Bleeding diathesis and gastro-duodenal ulcers in inherited cytosolic phospholipase-A2 alpha deficiency.

Arachidonic acid (AA), when cleaved from phospholipids by cytosolic phospholipase A2 alpha (cPLA2a), generates eicosanoids, with pro-hemostatic, pro-inflammatory, vasoactive and gastro-protective functions. We describe a patient (27-year-old man) and his twin-sister with early-onset bleeding diathesis and recurrent gastro-intestinal (GI) ulcers. Platelet aggregation/δ-granules secretion by collagen was impaired, but normal by AA; serum levels of thromboxane (Tx) B2 and 12-hydroxyeicosatetraenoic acid, and urinary levels of 11-dehydro-TxB2 were extremely low. Patients were homozygous for 1723G>C transition in PLA2G4A gene, which changed the codon for Asp575 to His. GI ulcers affected 5/14 heterozygous (< 40 years) and 1/16 wild-type homozygous (> 60 years) family members; none had bleeding diathesis. The proband, his sister and mother also had mildly reduced factor XI levels. Platelet messenger RNA expression did not differ among subjects with different PLA2G4A genotypes. Conversely, platelet cPLA2a was undetectable by Western Blotting in the proband and his sister, and decreased in 1723G>C heterozygous subjects, suggesting that the variant is transcribed, but not translated or translated into an unstable protein. We described a syndromic form of deficiency of cPLA2a , characterised by recurrent GI ulcers and bleeding diathesis, associated with mild inherited deficiency of factor XI. Unlike other reported patients with cPLA2a deficiency, these patients had extremely low levels of platelet TxA2 biosynthesis.

The protective role of Aegle marmelos on aspirin-induced gastro-duodenal ulceration in albino rat model: a possible involvement of antioxidants.

BACKGROUND/AIM: Gastro duodenal ulcer is a common disorder of the gastrointestinal tract. Several Indian medicinal plants have been traditionally and extensively used to prevent different diseases. In the present research studies, Bael fruit (Aegle marmelos (AM), family: Rutaceae) which are also called as Bilva in ancient Sanskrit was used as a herbal drug and its antioxidative role in aspirin- induced gastroduodenal ulceration in albino rat was evaluated using essential biochemical parameters. PATIENTS AND METHODS: Mucosal thickness (MT), ulcer index (UI), different biochemical parameters, such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH), and lipid peroxidation (LPO) were measured in all the groups, to study the possible involvement of antioxidants with gastroduodenal protection. RESULTS: A significant decrease in MT, SOD and CAT activities and GSH level and a significant increase in UI, AST, ALT, and ALP activities and LPO level were observed in aspirin treated stomach and duodenum of albino rats. CONCLUSIONS: Pretreatment with AM fruit pulp extract for 14 consecutive days showed the reverse effects of aspirin suggesting gastro-duodenal protective and anti- ulcerogenic properties of AM through its antioxidant mechanism.

Attenuation of cysteamine-induced duodenal ulcer with Cochinchina momordica seed extract through inhibiting cytoplasmic phospholipase A2/5-lipoxygenase and activating γ-glutamylcysteine synthetase.

