Helicobacter pylori-induced immunological responses in patients with duodenal ulcer and in patients with cardiomyopathies

The interaction between the bacteria and the host is a key factor determining the clinical consequences of H. pylori infection. The immune system plays an important role in either promoting or preventing the disease. The mucosal production of TNF-alpha, IL-6, IL-8 and IL-10 and the CagA status were investigated in H. pylori-positive patients with duodenal ulcer (DU). The concentrations of these cytokines in gastric antral mucosal specimens from patients infected with H. pylori (n = 40) were determined by ELISA and compared with data on mucosal specimens from H. pylori-negative patients (n = 12). The local TNF-alpha, IL-6 and IL-8 concentrations in the antral biopsy samples were significantly higher (p < 0.001) in the patients infected with H. pylori than in the samples from the H. pylori-negative subjects. CagA positivity was demonstrated in 39 (97.5%) of the 40 patients with DU, and in 41 (70.7%) of H. pylori-positive (58 of 100) healthy blood donors. In complementary studies focusing on extragastric disease, it was found that 57% of patients with ischaemic heart disease were seropositive as concerns H. pylori, and 91% of them had antibodies against human heat shock protein 60, too. This study suggests that, besides the bacterial virulence factor, the host response of an increased mucosal production of inflammatory cytokines can be relevant to the gastric pathophysiology in H. pylori-induced DU. At the same time, in ischaemic heart diseases the role of autoimmune processes induced by H. pylori cannot be excluded.     

Failure of secretin release in patients with duodenal ulcer.

The release of secretin was studied in 12 normal subjects and 23 patients suffering from proved duodenal ulceration. After infusing acid directly into the duodenum mean plasma levels (plus or minus S.E.M.) of secretin rose in normal subjects to 52.6 plus or minus 4.8 ng/1 at six minutes but to only 37.5 plus or minus 3.6 ng/1 in duodenal-ulcer patients, a significant difference. The impairment of secretin release was as great in patients with a recent onset as in those who had had symptoms of a duodenal ulcer for a long time, raising the possibility of it being a primary defect. Patients who smoked 20 or more cigarettes a day had a particularly reduced secretin release, in accord with the greater incidence of ulcers in heavy smokers.     

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.     

Risk factors associated with gastric cancer in patients with a duodenal ulcer

Background: Although gastric cancer (GC) and duodenal ulcer (DU) are both strongly associated with Helicobacter pylori infection, a DU is negatively associated with the risk of GC. The aim of the study is to evaluate histologic risk factors for GC among patients with a DU. Materials and Methods: A total of 541 consecutive patients with GC were prospectively evaluated for the presence of a DU. Control patients with only a DU (n = 89) were recruited from health screening population. Histologic grading was assessed using the updated Sydney system for six gastric biopsies from three regions. GC risk among patients with a DU was evaluated using logistic regression analysis. Results: Among patients with GC, 7.6% (41/541) had a concomitant DU or an ulcer scar. Corpus‐predominant/pangastritis were more frequently found in concomitant GC patients with a DU (90%) than in patients with a DU alone (62%) (p = .001). In patients with a DU, moderate–severe chronic inflammation at the lesser and greater curvatures of corpus was associated with GC risk (OR, 3.70; 95% CI, 1.46–9.36, and OR, 7.72; 95% CI, 3.18–18.7, respectively). Additionally, moderate–severe intestinal metaplasia (IM) at the antrum and corpus lesser curvature was associated with GC risk (OR, 7.52; 95% CI, 3.06–18.5, and OR, 9.25, 95% CI, 2.39–35.8, respectively). Conclusions: A DU is not rare in patients with GC in a high‐risk region of GC. Patients with a DU with chronic corpus gastritis and IM have an increased risk of GC, thus those patients should be followed up for GC development.     

Effect of alkalies on gastric acidity in patients with duodenal ulcer

Acidity of the gastric juice was measured following single oral dose of fluid and powdered alkalizing agents. It was found that liquid form of such an agent (Alugastrin) in a dose of 30 mL effectively increases intragastric pH to 5.0-6.0 and maintains it at 3.0-4.0 for 60 to 90 minutes. This agent similarly neutralizes gastric content in patients with or without duodenal ulcer. Tablet forms of alkalizing agents (Gastrin and Wikalina) increase pH to 7.5 within 10 minutes and maintain it at 3.0-4.0 for 90 minutes whereas other brands (Alusal and Magnosil) slightly alkalize gastric content for 30 minutes. The studies indicate that preparations Alugastrin, Gastrin and Wikalina efficiently alkalize gastric juice for longer period of time than Maalox. Therefore, more frequent--every 1 to 1.5 hours--administration of alkalizing agents is recommended in order to increase intragastric pH in those diseases which require the elimination of hydrochloric acid.     

The microflora of ulzerous zone mucosa in patients with duodenal ulcer

Bacteriological study of the biopsies taken from gastric and duodenal mucosa of 10 healthy volunteers and 74 patients with duodenal ulcer, was carried out. In the gastroduodenal zone of healthy subjects microorganisms of 6 genera (Streptococcus, Candida, Staphylococcus, Bacillus, Helicobacter and Lactobacillus) were detected. H. pylori was isolated in 20% of cases only in biopsy specimens taken from the antral section of the stomach of healthy as monoculture or in combination with C. albicans. In patients with duodenal ulcer activation of opportunistic microflora was observed in the periulcerous zone. More often H. pylori occurred in associations with fungi of the genus Candida, streptococci, staphylococci, enterobacteria, Pseudomonas and other microorganisms (of more than 30 genera). Quantitatively the dominating microorganisms (3.8-5.7 lg CFU/g) were H. pylori, fungi of the genus Candida, bacteria of the genera Streptococcus, Peptostreptococcus, Bacteroides, Gemella, Prevotella, Veillonella, Peptococcus, Bacillus, different species of opportunistic enterobacteria, as well as bacteria of the genera Staphylococcus, Micrococcus, Corynebacterium, Neisseria, Pseudomonas, etc. Opportunistic bacteria detected in the ulcerous zone, as a rule, expressed hemolytic, lecithinase, RNAase, caseinolytic, catalase and urease activity. Sonicated filtrates of such cultures produced a cytotoxic effect on cells HEp-2. Ulcer is an infected wound that needs sanitation.