Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

About one-half of patients with insulin- or non-insulin-dependent diabetes have delayed gastric emptying (diabetic gastroparesis). Some of them complain of epigastric pain, nausea, vomiting or postprandial fullness (diabetic dyspepsia), although only a minority are severely symptomatic. Diabetic gastroparesis is clinically relevant not only by virtue of the symptoms induced but also because it may contribute to inadequate glycaemic control and impaired absorption of orally administered drugs. Recent data suggest that abnormal blood glucose control, not only autonomic neuropathy, contribute to the pathogenesis of disordered gastric motility. In most cases diabetic gastroparesis is diagnosed clinically in the absence of demonstrable lesions of the upper gastrointestinal tract. To evaluate gastric emptying, scintigraphy is the 'gold standard'. Gastrokinetic drugs are of help in the treatment of gastroparesis: erythromycin is the first choice in acute presentations and cisapride for chronic symptoms. New macrolides with prokinetic action and devoid of antibacterial properties are very promising and should add another pharmacologic approach to control dyspepsia and gastroparesis in diabetic patients in the future.
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PMID:Gastroparesis and dyspepsia in patients with diabetes mellitus. 749 57

GI motility changes little--if at all--with age in healthy patients. However, a variety of diseases, including diabetes and Parkinson's disease, may cause autonomic neuropathy that is manifest as a motility disorder in the GI tract. Autonomic neuropathy can cause dysmotility in the esophagus, stomach, and gut. Symptoms are often nonspecific, including difficulty in swallowing, nausea, vomiting, heartburn, indigestion, diarrhea, and constipation. Nonpharmacologic treatment includes management of underlying diseases, avoidance of anticholinergic medications, and dietary changes. Agents with prokinetic action are the therapy of choice when drug treatment is indicated.
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PMID:GI motility disorders: diagnostic workup and use of prokinetic therapy. 790 Nov 29

Diabetic patients often suffer from symptoms arising from the gastrointestinal tract. Several factors are considered responsible for these alterations, including abnormalities of gastric motility. Recently Helicobacter pylori (HP) has been identified in a relevant aliquot of subjects with or without gastrointestinal abnormalities, but only scarce and controversial data are available on the prevalence of HP and the association between HP and chronic gastritis or peptic ulcer in diabetic patients. In addition, the possible association between alterations of gastric motility induced by autonomic neuropathy (AN) and the presence of HP has never been evaluated in diabetic subjects. In this study we document the presence of HP in the gastric biopsies of 73% out of a series of 29 patients affected by type 2 diabetes and non-ulcer dyspepsia (3 with oesophagitis, 10 with gastritis, 7 with bulbar duodenitis, and 9 with a normal endoscopy), with a significantly higher prevalence (P < 0.01) in subjects with AN (74%) than in subjects without AN (26%). Two other tests have been compared with the histological evidence of HP (used as golden standard), i.e. the urease test (CP-test) and the assay of anti-HP G-immunoglobulins, both of which were positive in a significantly (P < 0.01) higher percentage of neuropathic patients in comparison with non-neuropathic patients. The sensitivity and the specificity of the CP-test were 96% and 100%, respectively. Similarly, both the sensitivity and the specificity of the assay of IgG HP-Ab were 100%. Since patients affected by non-ulcer dyspepsia and NIDDM complicated by autonomic neuropathy are under a higher risk to be carriers of HP than non-neuropathic or non-diabetic patients. The assay of serum IgG HP-Ab could be used as a screening method, thus avoiding the more expensive and time-consuming endoscopy.
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PMID:Non-ulcer dyspepsia and Helicobacter pylori in type 2 diabetic patients: association with autonomic neuropathy. 879 6

