[Is gastric lymphoma an infectious disease?].
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Biomedical subjects
Publications and source records attributed to J P Gisbert.
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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.
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.
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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.
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.
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.
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).
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BACKGROUND: Serology is a good alternative, minimally invasive, diagnostic and screening test for Helicobacter pylori infection. Several immunoglobulin G (IgG) enzyme-linked immunosorbent assay (ELISA) commercial kits have been evaluated. Information on IgA ELISAs is relatively poor, and on the combined use of IgG and IgA ELISAs very scarce. OBJECTIVE: We intended to evaluate the sensitivity, specificity and predictive values of two quantitative commercial IgG and IgA ELISAs (Helico-G and GAP, respectively) and more particularly the accuracy of their combined use. PATIENTS AND METHODS: Serum samples and gastric biopsy specimen culture findings from 400 patients were evaluated. RESULTS: The sensitivity, specificity, positive and negative predictive values of the IgG ELISA Helico-G test in detecting IgG antibodies to H. pylori were 97.2, 85.4, 98.3 and 77.8%, respectively, when compared with those of the reference method used. The corresponding findings for detection of IgA antibodies with the GAP test were 96.4, 80.5, 97.7 and 71.1%, respectively. When considering a patient infected with H. pylori when both tests were positive, the sensitivity, specificity, positive and negative predictive values were 94.1, 85.3, 98.2 and 62.5%, respectively. On the other hand, when at least one test was positive, the corresponding values were 99, 80, 97 and 94%, respectively. CONCLUSION: The IgG ELISA Helico-G and IgA ELISA GAP, taken separately, are good and reliable tests for the detection of antibodies to H. pylori. Furthermore, the combined use of both serological methods provided more useful information compared with single IgG and IgA determinations.
BACKGROUND: To study basal gastrin levels in duodenal ulcer patients and in those with normal endoscopy, according to Helicobacter pylori infection. METHODS: Eighty-four duodenal ulcer patients and 164 with normal endoscopy were studied. Biopsy specimens were taken from gastric antrum and body, and investigated for microbiology (Gram stain and culture) and histology (hematoxilin-eosin stain). Basal gastrin levels were measured (RIA). RESULTS: In duodenal ulcer patients the percentage of chronic gastritis was higher (p < 0.001) than in patients with normal endoscopy without H. pylori infection, and similar to patients infected by H. pylori. In patients with normal endoscopy (n = 164), those infected with H. pylori (n = 115) had higher (p = 0.02) gastrin levels (mean +/- SD) than non-infected (64 +/- 34 vs 51 +/- 14 pg/ml) and similar to duodenal ulcer patients (62 +/- 20 pg/ml). In the multiple regression model analysis H. pylori infection was the only variable which correlated with gastrin levels (regression coefficient 9.48 [SE = 4.59]; multiple correlation coefficient 0.22 [p = 0.008]). Additional variables (age, sex, duodenal ulcer) were not correlated with gastrin levels. Patients with chronic gastritis had higher gastrin levels (p < 0.01) than those with normal histologic mucosa. CONCLUSIONS: In patients with normal endoscopy, those infected with H. pylori had significantly higher basal gastrin levels than non-infected individuals, and similar to duodenal ulcer patients. Therefore, hypergastrinaemia seems to be associated with H. pylori infection, and is not a distinctive feature of duodenal ulcer disease.
BACKGROUND: The aim of this study was to describe the prevalence of Helicobacter pylori infection in patients with gastric ulcer in addition to study its relationship with the ingestion of non steroid antiinflammatory drugs (NSAIDS). METHODS: One hundred sixty-one patients (mean age 54 years, 70% males) in whom gastric ulcer was endoscopically demonstrated were studied. Biopsies of the antrum and gastric body (hematoxillin-eosin, Gram staining and culture) were obtained during endoscopy. RESULTS: H. pylori was detected in 83% (CI = 78-89%) of the cases. In the patients not taking NSAIDS positivity was 87% (CI = 81-93%) while in those with NSAIDS this was only 63% (CI = 43-79%) (p = 0.008). The percentage of patients without H. pylori infection or NSAIDS intake represented 11% (CI = 6-16%). On multivariant analysis the only variable correlated with H. pylori infection was NSAIDS intake (OR = 0.25; CI = 0.09-0.66; chi 2 model = 7.27; p = 0.007) while the remaining variables (sex, age, smoking, alcohol and ulcer site) did not show a significant correlation. The percentage of chronic gastritis was higher (p < 0.001) in H. pylori positive patients in comparison with those who were uninfected (97% versus 67% in the antrum and 78% versus 41% in the gastric body). CONCLUSIONS: The prevalence of infection by Helicobacter pylori in patients with gastric ulcer is greater in those without non steroid antiinflammatory drug (NSAIDS) intake in comparison with those who have this history. The percentage of patients without H. pylori infection or NSAIDS ingestion was very low (11%), and thus it may be deduced that these elements represent pathogenic factors of major importance in gastric ulcer disease since the appearance of this entity in the absence of both is infrequent.
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.
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.
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AIM: To study basal pepsinogen I levels in patients with duodenal ulcer and in subjects with normal endoscopy, depending on Helicobacter pylori status. METHODS: One-hundred and one patients with duodenal ulcer and 74 controls with normal endoscopy were studied. Mean age and gender distribution were: 46 vs 42 years, and 74% vs 43% males, respectively. At endoscopy biopsies from the gastric antrum and body were obtained for histologic (H&E) and microbiologic (Gram and culture) study. Basal levels of serum pepsinogen I were measured (RIA). RESULTS: Among the subjects with a normal endoscopy, those with H. pylori infection had higher pepsinogen I levels (m +/- SD) than non-infected patients (77 +/- 27 vs 62 +/- 28 ng/ml; p < 0.05). Basal levels in duodenal ulcer patients were 107 +/- 38 ng/ml, higher (p < 0.001) than in the group with normal endoscopy (both with and without H. pylori). In multivariate analysis pepsinogen I levels were correlated with H. pylori infection (regression coef.= 17; SE= 8.1), duodenal ulcer (regr. coef.= 22; SE= 5.8) and smoking habit (regr. coef.= 24; SE= 5.2). CONCLUSION: Basal pepsinogen I levels were significantly higher in duodenal ulcer patients than in H. pylori infected subjects with normal endoscopy. The lowest levels corresponded to non-infected patients. Therefore, an additional factor other than H. pylori infection is likely involved in the hyperpepsinogenemia classically reported in duodenal ulcer patients.