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)

Considerable knowledge has recently accumulated on the mechanism by which Helicobacter pylori (H. pylori) induces chronic gastritis. Although H. pylori is not an invasive bacterium, soluble surface constituents can provoke pepsinogen release from gastric chief cells or trigger local inflammation in the underlying tissue. Urease appears to be one of the prime chemoattractants for recruitment and activation of inflammatory cells. Release of cytokines, such as tumor necrosis factor alpha, interleukin 1 and 6, and oxygen radicals, leads to a further tissue inflammation accompanied by a potent systemic IgA and IgG type of immune response. Chronic inflammation and antigens on glandular epithelial cells lead to a progressive destruction with loss of the epithelial barrier function. Within the gastric mucosa, patches of intestinal metaplasia develop, which may be a risk factor for subsequent development of gastric carcinoma. Hyperacidity in duodenal ulcer patients induces gastric metaplasia in the duodenal bulb, which represents a target for H. pylori colonization and ulcer formation. H. pylori can be detected in the majority of patients with peptic ulcers and, compared to age-matched healthy people, it is also found more often in patients with dyspepsia and gastric carcinoma. Although H. pylori can be detected in healthy people, the marked reduction of the ulcer recurrence rate by eradication of H. pylori (80 percent versus 20 percent relapse within one year) suggests that H. pylori is a major risk factor for duodenal ulcer formation. The potential role of H. pylori in non-ulcer dyspepsia and carcinogenesis is under investigation. Current regimens aimed at eradicating H. pylori use a combination of several drugs that are potentially toxic. Since the risk of complications may exceed the potential benefit in most patients, eradication treatment should be limited to clinical trials and to patients with aggressive ulcer disease. New drug regimens, e.g., the combination of proton pump inhibitors with one antibiotic, may provide less toxic alternatives. Beyond ulcer treatment, effective and well-tolerated eradication regimens may have a place in prophylaxis of gastric carcinoma.
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PMID:Pathophysiology and clinical relevance of Helicobacter pylori. 134 Oct 68

Helicobacter pylori (H. pylori) is a Gram-negative, curved bacillus known since 1983. It is supposed to play role in the pathogenesis of certain gastroduodenic diseases, e.g. non-ulcer dyspepsia (NUD), chronic inflammation, ulcers, etc. Serum samples of 70 patients who were examined for stomach complaints with gastroscopy and those of 22 healthy persons were analysed. The purpose of the study was to evaluate anti-H. pylori IgG, IgM and IgA antibodies using ELISA method. Whether the antibodies can be detected or not, 8 possible variations exist, each of them denoting certain state of infection. These states are not always going parallel with the macroscopic pictures revealed by gastroscopy, but there are some obvious congruences. Results show that serologic examination cannot replace gastroscopy but on the other hand in follow-up tests and examinations as well as in understanding the aetiology of different gastroduodenal diseases it can play an important role.
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PMID:[Clinical significance of serological markers of Helicobacter pylori]. 163 74

A total of 1158 sera were tested by an enzyme linked immunosorbent assay (ELISA) for IgG and IgA antibodies to Campylobacter pyloridis. When used to test sera from gastroendoscopy patients this method had a sensitivity of 91% and a specificity of 75%. Ninety-eight of 108 infected patients (91%) were seropositive whereas only 23 of 92 (25%) uninfected patients were seropositive (p less than 0.001). Positive serology was also associated with histological gastritis (p less than 0.001). When sera from occupational groups were compared to random blood donor sera, meat workers, freezing works veterinary surgeons and pest control officers had significantly higher seropositivity. Cook Island (33 of 85 (39%)), Samoan (57 of 129 (44%)) and Tongan (39 of 56 (70%)) blood donors also had greater seropositivity than random blood donors (15 of 102 (15%)), (p less than 0.001 for all three ethnic groups). Seropositivity increased with age. The results indicate that C pyloridis infection is common among certain groups within New Zealand. The implication of this finding with respect to the hypothesis that C pyloridis is aetiologically related to dyspepsia and peptic ulcer disease is discussed.
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PMID:Seroepidemiology of Campylobacter pyloridis. 346 97

