-
Gastroenterology Feb 1999It is unclear why only a minority of subjects infected by Helicobacter pylori develop duodenal ulcers (DU). The aim of this study was to investigate whether the number...
BACKGROUND & AIMS
It is unclear why only a minority of subjects infected by Helicobacter pylori develop duodenal ulcers (DU). The aim of this study was to investigate whether the number and type of H. pylori strains in the duodenum of patients with DU may play a critical role.
METHODS
Twenty-one patients with DU and 20 asymptomatic subjects with antral H. pylori infection were studied. Paired biopsy specimens were taken from the antrum and from each quadrant of the duodenal bulb. Analyses included extent of duodenal gastric metaplasia, severity of duodenitis, bacterial density, presence of the cagA gene, and vacuolating cytotoxin activity.
RESULTS
H. pylori was cultured from duodenal biopsy specimens in 95% of patients with DU and 80% of asymptomatic subjects. Both groups had a similar bacterial density and proportion of cagA-positive strains in the antrum (86% vs. 75%), but patients with DU had a 20-fold higher density of H. pylori and a higher proportion of cagA-positive strains in the duodenal bulb (81% vs. 30%). Active duodenitis was present only in patients with DU infected by cagA positive strains in the duodenum.
CONCLUSIONS
The results suggest that a high density of cagA-positive strains in the duodenum with severe duodenitis are important determinants of DU disease.
Topics: Adult; Antigens, Bacterial; Bacterial Proteins; Colony Count, Microbial; Cytotoxins; DNA Primers; Duodenal Ulcer; Duodenitis; Duodenum; Female; Genotype; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Polymerase Chain Reaction; Prevalence; Pyloric Antrum; Severity of Illness Index
PubMed: 9922305
DOI: 10.1016/s0016-5085(99)70121-6 -
Scandinavian Journal of... 1991Helicobacter pylori infection and chronic active gastritis are inextricably linked, and this organism is almost certainly responsible for inducing the resulting... (Review)
Review
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.
Topics: Anti-Inflammatory Agents, Non-Steroidal; Chronic Disease; Duodenitis; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans
PubMed: 1775921
DOI: No ID Found -
Arkhiv Patologii 2010There is a rise in the rates of acute erosive gastropathies in patients with cardiovascular and other somatic diseases. The role of acute erosive gastropathy-induced... (Review)
Review
There is a rise in the rates of acute erosive gastropathies in patients with cardiovascular and other somatic diseases. The role of acute erosive gastropathy-induced hemorrhages in the tanatogenesis of these diseases is underestimated; the problems of their prevention, diagnosis, and treatment remained unsolved. Many factors, mainly acute or chronic ischemia of the gastroduodenal mucosa, as well as its age-related involution, Helicobacter pylori infection, reflux gastritis, multiple organ dysfunction, drug-induced damage, etc., which are implicated in the pathogenesis of acute erosive gastropathies in patients with cardiovascular and other somatic diseases, are summarized.
Topics: Acute Disease; Duodenal Ulcer; Duodenitis; Gastric Mucosa; Gastritis; Gastrointestinal Hemorrhage; Humans; Intestinal Mucosa; Stomach Ulcer
PubMed: 21313773
DOI: No ID Found -
Srpski Arhiv Za Celokupno Lekarstvo 2004Helicobacter pylori (H. pylori) colonizes the gastric mucosa of a half of the mankind. Duodenal ulcer is found in 15-25%, gastric ulcer in 13%, while gastric... (Review)
Review
Helicobacter pylori (H. pylori) colonizes the gastric mucosa of a half of the mankind. Duodenal ulcer is found in 15-25%, gastric ulcer in 13%, while gastric adenocarcinoma develops in 1% of all infected individuals. Pathogenesis of H. pylori infection is related to the virulence factors of the bacterium, environmental (dietary habits, hygiene, stress) and host factors (age, sex, blood type). Colonization of the gastric mucosa is related to the motility of the bacterium, presence of lipopolysaccharide (LPS) and various bacterial enzymes. Gastric mucosal injury is the result of H. pylori LPS, vacuolization cytotoxin (vacA), cytotoxin associated protein (cagA), heat shock proteins and factors responsible for neutrophil chemotaxis and activity. H. pylori colonizes the gastric mucosa and zones of ectopic gastric epithelium. H. pylori infection is transmitted via oral-oral, fecal-oral and iatrogenic way (during endoscopy). Higher prevalence of the infection is associated with lower socioeconomic level, lack of drinking water, and living in a community. Acute H. pylori gastritis is superficial pangastritis progressing into the chronic phase after 7-10 days. Gastric mucosal atrophy and intestinal metaplasia can develop during the course of H. pylori infection. Clearly defined factors that influence the outcome of H. pylori infection include bacterial strain, distribution of gastritis, acid secretion and gastric mucosal atrophy.
