Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022104 (irritable bowel syndrome)
 8,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The determination of hydrogen in exhaled air by gas chromatography was used for investigation of patients with relapsing diarrhea of various genesis. An increased H level on an empty stomach, regarded as a sign of bacterial growth in the intestine, was detected in 45% of examines, mainly in celiac disease immunodeficiency, intestinal tuberculosis, diverticulosis, diabetic enteropathy, and erosive duodenitis. An increase in the H level in exhaled air after a lactose tolerance test (50 g of lactose) made it possible to diagnose lactose deficiency in 38% of patients with chronic relapsing diarrhea. In the irritable colon syndrome lactose deficiency was detected in 40% of patients.
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PMID:[Hydrogen test: its diagnostic possibilities in intestinal diseases]. 229 Mar 43

Celiac disease (CD) is the most common form of malabsorption in childhood when it presents with diarrhea and growth failure, a jejunal biopsy is considered the first diagnostic investigation by some authors. In adulthood, clinical symptoms of CD may mimic several different disease, such as peptic ulcer and IBS, and the first diagnostic investigation is an upper GI series. Radiological features of duodenum and small bowel were evaluated in twenty patients with adult onset celiac disease. Sign of duodenitis such as thickened folds, mucosal nodules, dilatation of duodenum and erosions were observed in 19 out of our 20 patients (95%); particularly, thickened folds in 17 (85%), nodularity in 16 (80%), duodenal dilatation in 12 (60%) and erosions in 4 (20%). In celiac disease the lesions are more severe in the upper part of small bowel, and duodenitis may be the unique sign of CD. Duodenitis may be part of a disease involving the entire small bowel; so, a duodenitis observed in the upper gastrointestinal tract requires the study of the entire small bowel--which seems to be very important in the case of celiac disease.
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PMID:[Radiological study of the duodenum in celiac disease in adults]. 317 71

Dyspepsia, defined as chronic or recurrent upper abdominal pain or nausea, is a common occurrence. Dyspepsia without an ulcer (non-ulcer dyspepsia) is diagnosed in patients at least twice as often as peptic ulceration. Diseases that may present with similar symptoms include gastroesophageal reflux, biliary tract disease, chronic pancreatitis, and irritable bowel syndrome. A careful history and physical examination, supplemented by selected tests, usually lead to a correct diagnosis. The pathogenesis of non-ulcer dyspepsia remains unknown. Gastric acid secretion, duodenogastric reflux, psychological factors, environmental exposures, and heredity probably do not play a major role. Some patients may have motility disturbances, but whether these disturbances cause dyspepsia is unknown. Campylobacter pylori infection and associated gastritis are common in non-ulcer dyspepsia, but their etiologic role is controversial, as is the importance of chronic duodenitis. By recognizing the heterogeneity of patients who present with non-ulcer dyspepsia, more rational management may be possible. Although an empiric trial of antacids or H2 blockers has been recommended to treat dyspepsia, most controlled trials show that although these substances reduce severity of symptoms, they are no more effective than placebos in non-ulcer dyspepsia.
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PMID:Non-ulcer dyspepsia: potential causes and pathophysiology. 328 48

One hundred fifty-one patients with non-ulcer dyspepsia, defined as chronic epigastric pain without concomitant symptoms of the irritable bowel syndrome and with no evidence of any organic disease other than macroscopic or microscopic gastritis/duodenitis seen at endoscopy on entry into the trial, were randomly assigned to treatment for four weeks with sucralfate or a placebo, 1 g three times a day one-half hour before meals, according to a double-blind model. Seventy-nine patients received sucralfate and 72 patients received a placebo. According to patients' subjective assessment of their symptoms at four weeks, 61 patients (77 percent) in the sucralfate group and 40 patients (56 percent) in the placebo group had become symptom-free or showed improvement, whereas the condition of 18 (23 percent) in the former group compared with 32 (44 percent) in the latter group remained unchanged or deteriorated. The difference between the groups was significant (p less than 0.01). The best response to sucralfate treatment (84 percent or more symptom-free or improved) was achieved in patients with mild or moderate symptoms and without macroscopic or microscopic inflammation of their gastric mucosa--a typical patient with non-ulcer dyspepsia. Our results indicate that sucralfate is significantly more effective than placebo in the treatment of non-ulcer dyspepsia.
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PMID:Sucralfate versus placebo in treatment of non-ulcer dyspepsia. 331 Jun 29

