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PubMed2003

Helicobacter pylori infection induces duodenitis and superficial duodenal ulcer in Mongolian gerbils.

BACKGROUND: There is no direct evidence for an animal model of Helicobacter pylori induced duodenal ulcer. AIM: In this study we evaluated the roles of bacterial strain and age of experimental animals in induction of duodenitis and duodenal ulcer in Mongolian gerbils after H pylori infection. METHODS: Specific pathogen free Mongolian gerbils were inoculated orally with three bacterial strains (H pylori ATCC 43504, TN2GF4, and K-6, a clinical isolate from a patient with gastric cancer in our clinic). These strains have both the cagA gene and VacA. Five week old gerbils were used to emulate prematurity infection and 14 week old animals were used as mature test subjects. Animals were observed for 12 weeks after inoculation. Interleukin 8 (IL-8) production in gastric epithelial cells (MKN74) after coculture with the H pylori strains was measured by ELISA. RESULTS: Gastritis and gastric ulcers were found in all gerbils infected with the three strains. However, duodenitis and gastric metaplasia were seen more frequently in gerbils infected with TN2GF4 and K-6 strains than in the ATCC 43504 infected or control groups (p<0.05). Superficial duodenal ulcers with severe duodenitis and gastric metaplasia were found in two gerbils inoculated at 14 weeks with the TN2GF4 strain but none at five weeks. The TN2GF4 strain stimulated significantly higher levels of IL-8 than ATCC 43504 and K6 strains (p=0.0039). CONCLUSIONS: When injected into adult Mongolian gerbils, a specific strain (TN2GF4) of H pylori can induce duodenitis with gastric metaplasia and superficial duodenal ulcers. Induction of duodenal ulcer in an animal model fulfills the requirements of Koch's postulates for establishing a role for H pylori as a causative agent.

Age Factors↗
PubMed1992

Helicobacter pylori, gastritis and duodenitis in the healing process of duodenal ulcer.

The occurrence of antral gastritis, duodenitis, gastric metaplasia and Helicobacter pylori (H. pylori) were compared between 63 endoscopically proven duodenal ulcer (DU) patients and 34 non-ulcer dyspepsia (NUD) patients with no ulcer history and no ulcer present as documented by endoscopy. The DU group showed a significantly higher rate of active antral gastritis (89% vs 41% p less than 0.05), a higher antral H. pylori carrying rate (76% vs 27% p less than 0.01), a higher rate of active chronic duodenitis (75% vs 32% p less than 0.05), and a higher rate of gastric metaplasia in the duodenal bulb (68% vs 27% p less than 0.05) than the NUD group. The H. pylori carrying rate in the bulb was 16% in the DU group and 0% in the NUD group. The difference is evident, although it is statistically insignificant. All 10 cases carrying H. pylori in the duodenum in the DU group had active chronic duodenitis with gastric metaplasia. Further evaluation of the variables (rate of active antral gastritis and duodenitis and the carrying rate of H. pylori in the antrum and bulb) showed no difference between different ulcer stages (active, healing, or scarred). The above findings strongly suggest a close relation between H. pylori and duodenal ulcer. However, the low occurrence rate of the bacteria in the bulb can only indicate a partial etiologic role of the bacteria in DU. No improvement in antral gastritis, duodenitis and H. pylori occurrence, despite the healing of an ulcer, is in agreement with the naturally high recurrence rate of duodenal ulcers.

Duodenal Ulcer↗
PubMed2001

The fine form of Helicobacter pylori on the metaplastic duodenal mucosa is associated with recurrent duodenal ulcers.

