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Biomedical subjects

D Boixeda

Publications and source records attributed to D Boixeda.

At least 19 recordsLinked to original sources

[Treatment of low-grade gastric MALT lymphoma with Helicobacter pylori eradication. Follow-up of the histological and molecular response].

BACKGROUND: Low grade gastric MALT lymphoma is associated to infection with Helicobacter pylori. Also, H. pylori eradication can produce histologic regression of the lymphoma. PATIENTS AND METHODS: This study reports the follow-up of a prospective series of 11 patients with low grade gastric MALT lymphoma, stage I, treated with eradicative therapy for H. pylori. After treatment, patients were followed up with sequential endoscopies to asses the histological and molecular regression of the lymphoma, using a score of the histological lesions and the amplification of the IgH gene with PCR analysis. RESULTS: Helicobacter pylori was eradicated in all patients. In 10(90.9%) histological regression of the lymphoma was demonstrated, in 6 of them in the first control after treatment. In the 10 patients with histological response, PCR analysis demonstrated a polyclonal rearrangement of the IgH gene in 6 (60%) and a clonal band in 4 (40%), that eventually disappeared at 12 (SD 4) months after treatment. In 4 patients with a previous polyclonal rearrangement, a clonal band was occasionally detected in any sequential controls; in 2 of these cases the clonal band disappeared 5 and 7 months after treatment and in the remaining 2 its evolution is not yet known. Nine patients have been followed up and are in remission 18 (SD 8) months after treatment. CONCLUSIONS: Eradication of H. pylori can produce histologic regression in stage I low grade gastric MALT lymphoma, and should be the first therapeutic option. Despite histological regression of the lymphoma, PCR analysis can detect a clonal rearrangement of the IgH gene in 40% of the cases, but its significance remains unknown. Sequential and prolonged follow-up is essential to assess whether this lymphoma can be actually cured with eradication therapy for H. pylori.

Adult

[new one-week triple therapies with metronidazole for the eradication of Helicobacter pylori: clarithromycin or amoxycillin as the second antibiotic].

BACKGROUND: To compare the efficacy of two "new" one-week triple therapies (with omeprazole, metronidazole and clarithromycin or amoxycillin) for the eradication of Helicobacter pylori and healing duodenal ulcer. METHODS: Randomised therapeutic trial. Eighty-eight consecutive duodenal ulcer patients with H. pylori infection were studied. At endoscopy, biopsies from both gastric antrum and body were obtained for histologic study (H&E). Two different therapies were administered for one week: omeprazole (O) (20 mg b.i.d.) and metronidazole (M) (500 mg b.i.d.) associated with clarithromycin (C) (500 mg b.i.d.) (group OMC, n = 44) or amoxycillin (A) (1 g b.i.d.) (group OMA, n = 44). Endoscopy with biopsies was repeated one month after completing therapy, and a 13C-urea breath test was also performed. Compliance was evaluated by tablet count. Analysis of data: multiple logistic regression, intention-to-treat. Eradication was defined as the absence of H. pylori by all diagnostic methods. RESULTS: Mean age (standard deviation) was 45(14) years, 75% males. Distribution of variables was similar in both therapeutic groups. Forty-two patients in each group completed the protocol. Eradication was achieved in 90.5% (95% CI = 78-96%) in group OMC and in 57% (42-71%) in group OMA (p < 0.001). In the multivariate analysis the type of therapy was the only variable which influenced on H. pylori eradication (OR = 7.1; CI = 2.2-24; p = 0.001). Ulcer healing was demonstrated in 88% (75-95%) of patients in group OMC and in 71% (56-83%) in group OMA (p = 0.1). Ulcer healing was higher when eradication was achieved (90%; 80-95%) than in H. pylori-positive patients (50%; 31-69%) (p < 0.001). Eradication of H. pylori was the only variable which influenced on ulcer healing (OR = 9.3; CI = 2.8-31; p < 0.001). CONCLUSION: The "new" triple therapy with omeprazole, metronidazole and clarithromycin (administered in a twice-a-day basis and only for one week) had an excellent efficacy for the eradication of H. pylori, significantly higher than that obtained with amoxycillin instead of clarithromycin. Both therapies achieved a high ulcer healing rate when H. pylori was eradicated, even with omeprazole administered only for one week.

Adult

Helicobacter pylori infection and insulin-dependent diabetes mellitus.

