver cirrhosis. 817 39

Gastrointestinal symptoms are often encountered in patients with diabetes mellitus. Symptoms may arise in any region of the alimentary tract; common symptoms are heartburn, nausea, vomiting, diarrhea, constipation, fecal incontinence, and abdominal pain. This article reviews practical approaches to the identification of the pathophysiologic mechanisms involved in diabetic enteropathies and their complications and briefly outlines strategies to treat these symptoms. Particular emphasis is placed on applied physiologic tests and the choice of pharmacotherapy (e.g., cisapride, erythromycin, or octeotide). The current role of pancreatic transplantations also is briefly reviewed.
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PMID:Gastrointestinal problems in diabetes. 879 4

Although relatively frequent. diabetic involvement of digestive tract motility has not been investigated extensively in different organs. The authors studied esophageal, gastric, and gallbladder motor function in 35 type 2 (noninsulin-dependent) diabetic patients to determine the extent of gut involvement. Of these patients, 27 (77%) had peripheral neuropathy, 12 (34%) had both peripheral and autonomic neuropathy, and 22 (63%) had gastrointestinal symptoms. Esophageal manometric abnormalities were recorded in 18 patients, and delayed radionuclide emptying of the esophagus was documented in 16 patients, with a 83% concordance between the two tests. Scintigraphic gastric emptying of solids was delayed in 56% of patients, whereas gallbladder emptying after cholecystokinin stimulation was reduced in 69% of them. In 74% of patients at least one of the viscera under investigation showed abnormal motor function; however, only 36% of patients displayed involvement of the three organs. Gastrointestinal symptoms, duration and therapy of diabetes, previous poor glycemic control, and retinopathy did not correlate with the presence or the extent of motor disorders. Neuropathy was not predictive of gastrointestinal involvement and its extent; however, when motor abnormalities were present in patients with neuropathy, these were usually more severe. Gastrointestinal motor disorders are frequent and widespread in type 2 diabetics, regardless of symptoms. Autonomic neuropathy has a poor predictive value on motor disorders (0.75 for the esophagus, 0.5 for the stomach, 0.8 for the gallbladder), thus suggesting the coexistence of other pathophysiologic mechanisms.
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PMID:Gastrointestinal motor dysfunction, symptoms, and neuropathy in noninsulin-dependent (type 2) diabetes mellitus. 1047 80

Gastrointestinal symptoms in diabetic patients are commonplace, and are believed to be due, at least partly, to neuropathy of the gut. In the present study, therefore, some important neurotransmitters in the myenteric plexus were investigated in non-obese diabetic mice, an animal model of human type 1 diabetes. For this purpose, immunocytochemistry was applied on sections from antrum, duodenum and colon, subsequently quantified by computerized image analysis. Whereas the number of vasoactive intestinal peptide (VIP)-positive neurons was increased in antral myenteric ganglia of diabetic mice, there was a decreased density of nerve fibres in muscularis propria. No difference was seen in the VIP of duodenum and colon. Acetylcholine-containing nerve fibres showed an increased volume density in muscularis propria of antrum and duodenum, but a decreased density in colon of diabetic mice, as compared with controls. There was a decreased number of neurons containing nitric oxide synthase (NOS) in myenteric ganglia of antrum and duodenum. No difference was seen in density of NOS-containing nerve fibres in muscularis propria. There was no difference regarding neuropeptide Y (NPY) and galanin between diabetic and control mice; nor was there any difference between pre-diabetic NOD mice and controls regarding all bioactive substances investigated. It is concluded that the diabetic state affects the innervation of gut in this animal model. The present findings may be of some relevance to the gastrointestinal symptoms seen in patients with diabetes.
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PMID:Diabetic state affects the innervation of gut in an animal model of human type 1 diabetes. 1096 18

Gastrointestinal symptoms such as nausea and vomiting, heartburn, abdominal pain, diarrhoea, constipation and faecal incontinence are common in patients with diabetes. Diabetes gastroenteropathy is a clinically relevant problem. In addition to the increased morbidity it causes, it results in severely impaired metabolic control, which in turn increases the risk of hyper-/hypoglycaemia. Moreover, the poorly controlled blood glucose level increases the risk of secondary diabetes complications, namely, retinopathy, nephropathy, neuropathy and cardiovascular affection. Gastrointestinal symptoms may also cause malnutrition in patients with diabetes, which, together with the disturbed immune defence in diabetes, may cause intercurrent infections. Gastrointestinal symptoms in patients with diabetes are attributed to disturbed gastrointestinal motility. Gastrointestinal dysmotility in diabetes is believed to be caused by autonomic neuropathy and/or hyperglycaemia. The neuroendocrine system of the gut secretes peptides/amines that play an important role in regulating gastrointestinal motility. It is conceivable, therefore, to assume that a disturbance in this regulatory system may contribute to the pathogenesis of gastrointestinal complications in diabetes. The present review gives an updated overview of the abnormalities in the gastrointestinal neuroendocrine system in diabetes, speculates upon the possible role of these abnormalities in the pathogenesis of diabetes gastroenteropathy and, finally, predicts the possible clinical implications of these findings.
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PMID:The possible role of the gut neuroendocrine system in diabetes gastroenteropathy. 1237 Nov 43


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