BACKGROUND AND AIM: Cysteamine is a reducing aminothiol used for inducing duodenal ulcer through mechanisms of oxidative stress related to thiol-derived H(2)O(2) reaction. Cochinchina momordica saponins have been suggested to be protective against various gastric diseases based on their cytoprotective and anti-inflammatory mechanisms. This study was aimed to document the preventive effects of Cochinchina momordica seed extract against cysteamine-induced duodenal ulcer as well as the elucidation of its pharmacological mechanisms. METHODS: Cochinchina momordica seed extract (50, 100, 200 mg/kg) was administrated intragastrically before cysteamine administration, after which the incidence of the duodenal ulcer, ulcer size, serum gastrin level, and the ratio of reduced glutathione (GSH)/oxidized glutathione disulfide (GSSG) as well as biochemical and molecular measurements of cytoplasmic phospholipase A(2) (cPLA(2)), cyclooxygenase-2 (COX-2), 5-lipoxygenase and the expression of proinflammatory genes including IL-1ß, IL-6, COX-2 were measured in rat model. Additional experiments of electron spin resonance measurement and the changes of glutathione were performed. RESULTS: Cochinchina momordica seed extract effectively prevented cysteamine-induced duodenal ulcer in a dose-dependent manner as reflected with significant decreases in either duodenal ulcerogenesis or perforation accompanied with significantly decreased in serum gastrin in addition to inflammatory mediators including cPLA(2), COX-2, and 5-lipoxygenase. Cochinchina momordica seed extract induced the expression of γ-glutamylcysteine synthetase (γ-GCS)-related glutathione synthesis as well as significantly reduced the expression of cPLA(2). Cochinchina momordica seed extract preserved reduced glutathione through increased expressions of γ-GCS. CONCLUSION: Cochinchina momordica seed extracts exerted significantly protective effect against cysteamine-induced duodenal ulcer by either cPLA2 inhibition or glutathione preservation.

Antiulcer activity of Andrographis paniculata (Burm.f.) wall. against cysteamine-induced duodenal ulcer in rats.

Antiulcer activity of Andrographis paniculata was evaluated by cysteamine induced duodenal ulcer model in rats. Male albino Wistar rats were pre-administered with 200 mg/kg body wt. of hydroalcoholic extact of Andrographis paniculata (HAEAP) orally, for 30 days prior to i.p. administration of 420 mg/kg body wt. of cysteamine as a single dose. Rats preadministered with 30 mg/kg body wt. of ranitidine served as standard drug. Ulcer index, thiobarbituric acid reactive substances, mucin, glutathione peroxidase and myeloperoxidase activities, reduced glutathione/oxidized glutathione (GSH/GSSG) ratio, glycoproteins and membrane bound enzyme activities were measured in duodenum of experimental animals. The ulcer score and myeloperoxidase activity were significantly minimized in rats treated with HAEAP. Mucin content was found to be preserved in rats treated with the extract. GSH/GSSG ratio and glutathione peroxidase activities were found to be maintained by the HAEAP. Level of lipid peroxidation products was found to be significantly low in HAEAP treated rats compared to ulcer control rats. The basolateral and brush border membrane bound enzyme activities which were depleted significantly in ulcer control rats were found to be maintained in rats pre-treated with the extract. The ulcer preventing effect was comparable to that of ranitidine treated rats. Level of glycoproteins was also found to be preserved in rats treated with the extract. The normal rats treated with the HAEAP did not show any abnormal alterations in the parameters studied. Histopathological observations also showed the ulcer preventing effect of the HAEAP. It is suggested that the ulcer preventing effect may be due to its mucin preserving and antioxidant nature.

Effect of andrographolide on cysteamine-induced duodenal ulcer in rats.

The aim of this study was to evaluate the gastroprotective efficacy of andrographolide isolated from Andrographis paniculata in rats induced with duodenal ulcers. Duodenal ulcers were induced by cysteamine administration in rats pretreated with 3 mg kg⁻¹ BW day⁻¹ of andrographolide for 30 days. Ulcer score, myeloperoxidase activity, TBARS level, GSH/GSSG ratio and enzyme antioxidants were measured in the duodenal tissue. Brush border and basolateral membranes were isolated to assay sucrase, maltase, alkaline phosphatase and total ATPases. Ulcer score was significantly minimised in rats pretreated with andrographolide. Elevation in myeloperoxidase and TBARS levels were found to be minimised significantly due to andrographolide treatment. Membrane-bound enzyme activities and the thiol redox status of glutathione were significantly maintained in duodenal mucosa of rats that received andrographolide. This study reveals that the major component of A. paniculata, andrographolide, has potent antiulcer properties that are most likely caused by minimising inflammatory changes, counteracting free radical formation and maintaining the thiol redox status in the duodenum.