Helicobacter pylori is associated with different diseases: duodenal ulcer, rosacea, ischaemic heart disease and gastric cancer. Given the abnormal immunological response and the high prevalence of gastrointestinal symptoms in diabetic patients, we conducted a study on H. pylori prevalence among these patients. We designed a case control study of a population-based cohort. Eighty insulin-dependent diabetes mellitus (IDDM) patients with an average age (24.05 +/- 8.3 years), and 100 control subjects (25 +/- 7.1 years) were selected to verify the seroprevalence of Helicobacter pylori in these populations. One serum sample was obtained from each subject for evaluation of antibodies against Helicobacter pylori, parietal cells (APA) and pancreatic islets cells (ICA). The seroprevalence of H. pylori among IDDM patients aged less than 24 years was significantly higher than among control subjects; the corresponding rate among IDDM aged greater than 24 years was significantly lower than among control subjects. Antibodies against parietal cells (APA) and islet cells (ICA) among H. pylori positive diabetic patients were significantly higher than among H. pylori negative diabetic patients. IDDM patients were subdivided on the basis of the evolutive course of diabetes. Seroprevalence of H. pylori as well as prevalence of ICAs decreased with IDDM duration. Nevertheless, no variation in the prevalence of APAs during the course of diabetes was observed. We observed an association between the seroprevalence of Helicobacter pylori and the duration of IDDM. The seroprevalence of H. pylori and ICA decreased with the evolutive course of diabetes mellitus among IDDM. The prevalence of ICA and APA in IDDM H. pylori positive subjects was higher than among controls.

Adolescent

Helicobacter pylori infection is markedly increased in patients with autoimmune atrophic thyroiditis.

Infection by viral or bacterial pathogens has been suspected in playing a role in the development of autoimmune thyroid disease. Because Helicobacter pylori might be involved in the development of nongastrointestinal conditions such as rosacea, ischemic heart disease, and diabetes mellitus, we evaluated the prevalence of H. pylori infection in patients with autoimmune thyroid disease. Fifty-nine patients with autoimmune thyroid disease were included: autoimmune atrophic thyroiditis (n=21), Hashimoto's thyroiditis (n=18), and Graves' disease (n=20). Twenty patients with nontoxic multinodular goiter served as controls for nonautoimmune thyroid disease, and 11 patients with Addison's disease served as controls for nonthyroid endocrine autoimmune disease. The levels of anti-H. pylori immunoglobulin G (IgG) were determined, and a radiolabeled urea breath test were performed. The prevalence of H. pylori infection was markedly increased in the patients with autoimmune atrophic thyroiditis (85.7%), compared with the controls with nontoxic multinodular goiter (40%) and Addison's disease (45.4%). Infection by H. pylori resulted in increased levels of gastrin, pepsinogen I, and pepsinogen II in the H. pylori-positive groups, compared with the H. pylori-negative groups. A positive linear regression was found between the levels of microsomal autoantibodies and those of anti-H. pylori IgG in patients with autoimmune atrophic thyroiditis (n=21; r=0.79; p < 0.01). Finally, and although the overall prevalence of H. pylori infection was not increased, the anti-H. pylori IgG levels and the results from the breath test were higher in the patients with Graves' disease and Hashimoto's thyroiditis patients than in the controls. Clearly, the prevalence of H. pylori infection is increased in autoimmune atrophic thyroiditis and results in abnormalities of gastric secretory function. The strong relation between the levels of anti-H. pylori IgG and the levels of microsomal antibodies suggests that H. pylori antigens might be involved in the development of autoimmune atrophic thyroiditis or that autoimmune function in autoimmune atrophic thyroiditis may increase the likelihood of H. pylori infection.

Addison Disease

A case of spontaneous peritonitis caused by Weeksella virosa.

A case of spontaneous peritonitis caused by Weeksella virosa is reported. This Flavobacterium has never been reported as a cause of spontaneous bacterial peritonitis. The patient responded to antimicrobial therapy. Clinical and therapeutic implications are discussed.

Flavobacterium

Diagnosis of hepatopulmonary syndrome with contrast transthoracic echocardiography and histological confirmation.

