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Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two urease-based tests--the urease slide test and the radiolabeled urea breath test, are commonly used for the diagnosis of Helicobacter pylori infection of the stomach. The reliability of these tests in chronic uremia was compared with serological tests for H pylori antibodies, and with direct detection of the organism by microscopy or culture of gastric antral biopsies. Twenty-seven patients with chronic renal failure and dyspepsia underwent upper gastrointestinal endoscopy. Twelve of these patients (46%) were judged to be infected with H pylori on the basis of identification of the organism on microscopy or culture of antral biopsy. Both urease-based tests were able to determine H pylori status, despite the markedly increased concentrations of urea in the gastric juice found in chronic renal failure. The urease slide test performed on antral biopsies obtained at endoscopy proved reliable in determining H pylori status with no false-positive nor false-negative results after 20 minutes and 24 hours of incubation. The 14C-urea breath test also differentiated the infected from the uninfected patients. The 20-minute 14CO2 excretion (kg %dose/mmol CO2 x 100) ranged from 50 to 834 in the H pylori-infected patients, compared with 0.3 to 27 in the H pylori-noninfected patients (P < 0.0001); the 90-minute values ranged from 88 to 398 in the former, compared with 1 to 79 in the latter (P < 0.0001). The excretion of 14CO2 (derived from bacterial hydrolysis of ingested 14C-urea) was higher in all the uremic patients compared with nonuremic controls, and in half of the H pylori-noninfected uremic patients there was a late increase in 14CO2 excretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The diagnosis of Helicobacter pylori infection in uremic patients. 146 85

Dietary fat has a less prominent role in realimentation than the alternate source of energy, carbohydrate. Presently available therapeutic diets, in typical feeding routines, provide only 3 to 120 g of fat per day. Three major factors contribute to fat underutilization: long-standing belief that fat is to blame for various vague symptoms of indigestion, misconception that daily fecal fat in excess of 7 g represents bowel dysfunction, and fear of fat-induced atherogenesis. None of these apply to refeeding starved and malnourished patients. The small intestine has a vastly underutilized capacity for fat absorption, and at the habitual fat intake of 100 g per day absorption is complete in the proximal one fifth of the gut. In patients requiring vigorous realimentation, the remaining small intestine should also be utilized. Dietary fat is well tolerated, and daily intakes of 500 g of polyunsaturated fat in a complete diet have not been associated with important side effects, while there was a significant improvement in body stores of fat and protein. Compared to diets high in carbohydrate, adequate intake of fat results in better nutrient utilization, less CO2 production and decreased lipogenesis and insulin requirements. Diets higher in fat are also better tolerated because of their lower volume and osmolality. The result is more effective absorption of calories and a faster nutritional recovery. Increased adipose tissue and protein reserve benefits patients who are in stress, immunocompromised, or debilitated. Adequate dietary fat should be considered for malnourished subjects with intact gastrointestinal function, and when intestinal absorptive capacity is reduced by surgery or disease.
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PMID:How much dietary fat in therapeutic nutrition? 219 11

14C-urea breath test was used to detect Campylobacter pylori colonisation in 129 consecutive non-ulcer dyspepsia patients. Fasting patients were given 3 microCi (110 kBq) of 14C-labelled urea after a test meal. Breath samples were collected at 10 minute intervals for 90 minutes and the C-14 activity was counted on a liquid scintillation analyser. Urea derived 14CO2 appears in the exhaled breath of Campylobacter pylori culture positive individuals within 20-30 minutes. Likelihood analysis revealed a most favourable cut off level of [0.07% dose 14C-urea/mmol CO2] multiplied by body weight at t = 40 minutes, to separate culture positive from culture negative subjects. Using this upper limit of normal, a positive likelihood ratio of 50 and a negative likelihood ratio of 0.05 was calculated. Sensitivity of the test was 95% and specificity 98%. The 14C-urea breath test is a simple, sensitive and non-invasive test, that detects viable C pylori microorganism and semiquantitatively assesses the bacterial load of C pylori colonisation. Administration of a single dose of colloidal bismuth subcitrate resulted in a rapid decrease in 14CO2 excretion, so this test can be used to confirm eradication of the bacterium in therapeutic trials without endoscopy, or need for culture.
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PMID:14C-urea breath test in C pylori gastritis. 259 50

Blood and urine acid-base parameters were investigated in 4 heifers with acid indigestion produced by intraruminal infusion of sugar in a dose of 12 g/kg b.wt. Observations were carried out for 9 days after sugar administration. It was found that rumen acidosis was accompanied by disturbances in blood acid-base balance characteristic of partially compensated metabolic acidosis. The most pronounced changes in acid-base parameters were observed within the first 24 hours after sugar infusion, i.e. during rapid increase of lactic acid levels in blood. These changes were reflected by a decrease of blood pH values to 7.138-7.275 reduction in standard bicarbonate to 12.2-17.0 mmol/l and deficiency in base excess ranging from 9.3 to 16.7 mmol/l. The maximum reduction in partial pressure of CO2 to 4.35-4.79 kPa occurred during the second day of the experiment. The duration of acid-base disturbances depended on their intensity in individual animals and oscillated between 4 and 9 days after sugar administration. When acidosis subsided, acid-base balance returned to normal or showed a tendency toward blood alkalization. The observed decrease of pH values in urine to 5.42-5.74 and renal acid excretion from 170 to 299 mmol/l indicate a significant role of kidney function in the correction of metabolic acidosis.
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PMID:[Acid-base equilibrium in experimental acid indigestion in cattle]. 382 57

