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F Di Mario

Publications and source records attributed to F Di Mario.

At least 55 records · Page 3Linked to original sources
PubMed1999

Efficacy of 7 day lansoprazole-based triple therapy for Helicobacter pylori infection in elderly patients.

BACKGROUND: The prevalence of Helicobacter pylori increases with age. However, data regarding the effects of anti-H. pylori treatments in the elderly are very scarce. METHODS: To evaluate the effect of three lansoprazole-based, 7 day, triple-therapy regimens on H. pylori eradication rates, symptomatology, chronic gastritis activity and serological markers of H. pylori infection in elderly subjects, we studied 150 symptomatic patients over 60 years of age with H. pylori-positive duodenal ulcer (DU, n = 34), gastric ulcer (GU, n= 19) or chronic gastritis (CG, n = 97). Patients were consecutively treated with one of the following regimens: (A) lansoprazole (LNS) 30 mg b.i.d. + clarithromycin (CLR) 250 mg b.i.d. + metronidazole (MTR) 250 mg q.i.d.; (B) LNS 30mg b.i.d. + amoxycillin (AMOX) 1 g b.i.d. + MTR 250 mg q.i.d.; and (C) LNS 30 mg b.i.d. + CLR 250 mg b.i.d. + AMOX 1 g b.i.d. RESULTS: Two months after therapy, the eradication rates of the three treatments, expressed using both intention-to-treat and per-protocol analyses were, respectively; group A, 86 and 91.5%; group B, 80 and 87%; group C, 82 and 89.1%. After therapy, a significant reduction in epigastric pain (P<0.001), heartburn (P=0.02), dyspepsia (P<0.001) and vomiting (P< 0.005) was observed independently of the success of H. pylori eradication. A significantly higher percentage of asymptomatic patients were in the GU-DU group than in CG group (87.7 vs 70.0%, P= 0.032). After therapy, 33 subjects still suffered from symptoms. Persistence of symptoms was significantly associated with an endoscopic diagnosis of oesophagitis and not with H. pylori infection. Patients cured of H. pylori infection showed a significant decrease in the histological activity of both antral and body gastritis (P< 0.0001), a significant drop in immunoglobulin (Ig) G anti-H. pylori antibodies (P< 0.0001) and pepsinogen (PG) C (P<0.0001) and an increase in the PGA/PGC ratio (P<0.0001). CONCLUSIONS: The 7 day, lansoprazole-based triple therapy was well tolerated and highly effective in the cure of H. pylori infection, the reduction of symptoms, chronic gastritis activity and serum levels of IgG anti-H. pylori antibodies and PGC. Persistence of symptoms after therapy was significantly higher in CG than GU and DU patients and was significantly associated with oesophagitis.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1999

Lack of association between Helicobacter pylori infection and extracardiac atherosclerosis in dyspeptic elderly subjects.

BACKGROUND: There are conflicting data on the association between Helicobacter pylori (HP) infection and cardiovascular diseases. AIM: To determine if there is an association between gastric HP infection and atherosclerosis of cerebral or peripheral arteries in elderly subjects. METHODS: 90 dyspeptic elderly subjects had upper gastro-intestinal endoscopy and the gastroduodenal pathology was identified. HP infection was confirmed by gastric histology and the rapid urease test. Vascular ultrasonography of extracranial cerebral arteries and leg arteries was performed to evaluate (i) the presence of an atherosclerotic lesion, (ii) the total length of all plaques documented and (iii) the number of arteries with atherosclerotic lesions. Statistical analysis was by the chi2 test, Yates's corrected chi2 test, the Mann-Whitney test and logistic regression. RESULTS: 59 subjects were HP-positive. These had a higher prevalence of peptic ulcer disease (P = 0.01) and higher serum levels of IgG anti-HP antibodies (P = 0.0001), but no significant differences in the number of atherosclerotic lesions, the total length of the plaques or the number of arteries with lesions. No significant association of HP positivity was found with diabetes mellitus, hypertension, cigarette smoking or coronary heart disease, nor with serum concentrations of HDL-cholesterol, fibrinogen, triglycerides or glucose. CONCLUSIONS: Elderly dyspeptic subjects with gastric HP infection had significantly more peptic ulcer disease but no more atherosclerotic lesions than those who were HP-negative. Atherosclerosis was not associated with HP infection. In this cross-sectional study of elderly patients with dyspepsia, no association between HP infection and extracardiac atherosclerosis was found.