We report a patient with cirrhosis and hepatopulmonary syndrome. This syndrome is an entity characterized by anomalies in the arterial oxygenation in patients with chronic hepatic disease and/or portal hypertension and demonstration of pulmonary vasodilatation (PV) in absence of primary cardiac or pulmonary disease. We show that the finding of PV with transthoracic contrast enhanced echocardiography (TCEE) in the diagnosis of PV is real and corresponds to direct measurement of capillary diameter by morphometry.

Adolescent

Association of Helicobacter pylori infection with cardiovascular and cerebrovascular disease in diabetic patients.

OBJECTIVE: Infection by Helicobacter pylori has been epidemiologically linked to some extradigestive conditions, including ischemic heart disease. Diabetic patients are an at-risk population for cardiovascular and thrombo-occlusive cerebral disease. The aim of the study was to examine a possible relationship between H. pylori infection and cardiovascular or cerebrovascular disease in diabetic patients. RESEARCH DESIGN AND METHODS: This was a cross-sectional case-control study with 127 diabetic patients (both IDDM and NIDDM). Special emphasis was placed on the detection of clinical macro- and microvascular complications, cardiovascular risk factors, acute phase reactants, and serological markers of increased cardiovascular disease risk. H. pylori infection was assessed through the determination of specific Ig-G titers, measured by a commercial enzyme-linked immunosorbent assay. RESULTS: Coronary heart disease was more prevalent in diabetic patients with than without H. pylori (odds ratio [OR] 4.07; 95% CI 1.21-13.6; P < 0.05). A history of thrombo-occlusive cerebral disease was also more frequent in H. pylori-positive diabetic patients (OR 4.8; 95% CI 1.24-18.51; P < 0.05). Other complications such as peripheral arteriopathy, advanced nephropathy, neuropathy, or retinopathy were no differently distributed according to serological status. Alterations in the levels of the following acute-phase reactants and blood chemistry determinations were significantly more profound in H. pylori-positive diabetic patients: high fibrinogen (P < 0.05), high erythrocyte sedimentation rate (P < 0.001), high triglycerides (P < 0.001), and low HDL cholesterol (P < 0.001). There values were also more deeply altered in H. pylori-positive diabetic patients with a history of coronary heart disease, thrombo-occlusive cerebral disease, or both, when compared with H. pylori-positive diabetic patients without those complications. CONCLUSIONS: Our data indicate a possible association of H. pylori infection and the development of coronary heart disease, thrombo-occlusive cerebral disease, or both, in diabetic patients. The importance of this link is highlighted by the possibility of an effective intervention against H. pylori infection.

Biomarkers

ABO blood groups, rhesus factor and Helicobacter pylori.

BACKGROUND: The aim of this study was to demonstrate an association between Helicobacter pylori infection, ABO blood groups and Rhesus factor; providing the association between duodenal ulcer and O group blood as well as the former and H. pylori infection. METHODS: Three-hundred and one healthy subjects were prospectively studied. In all of them ABO blood groups and Rhesus factor were determined by standard techniques. Systemic IgG antibodies against H. pylori were assayed using a quantitative enzyme-linked immunosorbent assay technique (Helico-G, Porton, Cambridge, UK). RESULTS: The overall seroprevalence was 52.2%. H. pylori infection distribution was similar among ABO blood groups and Rhesus factor. No statistically significant differences were observed in mean values of IgG antibodies among different blood groups. CONCLUSIONS: Distribution of H. pylori seroprevalence does not differ between different ABO or Rhesus factor blood groups. This excludes a possible link between this microorganism and the high ulcer prevalence in O blood group.

ABO Blood-Group System

[Gastroduodenal lesions and non-steroidal anti-inflammatory agents. What role does Helicobacter pylori play in this relationship?].