Topics: Duodenum; Gastric Mucosa; Helicobacter Infections; Helicobacter pylori; Humans; Intestinal Mucosa; Virulence
PubMed: 15794058
DOI: 10.2298/sarh0410340s -
Digestive Diseases and Sciences May 1992
Review
Topics: Duodenal Ulcer; Duodenum; Helicobacter Infections; Helicobacter pylori; Humans; Prevalence; Stomach
PubMed: 1563322
DOI: 10.1007/BF01296437 -
The Medical Journal of Australia Aug 1990Eighty-two patients, whose duodenal ulcers were recurrent or resistant to H2-receptor antagonist therapy, were entered in a treatment protocol of ranitidine followed by... (Comparative Study)
Comparative Study
Eighty-two patients, whose duodenal ulcers were recurrent or resistant to H2-receptor antagonist therapy, were entered in a treatment protocol of ranitidine followed by a four-week "triple therapy" course to eradicate Helicobacter pylori (HP) infection. The triple therapy consisted of colloidal bismuth subcitrate, tetracycline and metronidazole. Duodenal ulcer healed in all 78 patients available for endoscopy and H. pylori infection was shown to be eliminated in 75 patients (96%) at rebiopsy four weeks after cessation of therapy. In these 75 remaining patients the relapse rates for H. pylori infection and duodenal ulcer were studied endoscopically, yearly and at any recurrence of symptoms. At Year 1, 71 of 73 patients remained free of H. pylori infection (HP-negative) and duodenal ulcer. The corresponding figures subsequently were: Year 2, 57/57; Year 3, 34/34; Year 4, 15/15. No duodenal ulcers recurred in HP-negative patients who were followed for up to four years. Two patients of the original cohort of 75 HP-negative patients were HP-positive with endoscopic duodenitis at 12 months, and one at 36 months, but all were without reulceration. Distorted duodenal caps gradually returned to near-normal appearance in 80% of patients by two years. From this four-year follow-up study we conclude that duodenal ulcer disease will not recur provided the patient remains free of H. pylori.
Topics: Adult; Aged; Anti-Ulcer Agents; Campylobacter Infections; Duodenal Ulcer; Duodenitis; Duodenum; Female; Follow-Up Studies; Gastroscopy; Histamine H2 Antagonists; Humans; Male; Metronidazole; Middle Aged; Organometallic Compounds; Recurrence; Tetracycline
PubMed: 1974027
DOI: 10.5694/j.1326-5377.1990.tb136833.x -
Recenti Progressi in Medicina May 1997Up to today, the relationship between autonomous nonspecific duodenitis (ANSD) has not yet been defined. ANSD has been noticed in about 26% of dyspeptic population. With... (Comparative Study)
Comparative Study Review
Up to today, the relationship between autonomous nonspecific duodenitis (ANSD) has not yet been defined. ANSD has been noticed in about 26% of dyspeptic population. With reference to the presence of active inflammation, ANSD has been divided into chronic duodenitis (CD) (77.7%) and in active duodenitis (AD) (22.3%). The two duodenitis groups have been compared with a group of patients with duodenal ulcer (DU) in relation with the presence of duodenal gastric metaplasia (GM), of duodenal Helicobacter pylori (Hp) infection, of antral chronic gastritis (AG), of antral Hp infection, and in relation with the gastric secretion behaviour. The data concerning AD are superimposable to those of DU with presence of high percentage of duodenal GM, of duodenal Hp infection and of Hp positive AG. Furthermore, they present a gastric secretory profile similar to DU with prevalence of hyperchlorhydria and hyperpepsia. CD without activity, on the contrary, present values superimposable to dyspeptic population without duodenitis and DU. It is, therefore, that Hp positive AD can be considered as a possible precursor of DU. In periulcerous site, in fact, AD is present in more than 90% of cases.
Topics: Duodenal Ulcer; Duodenitis; Helicobacter Infections; Helicobacter pylori; Humans; Metaplasia; Stomach
PubMed: 9244958
DOI: No ID Found -
Archives of Disease in Childhood Nov 1990Twenty three children with coexistent duodenal ulcer and Helicobacter pylori infection were treated with either two weeks of amoxycillin (25 mg/kg/day) in addition to... (Clinical Trial)
Clinical Trial Randomized Controlled Trial
Twenty three children with coexistent duodenal ulcer and Helicobacter pylori infection were treated with either two weeks of amoxycillin (25 mg/kg/day) in addition to six weeks of cimetidine, or cimetidine alone. Endoscopy with antral and duodenal biopsies for urease test, microaerophilic culture, and histological studies were performed at entry, six weeks, 12 weeks, and at six months. Children with persistent H pylori infection at six weeks were given a further two weeks' course of amoxycillin. H pylori persisted in all children not receiving amoxycillin treatment but cleared in six of the 13 children (46%) treated with amoxycillin. With failure of H pylori clearance at six months, only two out of six (33%) ulcers had healed and 50% of patients had experienced ulcer recurrence. In contrast, when H pylori remained cleared all ulcers healed and no ulcer recurred. Persistent H pylori infection was associated with persistent gastritis and duodenitis despite endoscopic evidence of ulcer healing. Detection and eradication of H pylori deserves particular attention in the routine management of duodenal ulceration in children.