Aged↗
PubMed1999

Helicobacter pylori non-cytotoxic genotype enhances mucosal gastrin and mast cell tryptase.

AIMS: To determine the association, if any, between H pylori genotype and the gastric mucosal variations in the levels of gastrin, somatostatin, tryptase, and histamine. METHODS: 49 patients affected by duodenal ulcer and 48 by non-ulcer dyspepsia were studied. To identify the H pylori genotype, the presence of the cagA gene and vacA alleles m1, m2, s1, and s2 were analysed by polymerase chain reaction. Gastrin, somatostatin, tryptase, and histamine were measured in antral mucosal biopsies. RESULTS: 57 patients were infected with H pylori (30 with duodenal ulcer and 27 with non-ulcer dyspepsia). Gastrin and tryptase were increased in patients with H pylori infection, although the variations were statistically significant only for gastrin; somatostatin and histamine were not influenced by H pylori infection. In patients with non-ulcer dyspepsia the absence of the cagA gene and the presence of vacA alleles s2 and m2 were associated with higher values of tryptase and to a lesser extent of gastrin. These associations were not found in patients with duodenal ulcer. CONCLUSIONS: The cagA negative s2m2 strain of H pylori may be less dangerous for the gastric mucosa than other H pylori strains since it enhances tryptase production by gastric mucosal mast cells; this enzyme is thought to stimulate tissue turnover and favour wound healing.

Adolescent↗
PubMed1999

Polymorphonuclear oxidative burst after Helicobacter pylori water extract stimulation is not influenced by the cytotoxic genotype but indicates infection and gastritis grade.

H. pylori-associated gastric mucosal inflammation is characterized by the presence of polymorphonuclear (PMN) leukocyte infiltrate, which is more severe when the infecting strain is cagA positive. After appropriate stimuli, such as bacterial products, PMN release large amounts of oxygen derived free radicals and proteases, to kill the bacterium. H. pylori seems to be particularly resistant to the oxidative machinery of PMN, which can in turn damage the host gastric mucosa. We evaluated peripheral PMN oxidative burst response after stimulation with water extracts from cagA positive (WEcagA+) or negative (WEcagA-) H. pylori strains in infected (n=31) and non-infected patients (n=32) in comparison with healthy controls (n=16); the influence of gastric mucosal inflammatory infiltrate and activity grade on PMN oxidative burst were also assessed. PMN oxidative burst was measured by FACS analysis. H. pylori water extracts were obtained from bacterial culture. H. pylori genotype was determined by means of the polymerase chain reaction. The PMN oxidative burst in H. pylori infected patients was significantly higher than that in H. pylori negative or healthy controls, no differences being found when the results following WEcagA+ and WEcagA- stimulation were compared. The difference in PMN oxidative burst obtained after WEcagA- and E. coli (standard stimulus for PMN oxidative burst) stimulation discriminated H. pylori infected from non-infected patients with a sensitivity of 90% and a specificity of 97%. The grade of PMN oxidative burst correlated with PMN infiltration grade of the gastric mucosa. Our findings allow to conclude that PMN oxidative burst activation by H. pyloriWE is species- but not strain-correlated. PMN priming, probably consequent to the action of soluble mediators released by mononuclear cells, makes PMN hyper-responsive to H. pylori products, thus favoring the release in the gastric mucosa of infected patients of large amounts of oxygen-derived free radicals, which are not enough to eliminate the infection, but may contribute to damaging the gastric mucosa itself. Peripheral PMN oxidative burst response to H. pyloriWE might furthermore be of help in diagnosing H. pylori infection.

Adult↗
PubMed1999

Upper gastrointestinal diseases in the elderly: report of a meeting held at Vicenza, Italy, on 20 March 1998.

