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)

1. Hypoxic and hypercapnic ventilatory drives were measured in eight healthy male subjects before and after ingestion of ethanol, in a dose of 17 mmol/kg body weight. 2. A significant decrease in hypoxic ventilatory drive was observed at 20 min after ethanol (P less than 0.05). A significant depression in hypercapnic drive was observed at 70 min after indigestion of ethanol (P less than 0.05). The mean peak blood ethanol (24mmol/1) occurred at 20 min, at which time the lowest mean hypoxic drive was recorded. 3. Ethanol in moderate doses produced a depression of both hypoxic and hypercapnic ventilatory drives in normal subjects. This suggests that ethanol may play a role in the precipitation of acute respiratory failure in certain patients in whom the ventilatory drive is already impaired, as in chronic airways obstruction.
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PMID:Effect of ethanol on the ventilatory responses to oxygen and carbon dioxide in man. 114 93

The microbial flora and some of its metabolites and enzymes in the stomach were compared in patients with achlorhydria, pernicious anaemia, and primary hypogammaglobulinaemia and in patients with dyspepsia with normal gastric acidity. Detailed analysis of the flora of the gastric juice and of the mucosa from the antrum, body, and fundus in six patients with hypogammaglobulinaemia (mean pH 8.2), seven patients with pernicious anaemia (mean pH 7.3), and five patients with dyspepsia (mean pH 1.9) yielded 22 different genera of bacteria, mainly from the patients with achlorhydria, the most common being streptococci, micrococci, staphylococci, veillonella, and lactobacilli. A similar flora was found associated with the mucosa at all three sites. Various metabolites were also looked for. beta Glucoronidase and C14 lipase were found in patients with hypogammaglobulinaemia but not in those with pernicious anaemia or dyspepsia. Volatile fatty acids were not found. Relatively high concentrations of ethanol were found in the patients with hypogammaglobulinaemia compared with those with pernicious anaemia (p = 0.02). Similar concentrations of dimethylamine were found in all three groups, but the concentrations of trimethylamine were much higher in patients with pernicious anaemia and hypogammaglobulinaemia. The high concentrations of some microbial enzymes and ethanol differentiated the group with hypogammaglobulinaemia from the rest, and these may bear some relation to the high incidence of gastric cancer in patients with hypogammaglobulinaemia.
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PMID:Microbial and metabolic profile of achlorhydric stomach: comparison of pernicious anaemia and hypogammaglobulinaemia. 403 Nov 6

Reviewing medical and epidemiological reports, no definite clinical picture could be expected as a result of a low DMF exposure and experimental research on long term toxicity has always demonstrated some adverse effects but has not been sufficient to define a no-effect level in animals. This study was designed to assess the specificity of symptoms and the relevance of adverse effects as consequence of an exposure to airborne DMF concentration in the range of the present TLV (30 mg/m3 - 10 ppm). For this purpose 100 DMF-exposed workers, with homogeneous characteristics, were compared with 100 matched controls. Both groups were selected by a careful pair-matching. Mean DMF exposure was 22 mg/m3 (range 8-58 mg/m3). Exposed subjects and their matched controls were evaluated clinically and a questionnaire was used for the registration and the comparison of subjective complaints. A laboratory assessment was performed, including transaminase and gamma-glutamyl transpeptidase. Statistical analysis was based on McNemar Test procedure. The problem of dietary alcohol intake was particularly investigated. Among symptoms studied, headache, dyspepsia and digestive impairment of hepatic type could be specifically associated with chronic DMF exposure and increased levels of gamma-GT demonstrated minimal hepato-cellular damage, even without ethanol dietary intake. No chronic sickness was diagnosed and the disturbances observed are better considered as indicators of malaise and discomfort due to a toxic effect of DMF, whose consequences are discussed.
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PMID:Epidemiological study on workers exposed to low dimethylformamide concentrations. 653 79

In reviewing the literature we discussed the problem, whether there is a correspondence between the morphological picture of acute gastritis and the clinical expression including a complex of symptoms "acute gastritis", which should better be called acute dyspepsia. There is no good accord.--The histological main features of acute gastritis are infiltration of mucosa by neutrophils and the leucodiapedesis. this acute gastritis is very seldom the cause of clinical symptoms of acute dyspepsia. Alcohol, spices or drugs may produce a "toxic damage" of the mucosa, but they do not cause an acute gastritis, just as little as some viral diseases or staphylococcal toxins.
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PMID:[On acute gastritis (author's transl)]. 701 84