Matrix metalloproteinase-3 promoter polymorphisms but not dupA-H. pylori correlate to duodenal ulcers in H. pylori-infected females.

BACKGROUND: This study investigated if the H. pylori dupA genotype and certain host single nucleotide polymorphisms (SNPs) of matrix metalloproteinases (MMPs) and their inhibitors (TIMPs), including MMP-3, MMP-7, MMP-9, TIMP-1 and TIMP-2, might correlate with ulcer risk of H. pylori-infected Taiwanese patients. RESULTS: Of the 549 H. pylori-infected patients enrolled, 470 patients (265 with gastritis, 118 with duodenal ulcer, and 87 with gastric ulcer) received SNPs analysis of MMP-3-1612 6A > 5A, MMP-7-181 A > G, MMP-9exon 6 A > G, TIMP-1372 T > C and TIMP-2-418 G > C by PCR-RFLP. The 181 collected H. pylori isolates were detected for the dupA genotype by PCR. The rates of dupA-positive H. pylori infection were similar among patients with duodenal ulcer (22.8%), gastric ulcer (20.0%), and gastritis (25.5%) (p > 0.05). Males had higher rates of duodenal ulcer and gastric ulcer than females (p < 0.01). Of H. pylori-infected patients, the MMP-3 6A6A genotype were more common in patients with duodenal ulcers than in those with gastritis (87.7% vs. 74.9%, p < 0.05) in females. This genotype had a 2.4-fold (95% CI: 1.02-5.66) increased risk of duodenal ulcer, compared to those with the 5A carrier. Combining the MMP-3/TIMP-1 genotype as 6A6A/CC, the risk of duodenal ulcer increased up to 3.6 fold (p < 0.05) in H. pylori-infected females. CONCLUSIONS: The MMP-3 promoter polymorphism, but not the dupA-status, may correlate with susceptibility to duodenal ulcer after H. pylori infection in Taiwanese females.

[Substituted 1,5,6,7-tetrahydro-4H-benzimidazol-4-ones as inhibitors of urease].

A comparative kinetic study of the inhibition of urea hydrolysis by 9 substituted 1,5,6,7-tetrahydro-4H-benzimidazol-4-ones (BI I-IX) has been carried out. The inhibition had reversibl competitive character; the inhibition constants K(i), varied from 29 up to 754 microM in dependence of the structure of BI I-IX. Three BI I-III, having the K(i) values from 29 to 82 microM, may be used as the potential therapeutic agents for gastroenterology for treatment of stomach and duodenal ulcers.

[Parameters of plasma blood proteolysis and phenotypes of alpha1-proteinase inhibitor in children with duodenal ulcer].

The aim of this study was to determine correlation between proteolysis parameters and phenotypes of alpha1-proteinase inhibitor in blood plasma in children with duodenal ulcer. Activation of pepsin- and trypsin like proteinases was accompanied by the decrease in activity of alpha2-macroglobulin and the increase in activity of acid stable inhibitors. The phenotypes M1M3, M1M1, M2M2 of alpha1-proteinase inhibitor were determined. Activation of proteolysis was more pronounced in individuals with subtype M2M2. Activity of alpha1-proteinase inhibitor decreased by 2-fold in M2M2, insignifically differed from the control group in M1M1, and increased by 1,9-fold in M1M3 subtype. Low activity of alpha1-proteinase inhibitor was accompanied by high activity of acid stable inhibitors; this may be regarded as the protective reaction of the body. Determination of alpha1-proteinase inhibitor phenotypes may be a basis for employment of polyvalent proteinase inhibitors for therapy of ulcer.

Association between genetic polymorphisms in the cyclooxygenase-1 gene promoter and peptic ulcers in Japan.