The aim of this article is to summarize the recent progress in geriatric/gastroenterological topics, particularly of the upper gastrointestinal tract, which were the focus of the First International Meeting on Upper Gastrointestinal Diseases in the Elderly, held in Vicenza, Italy, in March 1998. The Meeting was divided into three sections: gastro-oesophageal reflux disease (GORD) in the elderly, Helicobacter pylori infection in the elderly, and nonsteroidal anti-inflammatory drugs (NSAIDs) and the upper gastrointestinal tract in the elderly. GORD presents unique clinical features in elderly patients. The changes in oesophageal function, particularly disorders of motility, only partially explain its unique clinical manifestation. The diagnostic, clinical and therapeutic characteristics of GORD in the elderly need to be studied with attention to avoid its severe local complications, i.e. bleeding, stenosis and Barrett's oesophagus, as well as the more generalized risks of disability, impairment of nutritional status and reduction in the quality of life. Epidemiological studies have demonstrated that the prevalence of H. pylori infection increases with ageing and that subjects living in nursing homes have discrete epidemiological characteristics which render them a high-risk group. The incidence of some histological modifications of the gastric mucosa, particularly intestinal metaplasia, gastric atrophy and gastric cancer, seems to be both age- and H. pylori-related; their study in elderly subjects could give the key to understanding the pathophysiological mechanisms of H. pylori gastric damage. NSAID-related gastroduodenal damage, particularly haemorrhage, increases with age. Ageing, per se, does not modify significantly gastric aggressive factors, such as acid and pepsin secretions; however, a selective and specific reduction in some gastric defensive mechanisms seems to occur with ageing. Clinical studies on prevention of NSAID damage have rarely been performed in an elderly population, and meta-analyses of published data can lead to conflicting conclusions from a pharmaco-economic perspective. The identification of risk factors of NSAID-related gastroduodenal damage must be the foundation of preventive medical care for elderly subjects.

Aged↗
PubMed1998

Optimal PPI-based triple therapy for the cure of Helicobacter pylori infection: a single center comparison of four 14-day schedules.

BACKGROUND: Helicobacter pylori eradication is accomplished using a wide array of drugs combined in a multitude of dosage schedules. The aim of the present study was to define the best 14-day eradication schedule using a PPI plus either two antibiotics or one antibiotic and bismuth. MATERIAL AND METHODS: For this study, 367 subjects (198 males, 169 females, age 22-87 years) with document H. pylori infection of the stomach were recruited from out-patients of the Gastroenterology Department of the Venezia Hospital. In all patients, H. pylori infection was identified by histology and the CLO-test. Patients were treated as follows: 1) PPI (P) plus clarithromycin (C) 250 mg plus amoxicillin (A) 1000 mg bid (P + C + A); 2) P plus C plus bismuth subcitrate (B) 120 mg qid (P + C + B); 3) P plus C plus tinidazole (T) 500 mg bid (P + C + T); and 4) P plus A plus T bid (P + A + T). After two months, an upper gastrointestinal endoscopy was repeated for end point histological evaluation and the CLO- test. Positivity of one of the two methods was considered sufficient to define H. pylori as "not eradicated". STATISTICS: Chi-squared test and Fisher exact test. RESULTS: Thirty-three subjects dropped out (six due to adverse events). P + C + B was proven significantly less effective than P + C + A, P + C + T and P + A + T, eradication rates being, respectively, 75.0%, 90.5%, 87.6%, 92.0%, (p = .005, per protocol analysis). CONCLUSIONS: All PPI-based triple therapies tested in this study were effective in curing H. pylori infection; however, P + C + B resulted in rates too low (< 85%) to be recommended. P + C + A and P + A + T resulted in the high cure rates and thus may be considered the treatment of choice.

Adult↗
PubMed1998

Cytotoxin-associated gene A-positive Helicobacter pylori infection in the elderly. Association with gastric atrophy and intestinal metaplasia.

