Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1522057 (Colitis)
 3,500 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Helicobacter pylori infection and chronic active gastritis are inextricably linked, and this organism is almost certainly responsible for inducing the resulting inflammatory changes. Acute ingestion studies have confirmed that H. pylori infection causes acute gastritis, and the progression to chronic gastritis has been documented. Duodenitis and H. pylori infection often occur concurrently, but colonization is restricted to those with significant gastric metaplasia. The association between H. pylori-induced inflammation and symptoms is at present unclear. In some treatment studies H. pylori eradication has been associated with a symptomatic response, whereas the acute inflammatory response appears frequently to subside H. pylori infection of the gastroduodenal mucosa is associated with both mucosal and systemic antibody responses. The mucosal response occurs both within the stomach and locally in the duodenum in patients with duodenitis. Mucosal cellular responses also appear active in patients with H. pylori gastritis. Cytokines are produced locally, which could have significant pathophysiologic effects. The concurrent use of non-steroidal anti-inflammatory agents in patients with H. pylori-induced gastritis may modify the subsequent inflammatory response. Although H. pylori is a major and consistent stimulus for inflammation within the gastroduodenal mucosa, our understanding of the development of these responses is far from complete. Inflammatory mediators are released during infection and probably play a major role in modulating the subsequent mucosal immune responses.
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PMID:Helicobacter pylori infection and inflammation. 177 21

Helicobacter pylori infection causes chronic-active gastritis and is associated with peptic ulceration. However, the link between gastric H pylori colonization and duodenal ulcers is not well understood. Therefore, a retrospective, case-controlled study was conducted to determine whether H pylori infection is associated with gastric metaplasia and mucosal inflammation in the duodenum. Biopsy specimens from the duodenal bulb were obtained from 31 of 47 children with H pylori-induced gastritis. Two control groups, matched for age and sex, consisted of 33 children with normal antral histologic evaluation and 33 with H pylori-negative gastritis. Coded duodenal sections were stained with periodic acid-Schiff, hematoxylin-eosin, and silver to examine for gastric metaplasia, mucosal inflammation, and Helicobacter-like organisms, respectively. Thirteen of 31 (42%) H pylori-infected children had gastric metaplasia, in contrast to 1 of 33 with normal histologic characteristics (P < .0001) and 2 of 33 with H pylori-negative gastritis (P < .001). H pylori was detected overlying ectopic gastric mucosa in only 2 of 13 cases. Duodenal ulcers were identified endoscopically in 10 of 13 children with gastric metaplasia and 9 of 18 H pylori-infected subjects without metaplasia (P = NS). Twenty-four of 31 (77%) children with H pylori gastritis had duodenitis compared with 4 of 33 (12%) with H pylori-negative gastritis (P < .001) and 2 of 33 (6%) with a normal antrum (P < .001). Duodenitis was present in 14 of 19 children with H pylori infection and duodenal ulcers and 10 of 12 infected patients without mucosal ulceration (P not significant). These findings demonstrate a higher frequency of both gastric metaplasia and mucosal inflammation in the proximal small intestine of H pylori-infected children. However, there was a lack of correlation between the presence of duodenal ulceration and both gastric metaplasia and duodenitis.
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PMID:Association of gastric metaplasia and duodenitis with Helicobacter pylori infection in children. 804 87

To investigate the prevalence and the significance of Helicobacter pylori duodenal colonization, endoscopic duodenal biopsies were performed in 168 children with chronic abdominal pain, gastroesophageal reflux, gastrointestinal bleeding, and malabsorption syndrome. Helicobacter pylori infection was detected in 68 children (40.4%): in 31 of them H. pylori was present in the gastric antrum, and in 37 in the duodenum also. Duodenitis was observed in 25 children with duodenal H. pylori; gastric metaplasia in 3. Scanning electron microscopy revealed the presence of the micro-organism in 3/13 cases; the bacteria were located in the intercellular spaces and alterations of the epithelial surface were found. In conclusion, H. pylori gastritis in children is often associated with duodenal colonization which can cause duodenitis, and also without gastric metaplasia, which indicates a possible role of the micro-organism in the pathogenesis of the lesions.
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PMID:Helicobacter pylori duodenal colonization in children. 917 19

