[Infection by Helicobacter pylori: where is the limit?].
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Biomedical subjects
Publications and source records attributed to D Boixeda.
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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.
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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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One hundred and forty-four episodes of spontaneous bacterial peritonitis (SBP) treated in our service between July 1988 and September 1995 were studied retrospectively to assess the clinical presentation, microbiological findings, possible pathogens, treatment and course. Ascites, abdominal pain and fever were the most common symptoms. Only 3.5% of cases were asymptomatic. The outcome was fatal in 12 (8.33%). Among the factors analyzed, only a prothrombin time of less than 35% correlated significantly with a higher mortality rate (60% and 8.33%, respectively; p < 0.01). Ascitic fluid culture was positive in 43.05% of cases; significant differences existed between these patients and those with negative ascitic fluid culture with respect to clinical findings or course. Gram-negative microorganisms were those most frequently isolated (48.38%). Treatment was initiated within 12 hours in 77.7% of the patients, between 12 and 72 hours in 11.8% and later in 10.41%. Intravenous cefotaxime was administered in 86.1% of cases and other drugs or drug combinations in only 13.9%; the mortality rate was much lower with cefotaxime (2.4% vs 45%; p < 0.01).
BACKGROUND: Helicobacter pylori infection is associated with low-grade gastric MALT lymphoma, and available data support that the eradication of the H. pylori can cause histological regression of the lymphoma. PATIENTS AND METHODS: Nine patients with low-grade gastric MALT lymphoma were treated with amoxicillin, metronidazole, and omeprazole for 14 days in a prospective study. Patients were followed up with sequential endoscopy, mapping gastric biopsies, and molecular studies with PCR amplification of the IgH gene in order to assess the response to H. pylori eradication and the evolution of the histological molecular responses. RESULTS: H. pylori was eradicated in all patients and reinfections were not demonstrated. After H. pylori eradication treatment, the lymphoma regressed both endoscopically and histologically in eight of the nine patients (88.8%). In four of the eight histologically cured patients, no clonal band was detected by PCR; in the remaining four patients; PCR identified a clonal band, which disappeared in all patients after a mean of 12 +/- 4 months. No clonal band was detected by the PCR analysis in any of the eight patients with histological regression after a median of 7 +/- 6 months (range 1-20). The seven followed-up patients have a persistent clinical and histological remission after a median of 14 +/- 5 months. CONCLUSIONS: (1) Low-grade gastric MALT lymphoma can be histologically cured with eradication therapy for H. pylori. (2) After histological regression, PCR amplification of the IgH gene can identify an eventually persisting clonal population. (3) Sequential histological and molecular studies are essential for the assessment of the evolution of the lymphoma. (4) The clonal population tends to disappear, but its disappearance may be delayed for months. (5) Patients with histological regression but with a persistent clonal band should not be treated unless the lymphoma can be histologically demonstrated. All these observations suggest that gastric lymphoma can be effectively cured, but the ultimate fate of these patients is unknown until long-term follow-up studies are available.
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Two cases are reported of spontaneous ascitic fluid Candida albicans peritonitis in two patients with liver cirrhosis secondary to HBV. In non of the two cases was there evidence of findings associated with secondary peritonitis, where ascitic fluid Candida infection has usually been reported.
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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.
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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.