To evaluate if the infection with strains of cytotoxin-associated gene A (CagA)-positive Helicobacter pylori is associated with either peptic ulcer and gastric atrophy or intestinal metaplasia in the elderly, we studied 71 H. pylori-positive patients older than 62 years old (34 men, 37 women; mean age, 77.5 years; range, 62-89 years) affected with gastric ulcer (GU) (n = 10), duodenal ulcer (DU) n = 22), or chronic gastritis (CG) (n = 39). H. pylori infection was documented by means of gastric histology, rapid urease test, and polymerase chain reaction (PCR) assay performed on gastric biopsies using two sets of primers: one for the ureC gene specific for H. pylori, and the second specific for the CagA gene. H. pylori-CagA positivity was significantly more common in patients with GU (9 of 10, 90%) than with DU (11 of 22, 50%; p < 0.05) or CG (17 of 39, 43.5%; p = 0.01). Gastric atrophy and intestinal metaplasia were significantly more common in CagA-positive patients than in CagA-negative patients (gastric atrophy: 40.54% vs 11.76, p = 0.007; intestinal metaplasia: 40.54% vs 14.70%, p = 0.01). No difference in prevalence of gastric atrophy and intestinal metaplasia was found in patients divided according to pathology (GU, DU, or CG). Logistic regression demonstrated that gastric atrophy and intestinal metaplasia were independent factors significantly associated with CagA-positivity (gastric atrophy: odds ratio = 4.53, 95% confidence interval 1.25-16.4; intestinal metaplasia: odds ratio = 3.44, 95% confidence interval 1.01-11.7). Our findings help to confirm the hypothesis that an infection with CagA-positive H. pylori strains may be catalytic in inducing gastric changes which can evolve into malignancies.

Aged↗
PubMed1998

Low dose of clarithromycin in triple therapy for the eradication of Helicobacter pylori: one or two weeks?

The aims of this pilot study were: (i) to compare the efficacy of low-dose clarithromycin (250 mg twice daily) for 1 or 2 weeks; and (ii) to evaluate possible therapeutic advantages in associating the low-dose clarithromycin with an anti-secretory agent or tripotassium dicitrate bismuthate (De Nol; Yamanouchi Pharm, Corugate Milano, Italy). A prospective, randomized, open trial was carried out on consecutive outpatients with dyspeptic symptoms and Helicobacter pylori infection. We enrolled 129 patients in one of the following schedules: (A) De Nol 120 mg q.i.d., clarithromycin 250 mg b.i.d. and metronidazole 250 mg q.i.d. for 2 weeks; (B) omeprazole 20 mg b.i.d., clarithromycin 250 mg b.i.d. and metronidazole 250 mg q.i.d. for 2 weeks; or (C) omeprazole 20 mg b.i.d., clarithromycin 250 mg b.i.d. and metronidazole 250 mg q.i.d. for 1 week. Results were evaluated by Per Protocol (PP) and Intention-To-Treat analysis (ITT). Eradication rate was 100% after treatment A, 92.6% after treatment B and 86.5% after treatment C by PP and 83.3, 75.7, and 68.1%, respectively by ITT. Side effects were reported by 16 subjects: 26.6% in group A; 9.1% in group B; and 7.5% in group C; in two cases side effects led to the withdrawal of the treatment. In conclusion, 500 mg clarithromycin per day in association with omeprazole and metronidazole, for 1 week gave comparable results to the same schedule for a 2 week period. The use of clarithromycin with bismuth and metronidazole produced a therapeutic gain compared with both of the anti-secretory schedules, although this was not statistically significant.

Adult↗
PubMed1998

Helicobacter pylori cytotoxic genotype is associated with peptic ulcer and influences serology.

OBJECTIVE: We studied 146 patients with peptic ulcer disease (n = 72), antral gastritis (n = 58), or duodenitis (n = 16) to ascertain whether the cytotoxic genotype of Helicobacter pylori (Hp) is associated with peptic ulcer disease and/or antral gastritis and whether it influences the circulating levels of total anti-Hp antibodies, anti-cagA antibodies, and pepsinogens. METHODS: A gastric juice sample was obtained from each patient. After DNA extraction, polymerase chain reaction was used to amplify the genes urease A (ureA), cagA, and vacA of Hp. RESULTS: A significant association was found between peptic ulcer disease and the cytotoxic genotypes, characterized by the presence of s1 and m1 alleles of vacA and by cagA. Patients with a cagA-positive genotype showed a significant increase in anti-cagA antibodies and also had significantly increased circulating levels of pepsinogen C. CONCLUSIONS: Cytotoxic Hp strains are mainly involved in determining peptic ulcer disease, but not antral gastritis. The higher levels of circulating pepsinogen C found in patients infected with cytotoxic genotypes may reflect the higher degree of inflammation sustained by these strains.