Helicobacter pylori infection and non-steroidal anti-inflammatory drugs (NSAIDs) are the two most important causal factors in gastroduodenal ulcer disease. The coincidence of both occurs frequently and, therefore, demonstration of a possible relationship, and the consequent attitude (giving or not eradication therapy) would have important implications. The lower H. pylori prevalence in gastric ulcer, in comparison with duodenal ulcer, seems to be due greatly to NSAIDs intake, although in a low number of patients this ulcer is not explained by either of these factors. Therefore, the finding of a gastroduodenal ulcer in an H. pylori-negative patient should suggest other possible causes, and among them NSAIDs outstands. Histologic gastritis found in a patient with NSAIDs intake is related to the subjacent presence of H. pylori and not with NSAIDs. It is not clear whether, in patients taking NSAIDs, the infection favors the appearance of dyspeptic symptoms. The possibility of H. pylori and NSAIDs having a synergistic effect on gastroduodenal ulcer disease is a debatable issue. H. pylori eradication in patients taking NSAIDs does not confer a clear advantage in ulcer healing, and the possible protecting effect of eradication on the development of an ulcer in subjects taking NSAIDs is doubtful. In an H. pylori-positive patient in whom an ulcer occurs while taking NSAIDs, it is not possible to know for sure whether the ulcer has been caused by the organism, by NSAIDs, or by both, and therefore it seems logical to administrate an eradication therapy. However, H. pylori eradication with the intention of preventing appearance of gastroduodenal lesions is not so evident. Finally, indications of traditional preventive treatment (with antisecretory drugs or mysoprostol) should not be influenced by the concomitant administration of H. pylori eradication therapy.

Anti-Inflammatory Agents, Non-Steroidal

[Omeprazole plus 2 antibiotics for the eradication of H. pylori, are 5 days of treatment sufficient?].

OBJECTIVE: Combinations of omeprazole plus two antibiotics for seven days have repeatedly been studied and high Helicobacter pylori eradication rates have been obtained, ranging from 80% and 90% in our country. Our objective was to verify whether length of such therapies (with omeprazole, metronidazole and clarithromycin or amoxicillin) can be shortened to five days with no loss of efficacy. METHODS DESIGN: randomized clinical trial. PATIENTS: forty-eight consecutive patients with duodenal ulcer were prospectively studied. The exclusion criteria were previous administration of antibiotics, bismuth or gastroerosive drugs, and associated diseases. During the initial endoscopy biopsy specimens from antrum and corpus were obtained (haematoxylin-eosin). Two therapies were administered for five days: omeprazole (20 mg/12 h) and clarithromycin (500 mg/12 h) plus metronidazole (500 mg/12 h) (n = 24) or amoxicillin (1 g/12 h) (n = 24). One month after therapy was completed a new endoscopy was performed, biopsy specimens were obtained, and the 13C-urea breath test was performed. Compliance of therapy was assessed by questioning the patient and counting the residual medication. DATA ANALYSIS: multiple logistic regression and "intention-to-treat" analysis. OUTCOME VARIABLE: eradication was defined as the absence of H. pylori by all diagnostic methods. RESULTS: Mean age +/- SD was 48 +/- 10 years, 73% were males. Twenty-three patients in each group completed the protocol and the distribution of investigated parameters was similar in both groups. Eradication was obtained in 91.7% (95% CI = 74%-98%) in the metronidazole group and 70.8% (51%-85%) in the amoxicillin group (chi 2 = 2.19; p = 0.13). In the multivariate analysis, OR for the effect of type of therapy on eradication was 4.5 (CI = 0.83-24.7; p = 0.077). No relevant secondary effects were reported. The most common secondary effect was a metallic taste of medication, which was perceived by half of patients in each group. CONCLUSION: The combination of omeprazole, clarithromycin, and metronidazole for only five days has a high eradicating efficacy (approximately 90%), similar to that obtained in previous studies with seven days of therapy. Nevertheless, the association of omeprazole, clarithromycin, and amoxicillin should probably be administered at least for one week to reach an optimal eradicating efficacy.

Amoxicillin

[One-week treatment with omeprazole, clarithromycin and amoxicillin: high efficacy in the eradication of Helicobacter pylori and cicatrization of duodenal ulcer].