Ingestion of sodium bicarbonate has been implicated as one of the proximate causes of spontaneous gastric rupture. However, the volume and rate of gas released from the reaction of ingested sodium bicarbonate and gastric acid has not been previously studied in detail. We, therefore, developed an in vitro method for measuring gas release after addition of sodium bicarbonate to a solution containing hydrochloric acid. From the results of our studies, we conclude that even though hydrochloric acid and sodium bicarbonate react instantaneously, the resulting gas production is slow, mainly because CO2 produced from the dehydration of carbonic acid dissolves in water and is only slowly released into the gas phase. The major exogenous factors that determine the rate of gas release are the volume of the solution, the quantity of reactants, the air volume over the reaction mixture, the partial pressure of CO2 of the acid solution before the addition of bicarbonate, and the stirring rate. The presence of food, alcohol, and carbonic anhydrase had relatively little if any effect. Based on our results, we believe that ingestion of the recommended dose of sodium bicarbonate (one-half teaspoon) would result in only small amounts of sudden gas release, probably not enough to be an important factor in causing spontaneous gastric rupture. On the other hand, we measured the amount of sodium bicarbonate that people actually select to take for indigestion, and all exceeded the recommended dose. Some people selected doses of bicarbonate that would result in several hundred milliliters of gas release within 3 min; it seems likely that such injudicious ingestion of sodium bicarbonate, if taken when the stomach was distended with air, food, and liquid, could be an important factor in spontaneous gastric rupture.
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PMID:Gas production after reaction of sodium bicarbonate and hydrochloric acid. 609 Feb 55

Recently many reports have shown a strong association between Helicobacter pylori infection in the stomach and recurrent peptic ulcer. Moreover, prospective cohort serological studies showed that H. pylori infected individuals have significantly increased rate of gastric cancer in the USA. H. pylori is a gram-negative spiral organism which has urease activity and produces ammonia and CO2 from urea, and nestles in the gastric pits and overlaying mucus gel layer. Many diagnostic methods of H. pylori infection are available; ie bacterial culture, 13C-urea breath test, histology, serum IgG antibody against H. pylori. We developed a new method, ie tissue IgA antibody against H. pylori and detection of H. pylori DNA in the gastric juice by PCR method. Triple therapies with metronidazole, bismuth compounds, and amoxicillin or tetracyclin are difficult to use in Japan because of their sever side effects. Thus, new methods with proton pump inhibitor (PPI) and amoxicillin have been introduced. We treated 14 patients of whom were H. pylori positive-active peptic ulcer with 30 mg/day of lansoprazole, a new PPI, plus 1,500 mg/day of amoxicillin for 2 weeks and 8 (57%) patients were eradicated. Gastric carcinogenesis are multi-steps and multifactorials process. Hypothetical sequence of intestinal type of gastric cancer is that superficial gastritis-->atrophic gastritis-->intestinal metaplasia-->dysplasia-->gastric cancer and H. pylori infection may play a role in the early stage of the sequence. We examined mucosal IgA antibody against H. pylori in chronic gastritis and intestinal metaplasia detected by the Tes-Tape method in 25 resected specimens after gastrectomy for gastric cancer. Positivity rates of tissue H. pylori IgA antibody were lower in the mucosa of intestinal metaplasia than in non-metaplastic gastric mucosa and were negative in carcinoma. Causal relationship between H. pylori infection and gastric cancer is not proven and factors other than H. pylori infection are also important in the gastric carcinogenesis. Finally we introduce 2 reports: (1) NIH Consensus Conference: Helicobacter pylori in peptic ulcer disease (JAMA. 1994; 272: 65-69). The consensus panel concluded that 1. ulcer patients with H. pylori infection require treatment with antimicrobial agents in addition to antisecretory drugs whether on first presentation with the illness or on recurrence; 2. the value of treating nonulcerative dyspepsia patients with H. pylori infection remains to be determined; and 3. the interesting relationship between H. pylori infection and gastric cancer requires further exploration. (2) World Health Organization: Working Group Meeting (Reported in World Congress of Gastroenterology, Los Angeles, 1994). H. pylori plays a causal role in the chain of events leading to cancer of the stomach. Group I: definite carcinogen.
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PMID:[Helicobacter pylori in peptic ulcer and gastric cancer]. 785 88

This paper describes a new gas-analytical method used in a 55-year-old female patient with dyspepsia. Symptoms included epigastric fullness and inflation. Evaluation indicated an increased gas production in the proximal end of the small intestine that entered into the stomach via duodenogastric reflux. High CO2 content of eructed gas was confirmed in eructed gas samples using a tube in situ. Authors propose that this new analytical method of eructed gas may be applied in clinical practice in patients with dyspepsia.
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PMID:[Dysmotility-type dyspepsia and eructation. Introduction of a new gas-analytical method]. 2136 5