Adult↗
PubMed1998

Analysis of Helicobacter pylori vacA and cagA genotypes and serum antibody profile in benign and malignant gastroduodenal diseases.

BACKGROUND: Helicobacter pylori species comprise different strains, cytotoxic and non-cytotoxic, which can be identified on the basis of their genomic pattern. AIMS: (1) To evaluate the polymorphism of the vacA gene and to ascertain whether the cagA gene is present in patients with gastric adenocarcinoma. (2) To study the anti-H pylori antibody profile using western blotting. PATIENTS: Twenty one patients with gastric adenocarcinoma and 71 with H pylori associated benign disease (nine gastric ulcer, 29 duodenal ulcer, 25 antral gastritis, and eight duodenitis). METHODS: The polymerase chain reaction was used to verify the presence or absence of cagA and to study the polymorphism of vacA in gastric mucosal samples obtained during endoscopy for patients with benign diseases and at surgery for patients with gastric adenocarcinoma. Fasting sera were used to assess anti-H pylori antibodies against different H pylori antigens by western blotting. RESULTS: CagA gene and the allele s1 of vacA were significantly less frequent in patients with antral gastritis (60% and 60%) compared with patients with gastric adenocarcinoma (94% and 100%) and with other non-malignant gastroduodenal diseases (93% and 87%) (chi 2 = 16.01, p < 0.001; and chi 2 = 13.97, p < 0.01). In patients with gastric adenocarcinoma, antibodies against a 74 kDa H pylori antigen were less frequently found than in patients with benign diseases. CONCLUSIONS: H pylori infection caused by cagA positive/vacA s1 strains is a frequent finding in patients with gastric adenocarcinoma. Prospective studies are needed to confirm whether the low incidence of positive serological response to the 74 kDa H pylori antigen in patients with gastric adenocarcinoma is important.

Adenocarcinoma↗
PubMed1998

The long-term clinical outcome of elderly patients with Helicobacter pylori-associated peptic ulcer disease.

The objective of this study was to evaluate the long-term efficacy of Helicobacter pylori (HP) eradication treatment in elderly patients with HP-associated peptic ulcer. A total of 56 subjects, 25 affected with gastric ulcer (GU, 9 males, 16 females, mean age 77.8 years, range 67-93) and 31 with duodenal ulcer (DU, 19 males, 12 females, mean age 76.5 years, range 65-87) were confirmed to be HP-positive by gastric histology and the rapid urease test. All patients were then consecutively treated with omeprazole for 4 weeks plus one or two antibiotics for 1 week as anti-HP treatment. Clinical checkups were then performed every 3 months for 1 year for the evaluation of symptoms and clinical recurrences. Endoscopy with gastric biopsies was repeated after 1, 3 and 12 months for the evaluation of ulcer healing, HP infection and chronic gastritis activity. Statistical analysis was performed by means of the Student t test for unpaired data, the Fisher exact test (two-tailed), and the McNemar chi 2 test. After 4 weeks of treatment, endoscopy confirmed healing of the ulcer in all patients, regardless of the treatment used to cure HP infection. Two months after the end of therapy, a total of 44 patients were HP-negative and 12 patients were still HP-positive. During the 1-year follow-up period 1/44 (2.2%) of the HP-eradicated patients and 5/12 (41.6%) of the still HP-positive patients suffered relapses (p = 0.001): the difference between the two groups remained statistically significant when patients were divided into the subgroups, GU (p = 0.01) and DU (p = 0.04). Two months after the end of therapy, there was still a significant reduction of symptoms both in HP-eradicated (p < 0.0000) and in HP-positive (p = 0.002) patients. After 1 year, however, there was a significantly decreased symptomatology only in HP-eradicated subjects (p < 0.0000) and not in patients still HP-positive. After both 2 months and 1 year of follow-up, chronic gastritis activity demonstrated a significant improvement only in HP-eradicated patients (p = 0.0000). In conclusion, the eradication of HP infection significantly improved the long-term clinical outcome of peptic ulcer disease in the elderly, reducing the recurrences of GU and DU, the patient's symptomatology and the histological signs of chronic gastritis activity. The cure of HP infection is, therefore, strongly recommended in elderly patients with HP-associated peptic ulcer disease.