Topics: Adolescent; Amoxicillin; Child; Child, Preschool; Cimetidine; Drug Therapy, Combination; Duodenal Ulcer; Duodenitis; Female; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Prospective Studies; Recurrence
PubMed: 2248531
DOI: 10.1136/adc.65.11.1212 -
Journal of Veterinary Diagnostic... Mar 2020Focal duodenal necrosis (FDN) is an intestinal disease of egg-layer chickens characterized by multifocal necrosis of the duodenal loop and proximal jejunum. Affected...
Focal duodenal necrosis (FDN) is an intestinal disease of egg-layer chickens characterized by multifocal necrosis of the duodenal loop and proximal jejunum. Affected flocks usually have decreased egg weights and drops in egg production. Previous studies have associated this condition with infection. We tried to reproduce FDN by experimental infection of egg-laying chickens using different -positive and -negative strains, and duodenal homogenate obtained from FDN lesions. Chickens challenged with and/or duodenal homogenate developed duodenitis after challenge. Gross lesions included mucosal erosions, hyperemia, mucosal hemorrhages, and watery intestinal content. Microscopic lesions included mild enterocyte degeneration and necrosis, and mild-to-moderate hemorrhage and lymphoplasmacytic and heterophilic infiltration of the lamina propria. Two -positive strains closely related to necrotic enteritis pathogenic strains, by genomic composition, were re-isolated from lesions. Necrosis of intestinal crypts was observed in chickens challenged with duodenal homogenate with or without coinfection. Characteristic microscopic FDN lesions with significant necrosis and loss of villus enterocytes were not reproduced.
Topics: Animals; Chickens; Clostridium Infections; Clostridium perfringens; Duodenum; Enteritis; Poultry Diseases; Stomach Diseases
PubMed: 31983302
DOI: 10.1177/1040638720901726 -
Clinical Rheumatology Feb 2020The aim of this study was to determine the frequency of Helicobacter pylori in SLE patients and to compare clinical characteristics and gastroduodenal lesions in...
OBJECTIVE
The aim of this study was to determine the frequency of Helicobacter pylori in SLE patients and to compare clinical characteristics and gastroduodenal lesions in patients with and without H. pylori infection.
METHODS
Adult SLE patients were selected and subjected to endoscopy. Gastroduodenal lesions were examined by endoscopy and biopsy (antrum and corpus). Biopsies were evaluated by hematoxylin and eosin and Giemsa staining. Immunochromatographic membrane-based assay using amplification was used to test for H. pylori antigen (coproantigen) in stool samples in all participants. Clinical characteristics and gastroduodenal lesions were compared between patients with and without H. pylori infection.
RESULTS
A total of 118 SLE patients were included (mean age 44.7 ± 11.7 years, mean disease duration 11.6 ± 6.0 years), of whom 101 (85.6%) were receiving non-steroidal anti-inflammatory drugs (NSAIDs). The coproantigen test was positive in 32 (27.1%) patients. H. pylori was present in twenty six patients (22.0%) in the gastric biopsy. The frequency of gastric erosions and gastric ulcers were 55.1% and 0.8%, respectively. Gastric erosions were less frequent in SLE patients with H. pylori infection than those without H. pylori (43.5.7% vs. 62.5%; p = 0.04). The age, disease duration, disease activity, chronic damage, gastroprotective drugs, and immunosuppressive therapy did not differ between the two groups.
CONCLUSIONS
We found a high frequency of H. pylori infection in SLE patients. The severity of SLE and reception of gastroprotective therapy do not seem to be related to H. pylori infection. Immunosuppressive therapy may not be protective against H. pylori infection in SLE patients.Key Points• In patients with systemic lupus erythematosus (SLE), the frequency of Helicobacter pylori infection was 39% and gastric erosions were frequent.• Disease activity, chronic damage, gastroprotective drugs, and immunosuppressive therapy may not affect the prevalence of H. pylori infection in SLE patients.
Topics: Adult; Anti-Inflammatory Agents, Non-Steroidal; Antigens, Bacterial; Biopsy; Case-Control Studies; Duodenitis; Endoscopy, Digestive System; Feces; Female; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Lupus Erythematosus, Systemic; Male; Middle Aged; Stomach Diseases; Stomach Ulcer
PubMed: 31713731
DOI: 10.1007/s10067-019-04805-w