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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).

Basal and stimulated gastrin levels and gastric acid output five months after therapy for Helicobacter pylori eradication in duodenal ulcer patients

The aim of our study was to demonstrate the effect of Helicobacter pylori eradication on basal and stimulated serum gastrin levels and gastric acid output 5 months after therapy of patients with duodenal ulcer. Thirty-two patients (24 men and eight women with a mean age of 45 years) who had had endoscopy and were diagnosed as having duodenal ulcer entered the study. In all patients three biopsy specimens were taken from the duodenal bulb, gastric antrum, body, and fundus. These specimens were then sent for microbiological and histological examination. Triple therapy consisting of bismuth, metronidazole, and tetracycline was administered. Endoscopy was repeated 1 and 5 months after therapy, and biopsy specimens were again taken from the gastric antrum and body. Before treatment, serum samples were taken to measure basal and stimulated (90 min) gastrin levels after ingestion of two beef cubes, and basal and stimulated acid outputs (after pentagastrin) were studied. Measurements of gastrin and gastric acid output were repeated 5 months after therapy. H. pylori was eradicated in 26 patients (81.3%). Basal gastrin levels (mean +/- SD) at diagnosis and after eradication were 44 +/- 12 and 35.8 +/- 2 pg/ml, respectively (p < 0.05). Similarly, stimulated gastrin levels (integrated values) decreased from 5,303 +/- 1,526 pg/ml/min before therapy to 3,779 +/- 1,204 pg/ml/min after eradication (p < 0.001). However, basal (4.9 +/- 4mEq/h) and stimulated (28.5 +/- 10mEq/h) acid output did not vary after eradication (3.9 +/- 4 mEq/h and 26.2 +/- 12 mEq/h, respectively). We conclude that basal and stimulated gastric acid output are not changed by H. pylori eradication in duodenal ulcer patients 5 months after therapy, in spite of its association with a significant decrease in basal and stimulated gastrin levels.

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 20mg twice daily plus two antibiotics (amoxycillin 1 g twice daily, clarithromycin 500mg twice daily, metronidazole 500mg 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.

Verification of decreased basal and stimulated serum pepsinogen-I levels is a useful non-invasive method for determining the success of eradication therapy for Helicobacter pylori.

BACKGROUND We wanted to demonstrate the effect of Helicobacter pylori eradication on basal and stimulated pepsinogen-I levels in duodenal ulcer patients and to verify whether modification of such levels is a useful method for determining the success of eradication therapy. METHODS Thirty-two patients (24 men; mean age, 45 years) with active duodenal ulcer were studied. In all patients three biopsy specimens were taken from the duodenal bulb, gastric antrum, body and fundus for microbiologic and histologic examination. Triple therapy consisting of bismuth, metronidazole, and tetracycline was administered. Endoscopy was repeated 1 month after completing therapy, and biopsy specimens were again taken from the gastric antrum and body. Serum samples were taken at initial and repeat endoscopies, to measure basal and stimulated (120 min) pepsinogen-I levels after injection of pentagastrin. RESULTS H. pylori was eradicated in 26 patients (81%). Significant histologic improvement, in both the antrum and body, was observed (p < 0.001). Basal pepsinogen-I levels (mean and 95% confidence interval) at diagnosis and after eradication were 106 (92-119) and 87 (74-100) ng/ml, respectively (P < 0.001). Similarly, stimulated pepsinogen-I levels (integrated values) decreased from 4790 (4199-5381) before therapy to 3970 (3383-4557) ng/ml.min after eradication (P < 0.001). Pepsinogen I levels did not change in patients in whom H. pylori was not eradicated. The area under the receiver operating characteristic curve for decreased basal and stimulated pepsinogen-I levels was 0.77 (SE, 0.09) and 0.79 (SE, 0.1), respectively. CONCLUSION H. pylori eradication in duodenal ulcer patients was associated with a significant decrease in basal and stimulated pepsinogen-I levels. Measurement of these levels could determine how successful response to therapy has been in both the eradication and resolution of associated gastritis. Other advantages of this procedure are that it has low cost and results are evident at an early stage.

Increased Incidence of Helicobacter pylori in Gastric Cancer, as Shown by the Rapid Urease Test

Nowadays it is widely accepted that Helicobacter pylori infection is the main etiologic factor in chronic gastritis type B (CGB). However, its contribution to the developement of gastric ulcer remains controversial. In vivo studies on gnotobiotic piglets [1,2] and healthy humans [3, 4] have shown that a typical CGB picture can be reproduced by the ingestion of this microorganism. A further point supporting a relationship between H. pylori and CGB is the possibility of inducing a partial or complete histologic recovery of the disease after the clearance of bacteria by bismuth salts or antibiotics [5–8].

Helicobacter pylori in Subtotal Gastrectomies

Surgery has long been the cornerstone in the management of peptic ulcer disease (PUD) refractory to medical treatment. Although the number of elective interventions has substantially decreased after the marketing of H2 receptor antagonists, the surgical approach maintains its full validity in the management of complicated PUD.