Helicobacter pylori infection causes chronic gastritis (nonatrophic gastritis), which progresses to atrophic gastritis and intestinal metaplasia over a period of decades. Atrophy may result from inflammation and apoptosis caused by H. pylori infection. H. pylori is an important risk factor for peptic ulcer disease. Duodenitis in the gastric metaplasia of the duodenum, hypergastrinemia, and impaired proximal duodenal mucosal bicarbonate secretion are considered causal factors for duodenal ulcer disease. Low-grade B-cell gastric lymphoma of mucosa-associated lymphoid tissue (MALT) develops in response to H. pylori infection. Studies of Mongolian gerbil model demonstrated that H. pylori had an initiator or promoter effect on gastric carcinogenesis.
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PMID:[Causal relationship between Helicobacter pylori infection and upper gastroduodenal diseases]. 1121 92

Histopathologic and clinical data strongly suggest a causal relation between Helicobacter pylori infection and gastritis, peptic ulcer disease, or both. However, little has been written about the potential association between H. pylori infection and Brunner's gland adenoma. Therefore, we carried out a prospective study to determine the presence of H. pylori infection among patients with Brunner's gland adenoma. From November 1996 till October 1999, 19100 patients who had undergone upper gastrointestinal endoscopy at two clinical centers in Zagreb, Croatia, were candidates for participation in the study. Brunner's gland adenoma was diagnosed on the basis of histologic samples taken from the polyp (four patients) or after the entire polyp was made available upon endoscopic removal (three patients). When all endoscopic examinations had been performed, biopsy samples were taken from the antrum and body of the stomach, so that gastritis could be classified and H. pylori determined by histology. Biopsy samples were also taken from the duodenal bulb to verify duodenitis. Two other samples were taken from the antrum for rapid urease test. The patients were considered positive for H. pylori when both histology and rapid urease test were positive. Brunner's gland adenoma was diagnosed in seven patients (five women and two men; median age, 49 yrs). Five (71%) patients with diagnosed Brunner's gland adenoma had concurrent H. pylori infection. Duodenitis associated with gastric metaplasia was observed in six patients. Complete eradication of H. pylori was achieved in only two patients. Symptoms disappeared or markedly diminished in all patients with significant improvement during therapy or immediately upon endoscopic removal of the polyp. Although limited by a very small number of patients, our results suggest that concurrent H. pylori infection is very common in patients with Brunner's gland adenoma. However, the role of H. pylori infection in the pathogenesis and development of Brunner's gland hyperplasia remains unclear.
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PMID:Helicobacter pylori infection in patients with Brunner's gland adenoma. 1239 18

HIV infection leads to progressive deterioration of immunity. Upper gastrointestinal symptoms are often reported in patients with this infection. The aim of the study was to evaluate morphological changes in upper gastrointestinal tract mucosa and prevalence of opportunistic infections and Helicobacter pylori in HIV-infected people in relationship to the degree of immunosupression. We studied 94 HIV-infected patients with dyspeptic symptoms, 47 suffered from severe immunodeficiency expressed by low CD4+ lymphocyte count below 200/ mm3. Control group consisted of 52 non HIV-infected patients. During endoscopy, gastrointestinal tract mucosa was evaluated and biopsy samples were taken from gastric body and antrum for histopathological analysis and rapid urease test. In patients with CD4+ lymphocyte count below 200/mm3, endoscopic examination revealed significantly more frequent esophageal candidiasis (36%); whereas reflux esophagitis (13%) was significantly less often diagnosed in comparison to the rest of the patients. Duodenitis and duodenal erosions were also less frequent in them. Prevalence of Helicobacter pylori infection in gastric antrum was significantly lower in HIV-infected patients with severe immunodeficiency (40%) in comparison to the rest of the patients (72%) and control group (69%). Chronic active gastritis of the antral mucosa was less frequent in HIV-infected patients with CD4+ lymphocyte count below 200/mm3.
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PMID:[Studies on relationship between immunodeficiency in HIV-infected people and condition of upper gastrointestinal tract mucosa, prevalence of mycosis and Helicobacter pylori infection]. 1678 59