The clinicofunctional and morphological status of the stomach, biliferous system, pancreas, large and small intestine was studied in 83 patients with Sjogren's syndrome and disease (SS and SD). Chronic gastritis with secretory insufficiency was shown to develop in SD. Morphological changes of the gastric mucosa were represented by chronic gastritis with glandular involvement and chronic atrophic gastritis of immune genesis. Pathology of the extrahepatic system of bilification was detected in 87% of patients. The most common pathologies diagnosed in these patients were chronic cholecystitis (51%) and biliary dyskinesia (25%). Changes of the chemical composition of the bile (arise of its lythogenic properties) were observed. Various disorders of pancreatic function were detected in 85% of SS and SD patients. X-ray and endoscopic investigations revealed duodenal, intestinal and colon hypokinesia, less frequently signs of enteritis and colitis in one-third of the patients. The irritable colon syndrome was found in 40%. On the whole, involvement of different parts of the intestine was observed in 92%. Morphological changes in the duodenal and sigmoid colon mucosa were typical of chronic diffuse duodenitis and sigmoiditis in a subacute SD course, and chronic atrophic duodenitis and sigmoiditis in a chronic SD and SS course.
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PMID:[Lesions of the digestive organs in Sjogren's disease]. 339 95

Dyspepsia or indigestion is one of the most common disorders that is managed by general practitioners and gastroenterologists. Non-ulcer dyspepsia can be defined as upper abdominal pain or nausea in patients in whom endoscopy reveals no evidence of peptic ulceration or gastric cancer. Non-ulcer dyspepsia is a heterogeneous disorder and can be the result of such diverse entities as the irritable bowel syndrome, duodenitis or gastro-oesophageal reflux, or may be idiopathic ("essential" dyspepsia). This review traces the development of modern thought on dyspepsia and non-ulcer dyspepsia, from the 16th century to the present.
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PMID:Dyspepsia and non-ulcer dyspepsia: an historical perspective. 354 May 42

Non-ulcer dyspepsia (NUD) is defined as dyspepsia in which investigation shows no evidence of focal gastroduodenal disease or oesophagitis. The aim of the present study was to determine the proportion of NUD patients with other identifiable diseases. We interviewed 327 consecutive patients who had at least 1 month of dyspepsia before a panendoscopy that showed no evidence of oesophagitis, malignancy, or peptic ulcer. Symptoms were assessed by a structured history questionnaire. The existence of gallstones was excluded radiologically. Of the subjects studied, 75 (23%) had irritable bowel syndrome and 71 (22%) gastro-oesophageal reflux, whereas 63 (19%) had both, 25 (8%) had aerophagy, and 14 (4%) had gallstones. Of the remaining 79 patients (24%) 6 had duodenitis and 10 gastritis, whereas 1 had both. Sixty-two subjects (19%) had entirely normal endoscopic results and no ascertainable cause of their dyspepsia (termed provisionally essential dyspepsia). It is concluded that, whereas three-quarters of NUD patients have diseases that fall into other diagnostic categories, nearly one-quarter have essential dyspepsia.
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PMID:The association between non-ulcer dyspepsia and other gastrointestinal disorders. 404 40

Forty three subjects with DU confirmed at endoscopy and healed after eight weeks of sucralfate therapy were subjected to a randomized double-blind controlled trial for six months. Twenty one subjects received sucralfate (1 g one hour before breakfast and dinner). Twenty two subjects received placebo. Symptoms were evaluated every month. The subjects were endoscoped at the end of the trial or earlier in case symptoms recurred. Sucralfate was found to be significantly more effective than placebo (6/21 vs. 17/22, p < 0.005) in preventing DU relapse. Age at presentation, age at onset, duration of illness, sex, periodicity, smoking, gastric stasis like symptoms, associated irritable bowel syndrome, degree of deformity of the bulb and initial presence of duodenitis were the factors examined for their effect upon the relapse. In the placebo group relapsers had significantly shorter mean duration of illness indicating that DU may relapse more frequently in earlier part of its natural course. Other factors did not influence the relapse rate. In the sucralfate group, higher ages at onset and at presentation were associated with significantly higher relapse rate. Sucralfate may be less effective in preventing relapse in elderly and late onset DU patients.
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PMID:Sucralfate in the prevention of duodenal ulcer relapse and factors influencing the relapse rate. 774 45

