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)

In children with vomiting, dyspepsia, and feeding problems, gastroesophageal reflux (GOR) and altered gastric emptying are common. We have used electrical impedance tomography (EIT) to study children with suspected gastric emptying disorders. Abnormalities of the gastric emptying curve suggestive of GOR were seen in some, with marked negative or positive shifts related to sharp increases or decreases in intragastric resistance. These findings could represent fluid leaving or entering the stomach, as might occur in GOR. To confirm the origin of the abnormal EIT curves, we devised and in vitro tank test system, and we performed simultaneous 2-h EIT and intraoesophageal pH monitoring after a glucose meal on six patients. In vitro, reflux of > or = 25 ml produced clearly detectable changes on the emptying curves. In vivo, the overall correlation between the times of 42 GOR episodes lasting > or = 1 min detected by pH study and the times of 38 negative peaks due to > or = 15% changes of the maximum intragastric resistivity detected by simultaneous EIT was significant; the correlation was highly significant in four of six patients. When the peaks were used to define GOR episodes on EIT gastric emptying curves, the two methods still showed good agreement. Retrospective examination of 50 patients who had undergone both EIT and 24-h intraoesophageal pH study during their diagnostic workup showed that EIT had a sensitivity of 94.6% and a specificity of 76.9% (with positive and negative predictive values of 0.92 and 0.83, respectively) for the detection of pathological GOR.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Detection of gastroesophageal reflux by electrical impedance tomography. 801 69

Dehydrocholic acid (Biliton) was given to 9 cows with a predisposition for the fat mobilization syndrome in daily doses of 5.5 g each. This was done two weeks after parturition and the results were compared with those from 9 untreated cows. Five other cows suffering from ketosis or indigestion symptoms were treated too. Decreased concentrations of liver lipids, free fatty acids (FFA), bilirubin, beta-OH-butyrate and urea as well as increased glucose in blood plasma indicated a favourable action of Dehydrocholic acid on metabolism and liver function. We did not observe a significant influence on milk and reproduction parameters. The use of Dehydrocholic acid is recommended for use in liver disturbances.
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PMID:[Effects of dehydrocholic acid (Biliton) on metabolism and liver function in cows]. 822 42

The effect of coffee on gastric emptying was addressed in a scintigraphic liquid-phase gastric emptying study in patients with non-ulcer dyspepsia. Ninety-three subjects (56 males, 37 females; mean age 40 years, range 17-77 years) diagnosed as having non-ulcer dyspepsia were enrolled in the study. The baseline study was to drink 500 ml of 5% glucose water and the coffee study was to drink 500 ml of 5% glucose water containing 4 g of regular instant coffee. The two studies were performed on separate days. Fifteen of the 93 subjects were chosen at random to undergo repeated coffee studies for evaluation of reproducibility. Overall the 93 subjects showed accelerated gastric emptying, as measured by half emptying time (T1/2) with coffee compared with baseline (35.7 +/- 10.5 vs 45.0 +/- 23.1 min, P < 0.001). However, 68 (73.2%) subjects showed accelerated emptying (-14.8 +/- 19.5 min), while 25 (26.8%) subjects showed delayed emptying (5.9 +/- 4.5 min) after ingestion of coffee. There was no significant difference in the change in gastric emptying with coffee in duplicate measurements from the 15 subjects who had two coffee studies (P = 0.082). We conclude that coffee accelerates liquid-phase gastric emptying in the majority of patients with non-ulcer dyspepsia.
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PMID:The effect of coffee on gastric emptying. 858 58