BACKGROUND/AIM: It is well known that Helicobacter pylori changes its shapes according to various environmental conditions. The aim of this study was to examine the morphological differences between H. pylori in the duodenum and that in the stomach. METHODS: Duodenal biopsy specimens were obtained from patients with duodenal mucosal lesions, and these specimens were then histopathologically examined. Morphological and genetic properties of cultured H. pylori isolates were analyzed. RESULTS: H. pylori was identified in 16 out of 50 duodenal biopsy specimens. Along with the regular form, we found a fine form of H. pylori in the gastric metaplastic mucosa of ten duodenal specimens that was shorter in length and thinner in diameter than the regular helical form. There were no detectable differences between the ureA-ureB polymorphism of the duodenal fine form and that of gastric regular form in a single patient. As compared with patients without H. pylori in the duodenum, the prevalence of recurrent duodenal ulcers significantly increased in patients with the fine form (p < 0.05), but not in patients with the regular form. CONCLUSION: The fine form of H. pylori in the metaplastic duodenal mucosa could result from its adaptation to the duodenal environment and may be associated with the recurrence of a duodenal ulcer.

Adolescent↗
PubMed1991

Serotonin-induced decrease of duodenal mucosal blood flow plus acid load produces duodenal mucosal lesion in rats.

To clarify the role of duodenal mucosal blood flow in the genesis of duodenal mucosal lesions, a single dose of serotonin, 20 mg/kg, was administered subcutaneously to rats. Serotonin significantly decreased both the duodenal mucosal blood flow and the output of gastric acid and pepsin. However, mild duodenal erosions were observed in only 2 of the 9 rats receiving that agent. The repeated intragastric administration of 1 ml of 0.1 N HCl hourly for 6 h failed to induce duodenal mucosal lesions. On the other hand, the administration of both serotonin and repeated doses of HCl produced marked duodenal mucosal lesions in all rats. It is concluded, therefore, that one of the factors responsible for the genesis of duodenal mucosal lesions is a decrease of duodenal mucosal blood flow combined with an acid load against the duodenal mucosa.

Animals↗
PubMed1989

Chronic nonspecific duodenitis. A multiple biopsy study of the duodenal bulb in health and disease.

A clinical, endoscopic and histopathologic study on chronic nonspecific duodenitis was performed in 174 subjects, 124 patients (control patients, patients with gastric or duodenal ulcer and nonulcer dyspepsia) and 50 healthy volunteers without clinical history of gastro-intestinal disease. Chronic nonspecific duodenitis was found in 6 healthy volunteers (12%), 5 control patients (7%), one gastric ulcer patient (7%), all duodenal ulcer patients and in 15 patients with nonulcer dyspepsia (83%). Chronic non-specific duodenitis is a focal process affecting the duodenal bulb. It can be missed when only one biopsy is studied. Superficial gastric metaplasia was directly correlated to gastric acid secretion and was found in 32 healthy volunteers (64%), 23 control patients (34%), six gastric ulcer patients (43%), 20 duodenal ulcer patients (20%) and in 17 patients with nonulcer dyspepsia (94%). This study suggests that chronic nonspecific duodenitis is a stage of duodenal ulcer disease.

Adult↗
PubMed2002

Correlation between the degree of duodenal bulbar deformity and the density of Helicobacter pylori infection in patients with active duodenal ulcers.

BACKGROUND: Duodenal ulcer with deformity of the bulb is evidence of a chronic process of ulcer disease. This prospective study was carried out to investigate the relationship between the degree of bulbar deformity and the density of Helicobacter pylori infection in patients with duodenal ulcer. METHODS: Patients with endoscopically proven active duodenal ulcers and a positive diagnosis of H. pylori infection were enrolled. Duodenal ulcers were divided into three types according to the degree of deformity of the bulb: type I, normal bulb; type II, mildly deformed; type III, markedly deformed. In each case, we evaluated the H. pylori density histologically. The density was graded according to the Sydney system (normal, mild, moderate, and marked). RESULTS: A total of 95 duodenal ulcer patients were studied, including 25 with type I, 40 with type II, and 30 with type III duodenal ulcers. H. pylori density was correlated with deformity of the duodenal bulb: 16/25 (64%) patients with a type I ulcer had mild infection, 19/40 (47.5%) patients with a type II ulcer had moderate infection, and 15/30 (50%) patients with a type III ulcer had marked infection. CONCLUSION: Patients with active type II or III duodenal ulcers had greater densities of H. pylori than did those with type I ulcers. A tendency for higher H. pylori density was seen as the degree of deformity of the duodenal bulb increased.