Disordered gastric motility and emptying are well known complications of diabetes mellitus (DM), but the pattern of intragastric distribution of food has not been extensively studied in diabetics. We examined the partition of a liquid nutrient meal between the proximal and distal stomach and the relationships between intragastric distribution of food and gastric emptying (GE) and the symptoms in DM patients with and without autonomic neuropathy (AN). Fourteen healthy volunteers and 20 DM patients (13 with AN; 9 with dyspepsia symptoms) ingested a liquid nutrient meal (250 ml; 437 kcal) labeled with [99mTc]phytate. Anterior and posterior serial images of the stomach were taken for 90 min with a gamma camera. Regions of interest for the proximal and the distal halves of the stomach and for the total gastric area were defined. Counts from each region along time allowed estimation of GE and the proportion of activity retained in the proximal stomach after meal ingestion (initial) and throughout GE (mean). GE half-times in controls (median; range: 66 min; 29-90 min) were not significantly different from diabetics (76 min; 5->150 min, P > 0.10), but abnormal GE was found in 11 DM patients (seven delayed and four rapid). In DM patients, initial retention in the proximal stomach (42%; 16-79%) was significantly lower (P < 0.02) than in controls (55%; 44-71%). Mean retention in the proximal stomach throughout emptying also was significantly lower (P < 0.05) in DM patients (43%; 18-58%) than in controls (51%; 32-69%). There were no differences between subgroups of patients with normal, delayed, or rapid gastric emptying regarding mean meal retention in the proximal stomach. Patients with evidence of AN or with dyspepsia symptoms had significantly decreased retention of food in the proximal stomach throughout gastric emptying. We concluded that patients with diabetes mellitus have abnormally decreased retention of gastric contents in the proximal stomach after a liquid meal, which seems to be related to the occurrence of autonomic neuropathy and dyspepsia symptoms, but not to disordered gastric emptying.
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PMID:Abnormal intragastric distribution of a liquid nutrient meal in patients with diabetes mellitus. 969 Mar 75

A high prevalence of upper gastrointestinal symptoms is described in diabetic patients and, at least in part, this has been attributed to abnormal emptying of the stomach. In an unselected small series of dyspeptic patients with Type 2 diabetes mellitus (DM2), we previously described a higher prevalence of Helicobacter pylori (Hp) infection associated with autonomic neuropathy (AN) than in non-diabetic subjects. To evaluate the prevalence of Hp and its relationship with AN, we studied 164 DM2 patients, matched for sex, age ( +/- 5 years) and body weight ( +/- kg) to 164 non-diabetic subjects, all affected with dyspepsia of unknown origin. Results document that the prevalence of peptic ulcer is similar in both groups of patients (20.1 vs 29.3% P = n.s.); chronic gastritis was 50% in the control group and 35.4% in the DN2 group (P < 0.01) and dyspepsia without ulcer and gastritis (simple dyspepsia) was significantly more frequent in DM2 patients than in non-diabetics (44.5 vs 20.7%, P < 0.01). Hp infection was documented by histology of gastrointestinal mucosa in 74.4% of the DM2 patients and in 50% of the controls (P < 0.01) (ulcer: 97 vs 71%, P < 0.05; gastritis: 72 vs 43.5%, P < 0.05; simple dyspepsia: 66 vs 35%, P < 0.01, respectively). Autonomic neuropathy was found in 65.2% of the DM2 patients (90.9% of patients with ulcer, 65.5% with gastritis and 53.4% with simple dyspepsia). A significant concordance (84.7%, P < 0.001) was found between the presence of AN and Hp infection. Data provide, for the first time, direct evidence for a higher frequency of Hp infection in dyspeptic patients affected with DM2 than in non-diabetic subjects. In addition, in diabetic patients the frequency of non-ulcer, non-gastritis dyspepsia is two times higher than in non-diabetics and is strictly associated with autonomic neuropathy, acting as a favoring factor for occurrence and recurrence of gastrointestinal disease.
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PMID:The role of autonomic neuropathy as a risk factor of Helicobacter pylori infection in dyspeptic patients with type 2 diabetes mellitus. 988 32