Colonising Campylobacter pyloridis were identified histologically in gastric biopsy specimens from 89% of 83 patients with non-ulcer dyspepsia and chronic gastritis, but not in 58 dyspeptic patients with normal mucosa. The presence and population density of organisms was associated with the presence of intraepithelial neutrophils. In vivo coating of the organisms by host immunoglobulin was investigated by immunoperoxidase staining of IgA, IgG, and IgM in 54 biopsy specimens. IgA coated bacteria were seen in all cases of active gastritis, and in 60% of biopsy specimens without intraepithelial neutrophils. Coating with IgG or IgM, or both, was correlated with activity of gastritis and was rarely seen in the absence of a neutrophil infiltrate.
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PMID:Local immune response to gastric Campylobacter in non-ulcer dyspepsia. 352 30

Antibody titres to Campylobacter pyloridis in serum and gastric juice were estimated by an enzyme linked immunosorbent assay (ELISA) to whole organisms obtained from bacterial culture in 39 patients with non-ulcer dyspepsia. Whereas 20 of the 21 patients with chronic gastritis had gastric C pyloridis, 17 patients with no C pyloridis had normal histology in the gastric antrum and body. Significantly raised serum IgG and IgA antibody titres to C pyloridis were found in colonised patients with gastritis. Patients with raised IgG antibody to C pyloridis were also shown to have significantly raised titres to other Campylobacter species, suggesting antigenic cross reactivity. Gastric juice antibodies were also studied and IgA titres to C pyloridis were detected in a proportion of patients with gastritis, together with low levels of IgM, but no IgG.
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PMID:Systemic and local antibody responses to gastric Campylobacter pyloridis in non-ulcer dyspepsia. 372 Dec 86

In 158 patients with symptoms of non ulcerative dyspepsia, endoscopic, histologic and immunohystochemical studies were performed over three years with the aim of investigating the immunological involvement in the Chronic non specific Duodenitis (CND). After excluding 112 patients with associated pathologies of those not fulfilling technics requisites, a population of 46 subjects was selected and subsequently it was subdivided into four groups. A group of 15 patients with histologically normal duodeno served as control; the rest (31 patients) were grouped according to duodenal compromise into three groups of minor-major severity; Grade 1 (n=12); Grade 2 (n=12); Grade 3 (n=7). The number of immunoglobuline producing cells by mn2 of mucosal area and semiquantitative evaluation of mononucleated cells with cytoplasmatic activity to hydrolitic enzymes (lysozyme or muramidase) were compared among the 4 sub-groups. It was observed a variation in the immunoglobulines rate among controls (IgA: M: G=82, 52: 11, 01: 6,45) regarding the most severe degree (61, 56: 27,30: 11,14). The increase of IgMy G compared with controls was highly significant (p is less than 0.001) and it was noted a correlative IgA diminution. The contribution of hydrolitic enzymes through the presence of "activated" histiocytes was maximal in the most degree-coinciding with the increase of IgM and IgG. This findings indicated that a marked local activation of the Immunitary System type B is observed in the Chronic Nonspecific Duodenitis and its increment, expressed as quali-quantitative variations of the different immunologlobulines and muramidase producing cells, should have lythic activity in the highest degrees. We conclude, proposing this disease as a model of immunological aggression which affects bulbar mucosae.
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PMID:[Evaluation of Ig and muramidase (lysozyme) in unspecified chronic duodenitis (bulbitis)]. 639 Oct 60