The frequency of Helocobacter pylori (Hp.) infection and active chronic antral gastritis among people with excessive alcohol consumption is not known. A high alcohol intake regularly causes acute gastroduodenitis. In this study, the prevalence of Hp. infection and active chronic antral gastritis in alcoholics compared with nonalcoholic controls was studied. Further, the frequency of gastrointestinal symptoms was registered. Diagnostic methods for Hp. were compared. Twenty-four alcoholics admitted to the hospital for detoxification underwent upper gastrointestinal endoscopy regardless of symptoms. Twelve individuals admitted to upper endoscopy mainly for dyspepsia, with low alcohol consumption and without gross pathology by upper endoscopy, were chosen as controls. Three diagnostic methods for Hp. were used: culture, direct microscopy, and histology. Hp. infection was found in 7 of the 24 alcoholics (29%) according to culture. In controls, 4 of 12 (33%) had a positive Hp. culture. In the alcoholic group, culture was more sensitive than histology. There was a good correlation between the different diagnostic methods in the control group. Histologically active chronic antral gastritis was found in 6 of the alcoholics (25%) and in 5 of the controls (42%). Five of the 7 Hp.-positive alcoholics and all of the Hp.-positive controls had an active chronic antral gastritis. Hp. infection is not more frequent in alcoholics than in controls. In both groups, there was a good correlation between Hp. infection and histologically, active chronic antral gastritis.
Alcohol Clin Exp Res 1994 Aug
PMID:Helicobacter pylori, active chronic antral gastritis, and gastrointestinal symptoms in alcoholics. 797

Alternations of stomach mucose caused by ethanol are in direct correlation with its concentration. ADH in stomach mucose is an efficient barrier against ethanol system toxicity. It stimulates higher secretion of HC1, dilutes protective barrier of mucose and phospholipids in membranes. Inflammatory reaction also participates in the damage of stomach mucose, with a share of products of arachidonic metabolism and free radicals. After ethanol administration the pancreas blood circulation diminishes and resistance in microcirculation increases. This can cause necroses in periphery of lobules. Activated phospholipase C may result in hypersecretion of Ca2+ dependent proteinkinases. Ischemic changes participate in alcohol impairment of pancreas and increase its vulnerability to enzyme attract and free radical reactions. Ethanol excesses may result in diarrhoea, dyspepsia, malnutrition and cause morphologic alternations of intestinal mucose (erosion, hemorrhagia). Absorption of nutrients and vitamins is affected by inhibition of active transport or by decrease of enzyme activity. Ethanol increases mucose permeability, alteres intestinal motility and damages absorption of water and electrolytes. In chronic alcoholics lower villi and changes in bacterial flora are described. The following mechanism of ethanol caused liver injury are observed: acetaldehyde toxicity, change in NAD+/NADH ratio connected with acidosis, cytoskeletal impairment, inhibition of protein synthesis and their secretion, relative perivenular hypoxia, activation of fibrogenesis, increased formation of free radicals with lipid peroxidation and immunological reaction. In hepatocyte there are morphological changes (megamitochondria, etc.) and functional changes (inhibition of glycolysis, inhibition of Krebs cycle and beta oxidation of fatty acids). Ethanol intake activates leukocytes, trombocytes, endothelial and Kupffer cells and their mediators, which result in increase of collagen and proteoglycans synthesis furthermore in fibrotic changes in liver.
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PMID:[Ethanol metabolism and pathobiochemistry of organ damage--1992. III. Mechanisms of damage to the gastrointestinal tract and the liver by ethanol]. 799 16

It's known that some psychologic factors could be implicated in dyspepsia. Therefore, the psychologic aspects of 38 dyspeptic patients (17 males, 21 females, aged 18-65 years), who underwent digestive endoscopy, were evaluated by means of Rorschach and MMPI test. Patients with previous peptic ulcer history, with chronic ethanol or NSAID intake, operated on digestive tract and patients with behavioural problems were excluded. The results of psychological tests enhanced two main groups: anxiety patterns (17 patients--49%) and normal patterns (21 patients--55%). Endoscopic and histological findings moreover showed: "anxious" group--12 patients with chronic gastritis (HP+ 50%), 5 patients with normal endoscopy; "normal" group--16 patients with chronic gastritis (HP+ 87.5%), 5 patients with normal endoscopy. This study suggests that in about 50% of dyspeptic patients anxious pattern is present. Moreover chronic gastritis is more frequently associated to Helicobacter pylori in non-anxious patients.
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PMID:[The psychological characteristics of dyspepsia. A controlled study with gastroscopic follow-up]. 820 2