Conglomerates of food and mucus or phytobezoars composed of vegetable matter are sometimes found in the stomach in the general population. Reports of phytobezoars in uremic patients are, however, scarce. Here we describe 2 uremic patients in which esophagogastroduodenoscopy was performed due to dyspepsia associated with weight loss and in which stomach phytobezoars were discovered. Theoretically, uremic patients should be at risk for producing bezoars. In fact, these patients frequently present predisposing conditions such as autonomic neuropathy, diabetes mellitus and delayed gastric emptying. Gastric bezoars cause anorexia. Anorexia is a frequent symptom in dialysis patients and is associated with malnutrition. In these patients, malnutrition is strongly associated with mortality and is quite difficult to reverse. Similarly, phytobezoars cause chronic anorexia. We suggest that clinicians working in dialysis units should consider the possibility of a gastric bezoar when evaluating anorexic uremic patients.
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PMID:Stomach phytobezoars in two uremic anorexic patients. 1186 60

Diabetic autonomic neuropathy (DAN) is a serious and common complication of diabetes. Despite its relationship to an increased risk of cardiovascular mortality and its association with multiple symptoms and impairments, the significance of DAN has not been fully appreciated. The reported prevalence of DAN varies widely depending on the cohort studied and the methods of assessment. In randomly selected cohorts of asymptomatic individuals with diabetes, approximately 20% had abnormal cardiovascular autonomic function. DAN frequently coexists with other peripheral neuropathies and other diabetic complications, but DAN may be isolated, frequently preceding the detection of other complications. Major clinical manifestations of DAN include resting tachycardia, exercise intolerance, orthostatic hypotension, constipation, gastroparesis, erectile dysfunction, sudomotor dysfunction, impaired neurovascular function, "brittle diabetes," and hypoglycemic autonomic failure. DAN may affect many organ systems throughout the body (e.g., gastrointestinal [GI], genitourinary, and cardiovascular). GI disturbances (e.g., esophageal enteropathy, gastroparesis, constipation, diarrhea, and fecal incontinence) are common, and any section of the GI tract may be affected. Gastroparesis should be suspected in individuals with erratic glucose control. Upper-GI symptoms should lead to consideration of all possible causes, including autonomic dysfunction. Whereas a radiographic gastric emptying study can definitively establish the diagnosis of gastroparesis, a reasonable approach is to exclude autonomic dysfunction and other known causes of these upper-GI symptoms. Constipation is the most common lower-GI symptom but can alternate with episodes of diarrhea. Diagnostic approaches should rule out autonomic dysfunction and the well-known causes such as neoplasia. Occasionally, anorectal manometry and other specialized tests typically performed by the gastroenterologist may be helpful. DAN is also associated with genitourinary tract disturbances including bladder and/or sexual dysfunction. Evaluation of bladder dysfunction should be performed for individuals with diabetes who have recurrent urinary tract infections, pyelonephritis, incontinence, or a palpable bladder. Specialized assessment of bladder dysfunction will typically be performed by a urologist. In men, DAN may cause loss of penile erection and/or retrograde ejaculation. A complete workup for erectile dysfunction in men should include history (medical and sexual); psychological evaluation; hormone levels; measurement of nocturnal penile tumescence; tests to assess penile, pelvic, and spinal nerve function; cardiovascular autonomic function tests; and measurement of penile and brachial blood pressure. Neurovascular dysfunction resulting from DAN contributes to a wide spectrum of clinical disorders including erectile dysfunction, loss of skin integrity, and abnormal vascular reflexes. Disruption of microvascular skin blood flow and sudomotor function may be among the earliest manifestations of DAN and lead to dry skin, loss of sweating, and the development of fissures and cracks that allow microorganisms to enter. These changes ultimately contribute to the development of ulcers, gangrene, and limb loss. Various aspects of neurovascular function can be evaluated with specialized tests, but generally these have not been well standardized and have limited clinical utility. Cardiovascular autonomic neuropathy (CAN) is the most studied and clinically important form of DAN. Meta-analyses of published data demonstrate that reduced cardiovascular autonomic function as measured by heart rate variability (HRV) is strongly (i.e., relative risk is doubled) associated with an increased risk of silent myocardial ischemia and mortality. The determination of the presence of CAN is usually based on a battery of autonomic function tests rather than just on one test. Proceedings from a consensus conference in 1992 recommended that three tests (R-R variation, Valsalva maneuver, and postural blood pressure testing)or longitudinal testing of the cardiovascular autonomic system. Other forms of autonomic neuropathy can be evaluated with specialized tests, but these are less standardized and less available than commonly used tests of cardiovascular autonomic function, which quantify loss of HRV. Interpretability of serial HRV testing requires accurate, precise, and reproducible procedures that use established physiological maneuvers. The battery of three recommended tests for assessing CAN is readily performed in the average clinic, hospital, or diagnostic center with the use of available technology. Measurement of HRV at the time of diagnosis of type 2 diabetes and within 5 years after diagnosis of type 1 diabetes (unless an individual has symptoms suggestive of autonomic dysfunction earlier) serves to establish a baseline, with which 1-year interval tests can be compared. Regular HRV testing provides early detection and thereby promotes timely diagnostic and therapeutic interventions. HRV testing may also facilitate differential diagnosis and the attribution of symptoms (e.g., erectile dysfunction, dyspepsia, and dizziness) to autonomic dysfunction. Finally, knowledge of early autonomic dysfunction can encourage patient and physician to improve metabolic control and to use therapies such as ACE inhibitors and beta-blockers, proven to be effective for patients with CAN.
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PMID:Diabetic autonomic neuropathy. 1271 21