Cyclooxygenase-1 (COX-1) has been regarded as a constitutively expressed enzyme that generates prostaglandins for gastrointestinal integrity. We attempted to clarify the association between potentially functional polymorphisms (T-1676C and A-842G/C50T) in the COX-1 gene promoter and gastroduodenal disorders in a Japanese population. The study was performed with 480 stocked DNAs from subjects (gastric ulcers in 93 subjects and duodenal ulcers in 44) with no evidence of gastric malignancy. We employed the PCR-SSCP method to detect gene polymorphisms. The severity of histological chronic gastritis in antral biopsy specimens was classified according to the updated Sydney system. The T-1676C polymorphism was not associated with either gastric mucosal atrophy or infiltration of inflammatory cells into gastric mucosa. In non-NSAID (non-steroidal anti-inflammatory drug) users, male gender and Helicobacter pylori (HP) infection were significantly associated with both gastric and duodenal ulcers, whereas the -1676T allele carrier was significantly associated with only gastric ulcers (OR, 2.86; 95% CI, 1.29-6.34). In NSAID users, the number of -1676T alleles was significantly associated with developing gastroduodenal ulcers (OR, 5.80; 95% CI, 1.59-21.1), whereas male gender and HP infection were not. The -842T/ C50T polymorphism was not detected in any of the 480 Japanese subjects. In conclusion, a carrier of the -1676T allele in the COX-1 gene promoter, as well as HP infection and male gender, seem to be significant risk factors for developing gastric ulcers, and the number of -1676T alleles was also a significant risk factor for the NSAID-induced ulcer, whereas the frequency of the A-842G polymorphism was thought to be very rare in the Japanese population.

Candida albicans aggravates duodenal ulcer perforation induced by administration of cysteamine in rats.

BACKGROUND: Candida sp are frequently isolated from the ascitic fluid of patients with perforated ulcers. The present study was performed to examine whether Candida infection may be involved in the process of ulcer perforation. METHODS: Male Wistar rats were divided into a saline group (n = 15) and a Candida group (n = 17). Cysteamine-HCl (Sigma; 31 mg/100 g) was administered thrice on day 1 to both groups of animals. Candida albicans at a density of 10(8) in 0.5 mL of saline was administered 1 h before, and 12 h and 24 h after the first administration of cysteamine in the Candida group. RESULTS: Perforated duodenal ulcers were observed in 94.1% of the rats in the Candida group, but only 26.7% of the rats in the saline group (P < 0.01). The area of the duodenal ulcers in the Candida group was 40.89 +/- 33.07 mm2, whereas that in the saline group was 16.53 +/- 20.4 mm2 (P < 0.05). The mortality rate was significantly higher in the Candida group than in the saline group. In the Candida group, colonization by C. albicans was recognized at the ulcer base, surrounded by marked granulocytic infiltration. The number of eosinophils infiltrating the ulcer base was also significantly greater in the Candida group than in the saline group. Immunohistochemical analysis revealed the expression of secretory aspartyl protease (SAP) in the region of the ulcer showing colonization by C. albicans in the Candida group. CONCLUSION: Candida albicans aggravates duodenal ulcer perforation in the experimental model of cysteamine-induced duodenal ulcer perforation. The present findings suggest that SAP and host-parasite relationships, including granulocyte-dependent mechanisms, may be involved in the aggravation of ulcer perforation by C. albicans.

Influences of chymase and angiotensin I-converting enzyme gene polymorphisms on gastric cancer risks in Japan.