Information on the utility of solid-phase gastric emptying studies (SPGES) in the evaluation of children with symptoms of upper gastrointestinal (GI) motor dysfunction is limited. This study was conducted to evaluate the impact of SPGES in the clinical management and outcome of children with upper GI symptoms suggestive of gastroparesis. The records of 45 children who underwent SPGES (31F; 3-17 years) were reviewed. All patients had GI symptoms suggesting gastroparesis. Patients were fed with Tc-99m-sulfur colloid-labeled chicken liver. Adult normal half-life (T1/2) values (F 103 +/- 14 minutes; M 66 +/- 13.6 minutes) were used. The relationships among symptoms, treatment, and outcome were evaluated. Of the 45 patients 9 had delayed, 16 had rapid, and 20 had normal gastric emptying. Six of 9 patients with delayed gastric emptying responded to cisapride. Four of 16 patients with rapid emptying were diagnosed with the dumping syndrome. Of the children with rapid gastric emptying, 87% were females. Twenty patients with normal emptying were diagnosed with gastroesophageal reflux (8), nonulcer dyspepsia (5), irritable bowel syndrome (2), Helicobacter pylori (1), lactose intolerance (1), eosinophilic gastroenteritis (1), duodenitis (1), and constipation (1). In patients who had SPGES for possible gastroparesis, 20% had gastroparesis, 36% had rapid gastric emptying, and 44% had normal gastric emptying. The high number of females in the rapid gastric emptying group might be secondary to normal adult female T1/2 values that were used. The practice of using adult normal T1/2 values in prepubertal girls may need to be revised. Patients with delayed gastric emptying responded to cisapride.
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PMID:The impact of solid-phase gastric emptying studies in the management of children with dyspepsia. 1455 21

Systemic mastocytosis (SM) is characterized by the accumulation of neoplastic mast cells in bone marrow and other organs. Gastrointestinal (GI) symptoms are common in both SM and cutaneous mastocytosis [urticaria pigmentosa (UP)], and are usually caused by the release of histamine and other inflammatory mediators. Occasionally, neoplastic mast cells may also directly infiltrate the GI tract. Previous studies have suggested that enumeration of the mast cells in GI biopsies may help establish the diagnosis of SM. However, mast cells have been reported to be increased in various inflammatory diseases, and mast cell density has not been systematically evaluated in other GI disorders. Recently, expression of CD25 by mast cells in bone marrow has been shown to be specific for SM. The purpose of this study was (1) to quantitate and compare mast cells in mucosal biopsies from patients with SM involving the GI tract, UP with GI symptoms, and a control group of diverse inflammatory disorders, and (2) to determine whether immunostaining for CD25 can be used to distinguish neoplastic from reactive mast cells in GI biopsies. Seventeen GI biopsies from 6 patients with SM; 17 GI biopsies from 5 patients with UP; and 157 control cases including 10 each normal stomach, duodenum, terminal ileum, and colon, Helicobacter pylori gastritis, bile reflux gastropathy, peptic duodenitis, celiac disease, Crohn disease, ulcerative colitis, lymphocytic colitis, and collagenous colitis, 20 biopsies from 16 patients with irritable bowel syndrome, 8 biopsies from 5 patients with parasitic infections, and 9 biopsies from 7 patients with eosinophilic gastroenteritis were immunostained for mast cell tryptase, c-kit (CD117), and CD25. Mucosal mast cells were quantitated, and the presence or absence of CD25 expression on mast cells was determined. In SM patients, mast cells in the small intestine and colon numbered >100/high-power field (HPF) in nearly all cases (mean 196/HPF; range 74 to 339). This was significantly higher than in GI biopsies from UP patients (mean 17/HPF; range 8 to 32, P<0.0001) and all inflammatory diseases (P<0.01). Mast cell density in other disorders ranged from a mean of 12/HPF in H. pylori gastritis to 47/HPF in parasitic infections. Interestingly, all SM biopsies (and none of the other cases) contained aggregates or confluent sheets of mast cells. In addition, mast cells in all SM cases were positive for CD25, whereas GI mucosal mast cells in UP and all other control cases were negative. In conclusion, quantitation of mast cells can be helpful to diagnose SM in GI mucosal biopsies, although mast cells are also markedly increased in parasitic infections. Aggregates or sheets of mast cells are only seen in SM. Immunoreactivity for CD25 in GI mucosal mast cells is specific for SM and can be used to confirm the diagnosis.
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PMID:Immunoreactivity for CD25 in gastrointestinal mucosal mast cells is specific for systemic mastocytosis. 1805 23


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