BACKGROUND: To evaluate the efficacy of one-week therapy with omeprazole, clarithromycin and amoxycillin in eradicating Helicobacter pylori and healing duodenal ulcer. PATIENTS AND METHODS: One-hundred and thirty-four consecutive duodenal ulcer patients (mean age 47 +/- 13 yrs, 66% males) with H. pylori infection were prospectively studied. At endoscopy, biopsies from both gastric antrum and body were obtained for histologic study (H/E). A 15C-urea breath test was also performed in 98 patients. Omeprazole 20 mg b.i.d., amoxycillin 1 g b.i.d., and clarithromycin 500 mg b.i.d. were administered only for 1 week, and no therapy was administered thereafter. Endoscopy with biopsies and breath test were repeated 1 month after completing therapy. RESULTS: Eradication was achieved in 87.3% of patients (n = 93; 95% CI = 82-93%). In the multivariate analysis the variables which influenced H. pylori eradication were: time of evolution of ulcer disease (p = 0.002) and active chronic gastritis in the antrum (p = 0.04) (chi 2 model = 15.8; p = 0.001). Ulcer healing was demonstrated in 89.5% of patients (84-95%), and healing rate was higher when eradication was achieved (94%; 90-98%) than in H. pylori-positive patients (59%; 36-78%) (p < 0.001). In the multivariate analysis the variables which influenced ulcer healing were: age (p = 0.02) and H. pylori eradication (p = 0.001) (chi 2 model = 21.2; p = 0.0001). An improvement of histologic gastritis was observed when eradication was achieved (p < 0.001). Compliance of therapy was complete in all patients but one and no relevant adverse effects were reported. CONCLUSION: One-week triple therapy with omeprazole, clarithromycin and amoxycillin administered on a twice daily basis achieves a high efficacy in eradicating H. pylori and healing duodenal ulcer. Moreover, this therapy regimen is simple and is associated with a low incidence of adverse effects and a low cost.

Adult

Erosive duodenitis: prevalence of Helicobacter pylori infection and response to eradication therapy with omeprazole plus two antibiotics.

OBJECTIVES: To study the prevalence of Helicobacter pylori infection in patients with erosive duodenitis (ED), the associated gastric histological lesions and their response to eradication therapy with omeprazole plus two antibiotics. METHODS: A prospective study was made of 57 patients with ED (mean age 46 +/- 16 years, 72% males). At endoscopy, biopsies from gastric antrum and body were obtained for histological study (haematoxylin and eosin). A 13C-urea breath test was also performed. Omeprazole 20 mg twice daily plus two antibiotics (amoxycillin 1 g twice daily, clarithromycin 500 mg twice daily, metronidazole 500 mg twice daily) were administered for 1 week. Endoscopy and breath test were repeated 1 month after completing therapy, and the breath test was performed again at 6 months. RESULTS: All patients were H. pylori positive. Overall eradication was achieved in 86% (95% CI 75-93%). Duodenal erosion healing was obtained in 45 patients (79%). Healing was achieved in 86% (CI 73-93%) of cases with successful eradication therapy, but only in 3/8 (37%; CI 8.5-75%) patients with therapy failure (P < 0.01). In the multivariate analysis, H. pylori eradication was the only variable which correlated with erosion healing (odds ratio 10; CI 2-51; P < 0.01). Histological improvement, in both the gastric antrum and body, was demonstrated when eradication was achieved (P < 0.001). Six months after diagnosis H. pylori absence was confirmed in all patients with initial therapy success (all of them asymptomatic), and infection was confirmed in the eight patients who were H. pylori positive after therapy (six of them symptomatic). At 6-month follow-up, endoscopy was normal in 6/7 H. pylori-negative patients with previously persistent ED, while erosions were still present in 4/5 H. pylori-positive patients with previously persistent ED. CONCLUSION: A high prevalence (100%) of H. pylori infection in patients with ED was observed. A 1-week twice daily therapy with omeprazole plus two antibiotics (clarithromycin plus amoxycillin or metronidazole) was very effective in H. pylori eradication, duodenal erosion healing, symptomatic improvement, and in disappearance of associated histological gastritis. These observations suggest that ED should be considered a variant form of duodenal ulcer disease and treated accordingly; that is, with H. pylori eradication therapy.

Adult

Unhealed duodenal ulcers despite Helicobacter pylori eradication.