BACKGROUNDS AND AIMS: The renin-angiotensin system plays an important role in homeostasis. Angiotensin II, which is generated by chymase and angiotensin I-converting enzyme (ACE), controls blood pressure as well as angiogenesis and cell proliferation. The aim of this study was to clarify the association of the chymase gene (CMA/B) and ACE polymorphisms with susceptibility to gastric cancer and peptic ulcer. METHODS: We assessed CMA/B A/G and ACE insertion/deletion (I/D) polymorphisms in H. pylori-positive gastric cancers (n = 119), gastric ulcers (n = 127), and duodenal ulcers (n = 105), and controls (n = 294) consisting of H. pylori-positive gastritis alone (n = 162) and H. pylori-negative subjects (n = 132) by PCR methods. RESULTS: In CMA/B polymorphism, the age- and sex-adjusted odds ratios (OR) of A/A and A/G genotypes relative to the G/G genotype for gastric cancer risk were 7.115 (95% confidence interval, 1.818-27.845) and 1.956 (95% confidence interval, 1.137-3.366), respectively. There was an increased risk for gastric ulcer in the A/A genotype (OR, 3.450; 1.086-10.960). However, there was no association between ACE polymorphism and susceptibility to gastric cancer and peptic ulcer. In allele combination analysis of CMA/B and ACE polymorphisms, the A/I allele combinations (CMA/B G/A or A/A and ACE I/I genotype) significantly increased the risk of gastric cancer development (OR, 4.749, 2.050-11.001) compared with the G/I allele combinations (CMA/B G/G and ACE I/I genotype). CONCLUSIONS: The CMA/B polymorphism was associated with an increased risk for gastric cancer and gastric ulcer development. The genotyping test of the renin-angiotensin system could be useful for the screening of individuals with higher risks of gastric cancer and gastric ulcer.

[A non-invasive method of evaluation of Helicobacter pylori urease activity: its perfection and introduction to clinical practice].

The authors have developed a highly sensitive method of non-invasive diagnostics of Helicobacter pylori, the most frequent human infection. Detection of urease activity is based upon measurement of the degree of the elevation of stable 13C isotope content in exhaled air after administration of C-urea as a test reagent. The method has been scarcely applied in Russia because the test preparation, 13C urea had not been produced domestically until 2002. The method can be easily applied by any healthcare institution; however, it requires special equipment and trained personnel to perform measurement of 13C content in exhaled air samples using mass spectrometers. The article presents the first experience in clinical application of the method.

[Oxidative stress in mechanism of psychosomatic disorders realization in duodenal ulcer in students].

AIM: To study the role of oxidative stress in mechanism of psychosomatic disorders involvement in pathogenesis of ulcerogenesis. MATERIAL AND METHODS: Psychosomatic disorders (PSD) and oxidative stress (OS) were assessed in 120 students with duodenal ulcer (DU) who had no concomitant pathology. Examination for PSD included interviewing by questionnaires. OS was judged by the level of lipid peroxidation products (malonic dialdehyde and dienic conjugates) and antioxidant activity--by glutathion peroxidase and superoxidedismutase. Melatonin was measured by enzyme immunoassay. RESULTS: A close correlation was discovered between the severity and features of PSD, lowering of melatonin, severity of OS and clinical features of the disease. CONCLUSION: DU students develop PSD which become leading factors of ulcerogenesis. One of the mechanisms of their participation in ulcerogenesis may be related with lowering of melatonin which is a potent stress regulator and corrector of lipid peroxidation and antioxidant activity.

Higher gastric cycloxygenase-2 expression and precancerous change in Helicobacter pylori-infected relatives of gastric cancer patients.

PURPOSE: This study was conducted to determine whether relatives of gastric cancer patients (GCF) showed greater gastric cycloxygenase-2 (COX-2) expression or a greater incidence of precancerous lesions after Helicobacter pylori infection and whether H. pylori eradication could reduce COX-2 expression. EXPERIMENTAL DESIGN: Three hundred subjects were enrolled in this study: half were relatives of 50 H. pylori-infected gastric cancer patients, and half were relatives of 50 H. pylori-infected duodenal ulcer (DU) patients (controls). Each relative underwent endoscopy to detect H. pylori infection and related gastric histology. One hundred and twenty GCFs were found to have H. pylori infection. After H. pylori eradication, 90 of the 120 GCFs were followed up with annual endoscopy examinations over the next 2 years. Gastric COX-2 intensity in all of the specimens collected from these patients was immunochemically stained and graded from 0 to 4. RESULTS: H. pylori infection, gastric atrophy, and intestinal metaplasia (IM) were more prevalent in GCFs than in relatives of H. pylori-infected patients with DUs (P < 0.05). H. pylori-infected GCFs also showed a greater COX-2 intensity than H. pylori-infected relatives of patients with DUs (89.1% versus 62.7%, P < 0.001; relative risk: 4.9; 95% confidence interval: approximately 2.34-10.29). Among the H. pylori-infected GCFs, COX-2 intensity correlated with atrophy and IM (P < 0.001). After H. pylori eradication, gastric COX-2 expression disappeared only in those relatives without IM (P < 0.001). CONCLUSIONS: GCFs are more likely to show greater gastric COX-2 expression and a higher incidence of precancerous lesions after H. pylori infection than the relatives of H. pylori-infected patients with only DUs. H. pylori eradication can reverse gastric COX-2 expression in patients without IM but not in patients with IM.