Dyslipidaemia may be treated with a number of safe and effective pharmacological agents that target specific lipid disorders through a variety of mechanisms. The bile-acid sequestrants--cholestyramine and colestipol--primarily decrease LDL cholesterol by binding bile acids, thereby decreasing intrahepatic cholesterol, and by increasing the activity of LDL receptors. Nicotinic acid lowers LDL cholesterol and triglyceride by decreasing VLDL synthesis and by decreasing free fatty acid mobilization from peripheral adipocytes. The HMG-CoA reductase inhibitors--fluvastatin, lovastatin, pravastatin and simvastatin--lower LDL cholesterol by partially inhibiting HMG-CoA reductase (the rate-limiting enzyme of cholesterol biosynthesis) and by increasing the activity of LDL receptors. The fibric-acid derivatives--bezafibrate, ciprofibrate, clofibrate, fenofibrate and gemfibrozil--primarily decrease triglyceride by increasing lipoprotein lipase activity and by decreasing the release of free fatty acids from peripheral adipose tissue. Probucol decreases LDL cholesterol by increasing non-receptor-mediated LDL clearance; as an anti-oxidant, probucol also decreases LDL oxidation; oxidized LDL which is thought to lead to atherogenesis. Although these agents have been proven safe in clinical trials, like any drug, they carry the risk for adverse effects. The bile-acid sequestrants may cause constipation, reflux oesophagitis, and dyspepsia, and may bind coadministered medications such as digitalis glycosides, beta blockers, warfarin, and exogenous thyroid hormone. Nicotinic acid use is commonly associated with flushing and pruritus and may also cause non-specific gastrointestinal complaints, hepatotoxicity (hepatic necrosis, hepatitis, or elevated liver enzymes), gout, myolysis, decreased glucose tolerance and increased fasting glucose levels, and ophthalmological complications including decreased visual acuity, toxic amblyopia, and cystic maculopathy. The HMG-CoA reductase inhibitors may produce liver enzyme elevations, creatine kinase elevations and rhabdomyolysis. The combination of a reductase inhibitor and a fibrate increases the risk for rhabdomyolysis. Possible adverse effects of the fibric-acid derivatives include abdominal discomfort, nausea, flatulence, increased lithogenicity of bile, liver enzyme elevations and creatine kinase elevations. Probucol may increase the QTc interval and may cause non-specific gastrointestinal complaints.
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PMID:Currently available hypolipidaemic drugs and future therapeutic developments. 859 27

The aim of this work was to ascertain if diabetes and obesity can affect gastric colonization by Helicobacter pylori. 59 hospitalized subjects with dyspepsia and endoscopic antral gastritis were selected. They were divided into three groups: I) 13 patients with normal body weight and without disease other than gastritis (control group); II) 15 patients with essential obesity of whom 10 had impaired glucose tolerance (IGT); III) 31 patients with type II diabetes mellitus, of whom 14 were obese. Three gastric biopsies were obtained from each patient for histologic examination and H. pylori detection by means of rapid urea test, culture and histological evidence of Helicobacter-Like Organisms (HLO). Age, sex, blood glucose, cholesterol, triglycerides, HDL-cholesterol, basal gastrine, duration of illness, body weight were statistically analysed. Differences between the three groups were not statistically significant. There was a higher prevalence of H. pylori infection both in obese and in diabetic patients with respect to control subjects. Prevalence became still higher in obese patients with impaired glucose tolerance. Among the three tests used for the detection of H. pylori, culture and rapid urea were reliable and specific, while the histologic test was highly sensitive but barely specific. Our data suggest that both obesity and type II diabetes may be associated with an increased incidence of H. pylori-colonization. This could be related to the reduced gastric motility observed in both pathologies and chemical changes in gastric mucosa following non-enzymatic glycosylation processes.
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PMID:Gastric infection by Helicobacter pylori and antral gastritis in hyperglycemic obese and in diabetic subjects. 872 11

The factors influencing appetite in humans are poorly understood. There is a weak relation between appetite and gastric emptying in normal subjects. Recent studies have shown that fasting and postprandial antral areas increase in patients with functional dyspepsia compared with normal subjects. We evaluated the hypothesis that antral area, and hence antral distention, is a significant determinant of postprandial fullness. Fourteen normal subjects had simultaneous measurements of gastric emptying by scintigraphy and antral area by ultrasound after ingestion of 350 mL 20% glucose. Fullness and hunger were assessed by visual analog scales. Measurements of the gastric-emptying half time (t1/2) by scintigraphy and ultrasound were not significantly different (129.6 +/- 11.8 min compared with 115.6 +/- 11.4 min). Fullness increased (P < 0.001) and hunger decreased (P < 0.001) after the drink. Both fullness and the magnitude of the increase in fullness after the drink were related to antral area (r > 0.56, P < 0.05), the increase in antral area (r > 0.59, P < 0.05), and the scintigraphic content of the distal stomach (r > 0.57, P < 0.05), but not to the ultrasound or scintigraphic t1/2 values. In contrast, hunger and the magnitude of the decrease in hunger after the drink were not related to either antral area, the increase in antral area, or the rate of gastric emptying. We conclude that postprandial fullness, but not hunger, was closely related to antral distention in normal subjects.
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PMID:Relation between postprandial satiation and antral area in normal subjects. 920 80