BACKGROUND: Our aims were 1) to study the influence of several factors (age, sex, smoking, previous ulcer disease, ulcer size, chronic gastritis, serum gastrin and pepsinogen I levels, therapy regimen and, especially, eradication of Helicobacter pylori) on duodenal ulcer healing; 2) to evaluate the frequency of duodenal ulcer healing failure despite eradication of H. pylori, to study why this failure occurs, and to verify its evolution without antisecretory therapy; and 3) to confirm whether a week's prescription of omeprazole is sufficient to obtain ulcer healing. METHODS: Three-hundred and eight patients (mean age, 45 +/- 13 years; 71% males) with duodenal ulcer and H. pylori infection were studied prospectively. Biopsy specimens were obtained at initial endoscopy, and serum gastrin and pepsinogen I levels were measured. A repeat endoscopy (with biopsies) was performed 1 month after eradication therapy had been completed, and a 13C-urea breath test was also carried out. Three eradication therapies were used: omeprazole plus amoxycillin for 2 weeks (OA group, n = 61); 'classic' triple therapy (with bismuth; CTT group, n = 65); and 'new' triple therapies for 1 week (NTT group, n = 182): omeprazole plus two of the following antibiotics: clarithromycin, metronidazole, and amoxycillin. When the ulcer did not heal despite successful H. pylori eradication, antacids were prescribed on an as-needed basis, and endoscopy was repeated 1 month later (2nd control endoscopy). If the ulcer was still present, the acid output (basal and pentagastrin-stimulated) was measured, a secretin test was performed, and a final endoscopy (3rd control endoscopy) was carried out after an additional month. The statistical method used was multiple logistic regression. RESULTS: Overall eradication was achieved in 69% (n = 212) of the patients, and ulcer healing in 76% (n = 233): 57% in the OA group, 80% in the CTT group, and 81% in the NTT group (P < 0.01 when comparing the OA group with the others). Ulcer healing was achieved in 90% of H. pylori-eradicated patients and in only 45% of patients with eradication therapy failure (P < 0.001). Similar results were obtained when only patients treated with NTT were considered: ulcer healing in 90% of patients with the organisms eradicated. Eradication of H. pylori (odds ratio (OR), 11.8; 95% confidence interval (CI), 6.3-22) and sex (OR, 2.5; 95% CI, 1.2-5.1) were the only variables that correlated with ulcer healing in the multivariate analysis. The ulcer persisted despite successful eradication of H. pylori in 22 patients. The duodenal ulcer had healed spontaneously in 73% of these patients at the 2nd control endoscopy. Finally, by the 3rd control endoscopy, only three patients still had duodenal ulcer. Therefore, ulcer healing was finally achieved in 98.1% (95-99%) of patients in whom H. pylori was eradicated. Gastrin, pepsinogen I, acid output, and the secretin test had normal values in all patients. CONCLUSIONS: Eradication of H. pylori favours ulcer healing, which is achieved in most patients in whom the organism is eradicated. Just 1 week of omeprazole therapy (that is, the antibiotic administration period in the new triple therapies) is enough to obtain a high ulcer healing rate. Most duodenal ulcers that do not heal initially despite H. pylori eradication will ultimately do so after several weeks without additional therapy.

Amoxicillin

Relation between histologic subtypes and location of gastric cancer and Helicobacter pylori.

BACKGROUND: Epidemiologic studies have consistently shown an association between Helicobacter pylori infection and gastric cancer, and it is now widely accepted that this organism plays a role in the pathogenesis of this tumor. Nevertheless, there are discrepant results on its relationship with the histologic type and location of gastric cancer within the stomach. The aim of this study was to determine the seroprevalence of H. pylori in a group of gastric cancer patients and the association between H. pylori and specific histologic types of gastric cancer and tumor location within the stomach. METHODS: Systemic IgG antibodies against H. pylori were assayed using an enzyme-linked immunosorbent assay technique in 48 patients (male to female ratio, 31:17; age range, 39-88 years; mean, 69 years) with histologically confirmed gastric cancer and 50 controls (male to female ratio, 33:17; age range, 40-77 years, mean, 64 years). RESULTS: Thirty-one cases of gastric cancer were of the intestinal type, and 12 of the diffuse type; the remaining 5 were unclassified. Thirteen gastric cancers were located in the distal stomach (antrum/pylorus), 12 in the body, and 5 in the proximal stomach (cardia/fundus); the remaining 17 were unclassified because the tumor extended towards more than one location. The overall seroprevalence of H. pylori in patients with gastric cancer and controls was 85.4% and 66%, respectively (P < 0.05). The seroprevalence increased with increasing age in cancer patients, but the difference was not significant. H. pylori seroprevalence among patients with the intestinal type of gastric cancer was higher than in those with the diffuse type (P < 0.05). The prevalence of H. pylori infection was higher among patients with the cancer located distally than in those with the cancer located proximally (P < 0.05). CONCLUSIONS: H. pylori seroprevalence was higher in gastric cancer patients than in controls. The prevalence of H. pylori infection in intestinal-type gastric cancer was clearly higher than in the diffuse type and in the control group. An association was found between H. pylori infection and tumors located distally (antrum/pylorus).

Adenocarcinoma