Acute Disease↗
PubMed1990

[The morphofunctional characteristics of the duodenal mucosa in patients with a duodenal ulcer at different phases of the disease].

Endoscopic, morphological, histochemical and biophysical properties of the duodenal mucosa as well as secretory activity of the stomach and pancreas were studied and compared in 398 patients with duodenal ulcer in different phases (active ulcer, healing ulcer, red and white scars). Sixteen patients were observed over time. Analogous studies were conducted in 88 patients with chronic diseases of the biliary and duodenopancreatic zone (with non-ulcerous duodenitis) and in 32 normal persons. The duodenal mucosa was established to undergo consistent morphofunctional reorganization related to the disease phase. Active duodenal ulcer was marked by duodenitis with thickening of the mucosa, shortening of the villi, reduction of the depth of the cryptae, gastric metaplasia, impairment of histochemical properties of epitheliocytes and decrease of the transmural potential difference, overproduction of acid and pepsin in the basal period, high sensitivity of the chief cells to stimulation, and insufficient output of bicarbonates by the pancreas. Gastric metaplasia of the duodenal epithelium, appreciable histochemical and morphometric alterations may be regarded as relatively specific traits of peptic duodenitis. As ulcer heals, a well-defined tendency may be noted towards normalization of all the parameters mentioned. However, they only correspond to normal in 25% of patients in the phase of a white scar. The conclusion is made that there is also a necessity of correcting morphofunctional abnormalities after duodenal ulcer healing.

Adolescent↗
PubMed1985

Changes in duodenal mucosal blood flow and mucus glycoprotein content during cysteamine-induced duodenal ulceration in rats.

The effects of cysteamine on duodenal mucosal blood flow and duodenal glycoprotein were studied during the development of duodenal ulceration in conscious rats. Cysteamine at an ulcerogenic dose (300 mg/kg s.c.) produced a remarkable decrease of duodenal mucosal blood flow which preceded the appearance of duodenal ulcers. The reduced blood flow was followed by a significant decrease of tissue levels of glycoprotein which also occurred prior to the time when duodenal injury had reached a maximum. Cysteamine was without significant effect on the rate of incorporation of 3H-glucosamine into duodenal glycoprotein at concentrations up to 10(-3) M. These results suggest that the reduction in duodenal mucosal blood flow in response to cysteamine could possibly contribute to a decrease of duodenal glycoprotein and that both may be at least in part responsible for the incidence of duodeno-ulcerogenecity.

Animals↗
PubMed1976

A comparison of basal and stimulated gastric acid and duodenal bicarbonate in patients with and without duodenal ulcer disease.

Basal gastric secretion and the maximum response to pentagastrin and basal secretion into the duodenumand its near-maximum response to secretin were measured in 20 control subjects and ten patients with duodenal ulcer disease. In control subjects the volumes of stimulated gastric and duodenal secretions were significantly correlated. In patients with duodenal ulcer, there were no significant correlations between basal gastric and duodenal secretion but after stimulation both volumes and outputs (but not concnetrations) of gastric and duodenal secretions were significantly correlated. The bicarbonate secretory capacity in patients with duodenal ulcer was not only normal but was also comparable to the gastric acid secretory capacity. The basal bicarbonate content of the duodenal aspirate, however, in patients with duodenal ulcer was only half that in control subjects, perhaps another example of inadequate entry of bicarbonate into the duodenum in patients with duodenal ulcer in spite of the normal bicarbonate secretory capacity.

Adolescent↗
PubMed2000

Effects of glucagon-like peptide-1(7-36)amide on antro-pyloro-duodenal motility in the interdigestive state and with duodenal lipid perfusion in humans.