Gastroduodenal safety of cyclooxygenase-2 inhibitors.

Cyclooxygenase-1 (COX-1) derived eicosanoids promote gastroprotective mucosal defenses and induce platelet aggregation. By sparing COX-1, COX-2 specific inhibitors provide effective anti-inflammatory and analgesic activity while substantially reducing the risk of peptic ulcer disease and GI bleeding compared to dual COX inhibitors (traditional NSAIDs). Clinical studies of the COX-2-selective inhibitors have demonstrated efficacy equivalent to nonselective NSAIDs with significantly lower rates of GI toxicity. The incidence of endoscopic ulcers in some studies with coxibs has approximated placebo. However, as the detection of endoscopic lesions is not always correlated with symptomatic ulcers and ulcer complications, outcome studies of GI safety were performed. The results of large outcome studies have evaluated rofecoxib and celecoxib in over 39,000 patients with osteoarthritis or rheumatoid arthritis. Results of these studies showed that patients taking a supratherapeutic dose of rofecoxib or celecoxib had significantly lower rates of GI-related adverse events than those taking a nonselective NSAID. The GI safety of coxibs for patients using low dose aspirin concomitantly with a coxib appears to be reduced, particularly with regard to ulcer complications. Such data provide support for the COX-2 hypothesis and demonstrate that coxibs provide effective treatment of pain and inflammation with a reduced risk of gastropathy.

Helicobacter pylori stimulates inducible nitric oxide synthase in diverse topographical patterns in various gastroduodenal disorders.

Overproduction of nitric oxide by inducible nitric oxide synthase (iNOS) acts cytotoxically and contributes to inflammation. We explored the roles of iNOS in the pathogenesis of Helicobacter pylori-associated diseases. Using reverse-transcribed PCR, we examined topographical patterns of iNOS mRNA expression in the gastroduodenal mucosa in H. pylori-negative controls and H. pylori-positive patients with duodenal ulcer (DU), gastric ulcer (GU), and ulcer-free gastritis. iNOS expression showed topographical variations among the tested disorders. As compared to controls, DU had a significantly higher expression of iNOS mRNA in the duodenum, GU in the antrum and duodenum, and gastritis in the antrum and corpus. H. pylori eradication yielded a significant reduction of iNOS mRNA in the duodenum of DU and in the antrum of GU. Diverse topographical patterns of H. pylori-induced iNOS expression may contribute to mechanisms by which H. pylori elicits different clinical disorders.

Inducible nitric oxide synthase expression in gastroduodenal diseases infected with Helicobacter pylori.