The 13C-octanoic acid breath test is considered a useful tool to measure gastric emptying both in physiological and pathological conditions. Many studies have concerned functional dyspepsia. Recently, breath test has been used in predicting a delayed gastric emptying in subsets of dyspeptic symptoms. In detail only postprandial fullness and vomiting are resulted significantly correlated with delayed solid emptying. Besides in the patients with dyspepsia and irritable bowel syndrome associated, intestinal disturbances did not seem to contribute to delay gastric emptying. In diabetic patients octanoate test has confirmed the percentages of delayed emptying obtained by means of scintigraphy. In other organic states (celiac disease, cirrhosis, renal failure, neurological disease, etc) most of reports have proved a delayed emptying of solids. In GERD and ulcer disease gastric function is resulted normal, being accelerated in distal gastrectomy and in hyperemesis gravidarum. From pathophysiological point of view Helicobacter pylori, extrinsic autonomic neuropathy (apart from diabetes) and autoimmunity do not seem to relate with gastric emptying, both in functional and organic disease.
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PMID:13C-octanoic acid breath test in functional and organic disease: critical review of literature. 1645 24

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. 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. 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. Gastroparesis can markedly impair quality of life, and up to 50% of patients have significant anxiety and/or depression. Often the distinction between dyspepsia and gastroparesis is based on clinical judgement rather than established criteria. Hyperglycemia, autonomic neuropathy, and enteric neuromuscular inflammation and injury are implicated in the pathogenesis of delayed GE. Alternatively, there are limited data to suggest that delayed GE may affect glycemic control. The management of diabetic gastroparesis is guided by the severity of symptoms, the magnitude of delayed GE, and the nutritional status. Initial options include dietary modifications, supplemental oral nutrition, and antiemetic and prokinetic medications. Patients with more severe symptoms may require a venting gastrostomy or jejunostomy and/or gastric electrical stimulation. Promising newer therapeutic approaches include ghrelin receptor agonists and selective 5-hydroxytryptamine receptor agonists.
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PMID:Diabetic Gastroparesis. 3108 77