The relationship between systemic and local humoral immune response to Helicobacter pylori is poorly understood. To further address this issue we measured, using ELISA, H. pylori-specific IgG and IgA antibodies in serum, saliva, gastric and rectal homogenates of H. pylori-infected patients. A total of 107 patients who underwent upper GI endoscopy and/or sigmoidoscopy were studied. The isotypic pattern of H. pylori-specific antibodies appeared to differ at the serum, salivary, gastric and rectal mucosa level. Serum H. pylori IgG titers were higher than those of the serum-specific IgA. On the contrary, in saliva samples H. pylori IgA titers were higher than specific IgG titers. In gastric homogenates, specific IgG and IgA titers were similar. H. pylori-specific IgG were detectable in rectal homogenates but no or very low H. pylori-specific IgA were found in the same material. Furthermore, no difference was found in H. pylori IgG and IgA in serum, saliva and gastric homogenates between duodenal ulcer and non-ulcer dyspepsia patients. Data of the present study indicate that, in H. pylori-infected patients, the specific immune response is as follows: (1) it involves the secretory immune system; (2) it is paralleled by the specific salivary IgA; (3) it does not differentiate duodenal ulcer from non-ulcer dyspepsia patients; and (4) it does not take place in the large bowel.
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PMID:Isotypic analysis of specific antibody response in serum, saliva, gastric and rectal homogenates of Helicobacter pylori-infected patients. 777 45

The authors report a case of a 42 year-old patient, female, already suffering in 1990 from pulmonary sarcoidosis at 0 radiological stage, together with uveitis and relapsing erythema nodosum, with dyspepsia and weight loss which benefited from corticosteroidal therapy, repeatedly applied at the relapses of Erythema Nodosum. This therapy induced clinical recovery and marked weight gain. After 3 years (in 1993), the appearance of chronic diarrhoea, weight loss, oedemas of the lower limbs and altered laboratory findings which suggested malabsorbtive syndrome, made us verify with clinical-instrumental examinations (serum AGA IgA and IgG, Xilose test, perendoscopic jejunal biopsy) the diagnosis of fully clinically expressed adult coeliac disease. The screening of close relatives, showed that the patient's brother, HLA like (HLA A1-B8), was suffering from a less expressive coeliac disease. After a wide review of the literature, authors emphasize particular aspects of both diseases, reporting clinical manifestations, possible morbid linkage and prognostic factors. They underline epidemiological, pathogenetic and genetic/immunological similarity. bound to support a possible non-causal linkage of the diseases, even within the family. The authors think this linkage to be underestimated, because it is not often searched for on identified.
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PMID:[Celiac disease (familial) associated with sarcoidosis. Clinical case and review of the literature]. 780 Jan 97

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

In a prospective study we examined 20 Helicobacter pylori (HP)-positive duodenal ulcer patients (5 female, 15 male; age 26-70 [mean 43] years), 20 HP-positive patients with non-ulcer dyspepsia (10 female, 10 male; age 26-79 [mean 48] years) and 10 HP-negative patients with non-ulcer dyspepsia (5 female, 5 male; age 21-76 [mean 45] years) during upper GI-endoscopy. HP was detected by histology (H&E, Giemsa), rapid urease test (CLO) and serology (Cobas Core Anti-H. pylori EIA). IgA anti-HP in gastric juice was determined by ELISA. HP-positivity included positivity in all methods, and HP-negativity failure to detect HP-infection by all methods used. Of the 20 duodenal ulcer patients, 10 patients (2 female, 8 male; age 26-70 [mean 42] years) had an endoscopically documented duodenal ulcer at an earlier endoscopy with no current ulcer, 10 patients had florid duodenal ulcer disease at the time of examination. Duodenal ulcer patients compared with non-ulcer dyspepsia patients were tended to have higher serum IgG anti-HP (551 +/- 240 vs. 338 +/- 159 U/ml) and significantly higher gastric juice IgA anti-HP (50.0 +/- 7.3 vs. 26.5 +/- 4.3 relative units). Concentrations of both serum IgG anti-HP and gastric juice IgA anti-HP tended to be higher in patients with positive ulcer history but no present ulcer compared with patients with florid ulcer disease (934 +/- 456 vs. 170 +/- 63 U/ml and 60.0 +/- 8.6 vs. 40.8 +/- 10.4 relative units).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Duodenal ulcer disease: a defect in the secretory immune response to Helicobacter pylori?]. 819 Dec 63


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