BACKGROUND: Nitric oxide (NO) is synthesized enzymatically from L-arginine by NO synthase, which is measured by inducible NO synthase (iNOS). Helicobacter pylori (H. pylori) infection produces a state of chronic immunostimulation in the gastric epithelium. Infection with cagA+ H. pylori has greater degree of gastric inflammation and epithelial cell damage. Therefore, we compared the levels of iNOS in patients with H. pylori infection in relation to cagA status and H. pylori-related disease. MATERIALS AND METHODS: One hundred and seven patients, including 51 patients with gastric cancer, 12 patients with gastric ulcer, 18 patients with duodenal ulcer and 26 patients with chronic gastritis, were enrolled in this study. Biopsies from the antrum and body were obtained for histologic examination, culture and reverse transcriptionase-PCR (RT-PCR) for detection of iNOS gene expression. The presence of H. pylori was confirmed by Giemsa staining or culture and the gene expression of cagA in H. pylori isolates was confirmed by PCR. RESULTS: H. pylori infection was detected in 70.1% (75/107) and cagA was detected in 84.8% (28/33). iNOS expression was detected in 49.5% (53/107) and there was no significant difference in iNOS expression according to H. pylori infection nor the cagA status in the gastroduodenal diseases. However, iNOS expression was more frequently detected in gastric cancer than the other H. pylori-related diseases (64.7% vs. 35.7%, p <.05). CONCLUSION: Although NO was thought be involved in the gastric carcinogenesis, the level of NO production was not related to H. pylori infection or cagA status.

Phospholipase C activity of Helicobacter pylori is not associated with the presence of the cagA gene.

BACKGROUND: Knowledge about the possible role of phospholipase C (PLC) activity of microbial pathogens in the development of disease is increasing. Recently attention has focused on investigating PLC activity elaborated by Helicobacter pylori, but the role of this enzyme in H. pylori pathogenesis is still unknown. The aim of this study was to correlate PLC-activity of H. pylori on the basis of the cagA status with the clinical diagnosis of the patients. MATERIALS AND METHODS: Helicobacter pylori was isolated from patients with gastritis (G; n = 38), duodenal ulcer (DU; n = 15), gastric ulcer (GU; n = 11) and gastric cancer (GC; n = 12). Polymerase chain reaction primers DZ3/R009 which amplified a 1350-bp fragment were used to detect the cagA gene. PLC activity was determined using p-nitrophenylphosphorylcholine as substrate. RESULTS: Of the strains, 60% were cagA(+) and 40% were cagA(-). All strains showed PLC activity (2.20 +/- 0.91 U mg(-1) protein). PLC activity showed no association with the cagA status: cagA(+) (2.21 +/- 1.03 U mg(-1) protein), cagA(-) (2.18 +/- 0.79 U mg(-1) protein). Patients with GU had the highest PLC activity (2.77 +/- 1.26 U mg(-1) protein) and patients with GC had the lowest activity (1.8 +/- 0.57 U mg(-1) protein). CONCLUSIONS: Although PLC activity was present in all strains tested, it may only have pathological importance in patients with GU. However, the extent of PLC activity was independent of the presence of the cagA gene.

Adenosine deaminase activity in the gastric mucosa of duodenal ulcer patients in relation to the severity of chronic gastritis and gastric acid secretion.

Earlier reports suggested that adenosine deaminase activity in the gastric corpus mucosa depends upon either gastric acid secretion or severity of chronic gastritis. Knowing that gastric acid secretion corresponds well with histological status of the gastric mucosa, the aim of this study was to determine the enzyme activity in relation to these two factors evaluated simultaneously. The study was conducted on Helicobacter pylori positive duodenal ulcer patients treated for two weeks with either omeprazole alone or omeprazole in combination with amoxycillin and tinidazole. It was found that these two therapeutic regimens decreased adenosine deaminase activity only in the gastric corpus mucosa and a decline was more deeper in patients on omeprazole monotherapy. Moreover, omeprazole monotherapy inhibited completely basal gastric acid secretion and did not change the severity of chronic gastritis, while omeprazole-based eradication therapy decreased both the gastric acid secretion and severity of chronic gastritis. One month after completion of eradication therapy adenosine deaminase activity returned to the pretreatment values but severity of chronic gastritis decreased further. The results of the present study indicate that adenosine deaminase activity in the gastric corpus mucosa depends primarily upon gastric acid secretion but not upon the severity of Helicobacter pylori associated chronic gastritis.