BACKGROUND: Glucagon-like peptide-1(7-36)amide (GLP-1) is a gut hormone released postprandially. Synthetic GLP-1 strongly inhibits gastric emptying in healthy subjects and in patients with diabetes mellitus. AIMS: To investigate the effects of GLP-1 on antro-pyloro-duodenal motility in humans. METHODS: Eleven healthy male volunteers were studied on two separate days. On the interdigestive study day, a basal period was followed by a 60 minute period of saline infusion and two further 60 minute periods of intravenous infusion of GLP-1 0.4 and 1.2 pmol/kg/min to achieve postprandial and supraphysiological plasma levels, respectively. On the postprandial study day, the same infusions were coadministered with intraduodenal lipid perfusion at 2.5 ml/min (2.5 kcal/min) followed by another 60 minutes of recording after cessation of GLP-1. Antro-pyloro-duodenal motility was measured by perfusion manometry. RESULTS: GLP-1 significantly inhibited the number and amplitudes of antral and duodenal contractions in the interdigestive state and after administration of duodenal lipid. It abolished interdigestive antral wave propagation. In the interdigestive state, GLP-1 dose dependently increased pyloric tone and significantly stimulated isolated pyloric pressure waves (IPPW). Pyloric tone increased with duodenal lipid, and this was further enhanced by GLP-1. GLP-1 transiently restored the initial IPPW response to duodenal lipid which had declined with lipid perfusion. Plasma levels of pancreatic polypeptide were dose dependently diminished by GLP-1 with and without duodenal lipid. CONCLUSIONS: GLP-1 inhibited antro-duodenal contractility and stimulated the tonic and phasic motility of the pylorus. These effects probably mediate delayed gastric emptying. Inhibition of efferent vagal activity may be an important mechanism. As postprandial plasma levels of GLP-1 are sufficient to appreciably affect motility, we believe that endogenous GLP-1 is a physiological regulator of motor activity in the antro-pyloro-duodenal region.

Adult↗
PubMed1999

Duodenal Helicobacter pylori infection differs in cagA genotype between asymptomatic subjects and patients with duodenal ulcers.

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.

Adult↗
PubMed1982

Frequency and extent of bulbar duodenitis in duodenal ulcer, endoscopic and histological study.

The present prospective investigation was aimed at ascertaining the true incidence of duodenitis in the presence of duodenal ulcer, and the extent of bulbar involvement. In 54 consecutive patients 3 biopsy specimens were collected from preestablished sites during endoscopy. Endoscopic findings were defined as the presence or absence of definite inflammation. Biopsy specimens were evaluated blind, and the degree of duodenitis was classified from 0 to 3 in accordance with the criteria proposed by Whitehead; grade 1 was further classified into 1a (within the range of normal mucosa) and 1b (mild duodenitis). Only grades 1b, 2 and 3 were regarded as duodenitis. Reliable histologic evaluation of all 3 biopsies was possible in only 36 out of the 54 patients. Results show that endoscopic and histologic findings are in agreement in 82% of the patients, but endoscopic judgement of inflammation was false in 17 out of 54 (35%) observations of histologically normal mucosa. Histological duodenitis is more frequent and more severe close to the ulcer than in the mid-bulbar area, and the mucosa of the mid-bulbar area appears to be significantly more affected by the inflammatory process than the apex. Duodenitis is present predominantly in the areas of the duodenal bulb in which ulcers usually develop, and therefore it might not be merely a phenomenon induced by the presence of the ulcer.

Adolescent↗
PubMed2001

[Stages of duodenal motility disorders in the formation of duodenogastric reflux in patients with chronic duodenitis complicated by opisthorchiasis].

Stages of the duodenogastral reflux development in the patients with chronic duodenitis with opistorchosis combination are presented as follows. The 1st stage manifests the earliest attributes of duodenal passage changes that are revealed with duodenodebitometria (the definition of physiologogical solution perfusion speed in duodenum). Structural changes are absent in this stage. The compensated changes of duodenal passage, so called "latent" and later stable duodenal hypertension are demonstrated in the patients with the 2nd stage. The patients with duodenal hypertension and nonstable duodenal regurgitation constitute the 3rd stage. The 4th stage is presented with subcompensated duodenal passage changes, that later transform to the decompensated ones with stable duodenal reflux into a stomach development.

Adolescent↗