Abundance of VIP in duodenal mucosa of coeliacs and duodenal ulcer patients

VIP levels were determined in gastroduodenal mucosal biopsies of 8 duodenal ulcer patients, of 5 coeliac sprue patients, and of 8 volunteers without upper gastrointestinal disease. In duodenal ulcer patients, mucosal VIP concentrations were significantly elevated in the proximal duodenum (e.g., in the duodenal bulb $\text{225±48}$ versus $\text{95±17}\text{pmol/g}$ in controls), while in coeliac sprue VIP levels tended to be increased in the whole duodenum and upper jejunum (e.g., descending duodenum $\text{409±161}$ versus $\text{81±16}$, $\text{p<0.05}$). In both disease entities, the rise in mucosal VIP may be a reaction of the peptidergic nervous system to chronic mucosal irritation and a reason for enhanced fluid and electrolyte secretion in the affected areas.     

Selective decrease of duodenal phosphoprotein phosphatase activity is a general property of duodenal ulcerogens

A phosphoprotein phosphatase (PPPase) is inhibited in rat duodenal mucosal cells very early after a single s. c. injection of the duodenal ulcerogens cysteamine, propionitrile and mepirizole. The effect seems to be independent of their effects on gastric acid secretion and on duodenal suppression of alkaline secretion. The enzyme inhibition is dose- and time-dependent under in vivo conditions. The inhibition of the PPPase activity is enzyme-selective at the level of mucosal cells in the duodenum. Under in vitro conditions, none of the duodenal ulcerogens inhibited PPPase activity. The results indicate that the effect of the ulcerogens on PPPase activity is probably exerted indirectly. When given simultaneously in vivo, propionitrile attenuated the inhibitory effects of cysteamine on the PPPase activity. However, both propionitrile and cysteamine potentiated the effect of mepirizole on PPPase depletion. These data indicate that cysteamine and propionitrile may act through the same mechanism when depleting PPPase activity. The mechanism of the decrease of duodenal protein phosphatase activity by mepirizole is probably different from the other duodenal ulcerogens.     

Different Helicobacter pylori strains colonize the antral and duodenal mucosa of duodenal ulcer patients

Background. We have investigated the possibility that the same patients may be colonized by Helicobacter pylori strains of different genotypes or phenotypes in the antrum as compared to in the duodenum. The strains were typed for DNA fingerprints, different lipopolysaccharides (LPS), and Lewis antigen expression on the O –side chains of LPS.
Materials and Methods. Polymerase chain reaction (PCR) amplifications using primer sequences (i.e., the Enterobacterial Repetitive Intergenic Consensus [ERIC]) and randomly amplified polymorphic DNA (RAPD) elements were performed to asses chromosomal DNA diversity between H. pylori strains. The expression of different LPS types and Lewis antigens in the various H. pylori isolates were determined by whole bacterial enzyme-linked immunosorbent assays using monoclonal antibodies.
Results. Duodenal ulcer patients had different H. pylori genotypes in the duodenum as compared to in the antrum as shown by ERIC-PCR (44%) and by RAPD-PCR (75%). Different DNA patterns were found among the strains that were isolated from various regions of the duodenum in 4 of 16 patients (25%) as shown by ERIC-PCR and in 8 of 16 patients (50%) as shown by RAPD-PCR. Sixty-three percent of the duodenal ulcer patients had H. pylori strains with a different Lewis antigen phenotype in the duodenum as compared to in the antrum, and 3 of 16 patients (19%) had strains with different Lewis antigens expressed by strains from different duodenal biopsies from the same patient.
Conclusion. The results suggest that a mixed population of different H. pylori strains with marked variation, both genotypically and phenotypically, colonize the same patient.     

The role of gastric and duodenal pH in the cysteamine-induced duodenal ulcer in the rat

Many secretory studies reported an increase in gastric acid secretion by the duodenal ulcerogen cysteamine. A detailed analysis of these experiments, especially the results from rats with chronic gastric fistula suggest that direct stimulation of gastric acid secretion may not be the primary mechanism of the duodenal ulcerogenic action of cysteamine. We used a different approach and measured the pH at the site of ulceration in the proximal duodenum. A duodenal ulcerogenic dose of cysteamine did not change the pH at the anterior or posterior wall of the duodenum during 4 hr. In the same dose and by the same route of administration, cysteamine nevertheless induced duodenal ulcers in 24 hr. These experiments demonstrate that in addition to the effect on gastric acid secretion, other factors are needed to the effect on gastric acid secretion, other factors are needed to explain the early duodenal ulcerogenic action of cysteamine.