The intake of larger quantities of alcoholic beverages leads to manifold functional disturbances and organ injury in the upper gastrointestinal tract. These damaging effects of alcohol are frequently the cause of complaints, such as heart burn, symptoms of dyspepsia and diarrhoea. Examples of more pronounced organ injury which can occur even following a single episode of heavy drinking are tears in the mucosa at the junction of the esophagus and the stomach (Mallory-Weiss-lesion) and hemorrhagic erosions in the stomach and/or the duodenum which may lead to massive bleeding. In the small intestine alcohol abuse interferes with the absorption of glucose, amino acids, lipids, water, sodium and vitamins (especially thiamine and folic acid). This inhibition of absorption of nutrients may contribute to nutritional deficiencies frequently observed in alcoholics. Acute alcohol ingestion can also damage the mucosa in the upper region of the small intestine and may lead to the disruption of the tips of the villi. Chronic alcohol abuse increases markedly the prevalence of bacterial overgrowth in the small intestine. The findings of human and animal studies suggest that the mucosal injury together with bacterial overgrowth favour the following sequence of events: Alcohol induced mucosal injury in the small intestine increases the permeability of the mucosa to macromolecules, such as endotoxin and/or other bacterial toxins, into the blood or lymph. This results in the release of potentially toxic cytokines and other mediators like Kupfer cells and other phagocytes. These cytokines and other mediators, in turn, exert multiple injurious effects on the microcirculation and membranes. The result is cell damage and even cell death (apoptosis, necrosis) in the liver and other organs. Chronic alcohol abuse is one of the most important risk factors for the development of cancers of the tongue, larynx, pharynx and esophagus. In many countries alcohol abuse is the most important cause for the development of chronic pancreatitis. In the initial phase the disease is frequently characterised by episodes of 'acute' pancreatitis. These episodes develop only on the basis of prolonged alcohol abuse leading to subclinical damage of the gland. The latter is found in about 20-50% of patients with chronic alcohol abuse while the clinically overt pancreatitis is observed in only 1%-3% of alcoholics. Despite numerous studies performed in animal experiments and man the pathogenesis of alcoholic pancreatitis until now has not been clarified.
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PMID:[Alcohol, the gastrointestinal tract and pancreas]. 1080 79

Previous studies have shown that patients with chronic alcohol ingestion may show a variety of morphological and functional alterations in the small intestine. In this study, we have focused on the neuroendocrine system in the duodenal mucosa in chronic alcoholics; an area little studied. Twenty-three defined chronic alcoholics admitted to the hospital for detoxification underwent clinical examination, followed by upper gastrointestinal endoscopy and blood tests on average 4 days after the most recent alcohol intake. Biopsy specimens were taken from the distal part of the descending duodenum for both immunohistochemical and routine histological examination. The control group consisted of 25 patients referred for upper endoscopy mainly because of dyspepsia (ulcer, reflux type), but who were otherwise healthy. A normal carbohydrate-deficient transferrin and a history of low alcohol consumption (<40 g/week) were required for inclusion in the control group. The tissue specimens were studied using antisera for the following neuropeptides: cholecystokinin, galanin, gastric inhibitory peptide (GIP), glucagon, motilin, neuropeptide Y, pituitary adenylyl cyclase activating peptide, secretin, serotonin, somatostatin, substance P, vasoactive intestinal polypeptide and protein gene product, as a general marker for neurones and cells of the diffuse neuroendocrine system. The density of nerve fibres was evaluated semi-quantitatively and the number of endocrine cells per unit length of mucosa was counted in sections cut perpendicularly to the mucosal surface. All the different peptidergic nerve fibres in the alcohol group showed higher densities than the corresponding controls. However, this was not a statistically significant difference. A slightly significant increase (P = 0.02) in the numbers of glucagon and GIP cells was seen in the alcohol group. Gastrointestinal symptoms were frequently present (87%) in chronic alcoholics. We suggest that chronic alcohol consumption in man may have a general effect on the peptidergic nerve system and some endocrine cell types in the duodenal mucosa.
Alcohol Alcohol
PMID:Neuropeptides in the duodenal mucosa of chronic alcoholic heavy drinkers. 1137 57

A neutral volatile substance in ruminal contents from sheep suffering from acute indigestion due to overfeeding has been identified as ethanol. Ethanol was consistently observed in ruminal material from both cattle and sheep after they had been fed large amounts of readily fermentable carbohydrate.
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PMID:ETHANOL ACCUMULATION IN THE RUMEN AFTER OVERFEEDING WITH READILY FERMENTABLE CARBOHYDRATE. 1410 63


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