Aged↗
PubMed1998

Strategy for the retreatment of failed Helicobacter pylori eradication therapy: a case series.

BACKGROUND: Helicobacter pylori eradication therapy can be unsuccessful in 5 to 20% of patients. AIM: To investigate the validity of a strategy using triple therapies for the retreatment of patients with eradication failure, avoiding retreatment with antibiotics prone to induce resistance after use in the first treatment. PATIENTS AND METHODS: From a consecutive sampling of 108 patients still Helicobacter pylori-positive after a first course of antibiotic-based treatment, 74 (68.5%) agreed to a second course of triple therapy. Group 1 (N = 17): treatment failures on an imidazole (1)-based therapy were retreated with clarithromycin (C)-based regimen; Group 2 (N = 28): failures on a C-based therapy with an I-based regimen; Group 3 (N = 7): failures on an IC-based therapy using an I-based regimen and Group 4 (N = 22): failures on a non-I/non-C based therapy with either an I-based, C-based or IC-based regimen. The presence of Helicobacter pylori was assessed by histology and the CLO-test at study entry and two months after stopping therapy. RESULTS: Nine patients were withdrawn from the study (12.2%) due to a lack of end point endoscopy. Helicobacter pylori was cured after the second course of therapy in all but seven patients [10.7% failure by Per Protocol analysis, 21.6% by Intention-To-Treat analysis]. No statistically significant differences were found between the four groups (Group 1: 92.9% PP, 76.5% ITT; Group 2: 90.9% PP, 71.4% ITT; Group 3: PP and ITT 85.7%; Group 4: PP and ITT 86.4%). Minor adverse events were experienced in nine, none of whom required withdrawal from the drug therapy. CONCLUSIONS: A second course of triple therapy with alternate antibiotics effectively eradicated Helicobacter pylori, with only very few treatment failures. This suggests that the therapeutic strategy employed may be recommended.

Adult↗
PubMed1997

Role of Helicobacter pylori infection on upper gastrointestinal bleeding in the elderly: a case-control study.

Nonsteroidal antiinflammatory drug (NSAID) use is known to be associated with a high incidence of upper gastrointestinal tract bleeding in the elderly. The increased prevalence of Helicobacter pylori (HP) infection, which also occurs with age, suggests that an interaction between NSAID use and HP infection may explain the higher incidence of ulcer complications in the elderly. The aim of the present study was to determine if a relationship exists between HP infection and NSAID use in elderly patients with upper gastrointestinal bleeding. This was a case-control study on 146 elderly patients (73/group). The bleeding group consisted of 37 males and 36 females (mean age 80.4 years, range 70-96) with symptoms (hematemesis, melena, anemia with loss of more than 3 g hemoglobin), and endoscopic stigmata of bleeding. The control group consisted of 73 age- and sex-matched patients with the same endoscopic diagnosis but with no endoscopic stigmata of bleeding. NSAID use was evaluated by interview at the time of endoscopy, and HP infection was confirmed in all cases by histology and the rapid urease test. Statistical analyses were performed using the chi-square test and logistic regression. In both groups, 46.57% of patients were affected with gastric ulcer, 36.98% with duodenal ulcer, and 16.43% with erosive gastritis. The bleeding group had a significantly higher percentage of NSAID users (53.42% vs 19.17%, P < 0.0001) and a lower percentage of HP-positive patients (47.94% vs 72.60%, P = 0.004). The NSAID use pattern was as follows: occasional users (sporadic, as needed during the previous week): 53.8% of bleeding cases and 50% of controls; acute users (continuous therapy for less than one month): 17.9% of bleeding cases and 28.5% of controls; and chronic users (continuous therapy for more than one month): 28.2% of bleeding cases and 21.4% of controls. The logistic regression demonstrated that NSAID use was significantly related to an increase risk of bleeding both in gastric (odds ratio: 4.98, 95% CI: 1.83-13.6) and duodenal ulcer patients (odds ratio: 10.2, 95% CI: 2.25-46.7) while HP-positivity presented a significant inverse relationship with bleeding only in subjects with gastric lesions (odds ratio: 0.20, 95% CI: 0.07-0.55). NSAID use and HP infection were also shown to be independent, unrelated factors, with the overall risk of bleeding in HP-positive NSAID users identified to be significantly less than in HP-negative NSAID users. In conclusion, in elderly patients: (1) NSAID use increases the risk of upper gastrointestinal bleeding while HP infection was associated with a low risk for gastric bleeding; and (2) the two factors are independent variables, therefore the HP-positive NSAID user has a lower risk than the HP-negative NSAID user.