The aim of this study was to study sugar maldigestion/malabsorption in patients with functional dyspepsia using H2 breath testing. End-expiratory breath H2 after separate challenges with lactose (25 g), fructose (25 g), and sorbitol (5 g) were used to determine malabsorption, as well as small bowel transit time (SBTT). Five hundred twenty patients with functional dyspepsia received all three challenges. Smaller groups were also tested after lactulose (10 g, N = 36) and glucose (50 g, N = 90) challenges. Fructose and sorbitol were closely linked with respect to absorption and malabsorption status. Only in the case of lactose maldigestion/malabsorption was there a greater than random prevalence of malabsorption (P < 0.001) for fructose and sorbitol. In contrast to lactose, ethnic origin did not influence fructose or sorbitol malabsorption, and females predominated among fructose and sorbitol malabsorbers. In Jews, the prevalence of lactose maldigestion/malabsorption decreased in the age group of 25-55 and subsequently rose after 55, while fructose and sorbitol malabsorption decreased progressively with advancing age. With respect to small bowel transit time (SBTT), in the case of sorbitol and lactulose, it was significantly greater (P < 0.05) than those for fructose and lactose. Multiple sugar malabsorptions are common when lactose maldigestion/malabsorption is present.
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PMID:Fructose and sorbitol malabsorption in ambulatory patients with functional dyspepsia: comparison with lactose maldigestion/malabsorption. 944 Jun 43

The purpose of this investigation was to study the metabolic situation in clinical cases of bovine ketosis and to diagnose additional diseases. Extensive clinical examination, clinical biochemistry, haematology and fine-needle aspiration biopsy of liver was performed on 17 ketotic and eight control dairy cows in the field, and on seven hospitalized hyperketonaemic fatty liver patients. Additional findings in the ketotic group were heat (n = 7), indigestion (n = 5), endometritis (n = 2), cystic ovaries (n = 1), and mastitis (n = 1), and in the fatty liver group displaced abomasum (n = 4), abomasal ulcers (n = 3), mastitis (n = 2), laminitis (n = 1), bronchopneumonia (n = 1), and hypomagnesaemia (n = 2). There were no additional findings in the control group. Aspartate aminotransferase (AST) and creatine kinase (CK) were elevated in the ketosis and fatty liver groups. Total bilirubin, gamma-glutamyl transferase (GGT) and glutamate dehydrogenase (GD) were elevated in the fatty liver group and in some animals in the ketosis group. Total bile acid was not different between the groups. The free fatty acid/cholesterol ratio was higher in the fatty liver group compared with the control and ketosis groups. There was no or only slight fatty degeneration of the liver cells in the control and ketosis groups. Glucose and insulin preinjection concentrations and changes from basal values after glucagon injection were significantly lower in the ketosis group if compared with the control group. The responses in the fatty liver animals after glucagon injection were more heterogeneous than in the control and ketosis animals, a sign of disturbance in the metabolic adaptation, which together with high free fatty acid (FFA) levels can lead to fatty liver in cows with concurrent diseases.
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PMID:Glucose and insulin responses to glucagon injection in dairy cows with ketosis and fatty liver. 946 72

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

As part of a symposium on laboratory medicine, a colloquium on point-of-care testing was held in June 1999 where four experts were invited to produce recommendations and opinions on the use of point-of-care testing under various clinical venues. Each commented on costs for providing POCT services. A total of eleven recommendations and four opinions were rendered and discussed in an open forum. While one expert concluded that some forms of POCT are less expensive than central laboratory testing if entire laboratory workstations are eliminated, another expert suggested that POCT offered little advantage if rapid transport systems are available. A recommendation was made that POCT be considered for analytes that have a required reporting turnaround time of <30 min, and that the goals for precision and accuracy should be dictated by the clinical need and not by analytical limitations. Recommendations for POCT in specific clinical situations include use of glycated hemoglobin and urine albumin testing with personal glucose monitoring at the time of consultation, use of glycated albumin for gestational diabetes, leukocyte esterase and nitrite testing in urine to screen for urinary tract infections, coagulation tests for monitoring patients on oral anticoagulant therapy and in the operating room, testing for H. pylori for patients with dyspepsia, and cardiac markers and urine drugs-of-abuse testing in the emergency department.
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PMID:Recommendations and opinions for the use of point-of-care testing for hospitals and primary care: summary of a 1999 symposium. 1116 17


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