Aged↗
PubMed1997

The effect of Helicobacter pylori infection on NSAID-related gastroduodenal damage in the elderly.

OBJECTIVE: To evaluate the effect of Helicobacter pylori infection on the prevalence and severity of non-steroidal anti-inflammatory drug (NSAID)-related upper gastrointestinal lesions in the elderly. PATIENTS AND METHODS: One hundred and twenty-eight symptomatic NSAID users (47 males, 81 females; mean age 79.5 years, range 67-95 years) were evaluated by endoscopy. NSAID use was evaluated at the time of endoscopy by interview and general practitioners' clinical records. Patients were separated by the following use patterns: (1) Occasional Users: patients who had taken NSAIDs sporadically, on an as-needed basis in the 7-day period before endoscopy; (2) Acute Users: patients who had taken NSAIDs regularly during the last month; and (3) Chronic Users: patients who had taken NSAIDs regularly for more than 1 month. H. pylori infection was diagnosed by gastric histology (modified Giemsa stain) and the rapid urease test. Statistical analysis was performed by means of the chi 2 test with standardized deviates. RESULTS: Of the 128 subjects, 107 (83.6%) presented with gastroduodenal damage: 3 patients (2.3%) had erosive oesophagitis; 38 patients (29.7%) had gastric ulcer (GU); 43 patients (33.6%) had duodenal ulcer (DU); 3 patients (2.3%) had both GU and DU and 20 patients (15.6%) had erosive gastritis. Seventy-four of the 128 patients (57.8%) were found to be H. pylori positive. In comparison to H. pylori-negative subjects, those who were H. pylori-positive had a significantly higher percentage of GU and DU (74.3% vs. 53.7%, P = 0.02) and a lower percentage of non-gastroduodenal lesions (10.8% vs. 24.0%, P = 0.05). No significant trend in H. pylori positivity was found in the 50/128 (39.06%) patients who presented with bleeding lesions (H. pylori positive 36.5%, H. pylori negative 42.6%, not significant). At endoscopy 78% of occasional NSAID users, 93.8% of acute users and 88.7% of chronic users presented with upper gastrointestinal lesions (not significant). No significant differences in NSAID use patterns were observed between H. pylori-positive and H. pylori-negative subjects. CONCLUSION: H. pylori infection in the elderly is associated with an increase in the NSAID-related GU and DU, but not with a higher prevalence of upper gastrointestinal bleeding.

Aged↗
PubMed1997

Impaired fibrinolysis and increased protease levels in gastric and duodenal mucosa of patients with active duodenal ulcer.

OBJECTIVES: Cathepsin B and L (cysteine proteases), urokinase- and tissue-type plasminogen activators (serine proteases), and type-1 inhibitor are involved in gastric mucosal injury. We determined tissue protease levels in duodenal ulcer and their relationship to ulcer phase, bleeding tendency, Helicobacter pylori infection, and use of H2-blockers. METHODS: Endoscopic biopsies of antral and duodenal mucosa were obtained from 61 patients with active or healed duodenal ulcer and control subjects. Antigen concentrations were measured by ELISA. RESULTS: Significantly higher levels of cathepsins, urokinase-type plasminogen activator, type-1 inhibitor, and significantly lower levels of tissue-type plasminogen activator were found in active ulcers. Bleeders had the highest cathepsins and urokinase-type plasminogen activator levels. Higher levels of urokinase-type plasminogen activator, cathepsin B, and type-1 inhibitor were observed in Helicobacter pylori-positive patients. CONCLUSIONS: Our results suggest that impaired fibrinolysis (tissue-type plasminogen activator), intramucosal proteases (cathepsins), tissue remodeling, and angiogenesis (urokinase-type plasminogen activator and type-1 inhibitor) are involved in duodenal ulcer formation and healing.

Adult↗