Basal and stimulated gastrin and pepsinogen levels after eradication of Helicobacter pylori: a 1-year follow-up study.

AIM: A decrease in gastrin and pepsinogen (PG) levels 1 month after Helicobacter pylori eradication has been described repeatedly, but the long-term progression of such a decrease has been scarcely studied. We therefore studied the effect of H. pylori eradication on basal and stimulated gastrin and PG levels for 1 year. Initially, the usefulness of measuring these parameters for the noninvasive diagnosis of H. pylori eradication was validated. Furthermore, an assessment was made of the association between H. pylori reinfection and a re-increase in gastrin and PG values. Finally, an evaluation was made of the variables influencing gastrin and PG concentration, with particular attention to H. pylori infection and histological lesions of gastric mucosa. METHODS: Two-hundred and twenty-two patients with duodenal ulcer were studied prospectively. Exclusion criteria were the administration of antibiotics, H2 antagonists, omeprazole or bismuth prior to endoscopy. In all patients serum basal levels of gastrin, PGI, and PGII were measured before and 1 month after completing eradication therapy. In the successfully eradicated patients, gastrin, PGI, and PGII were also measured at 6 and 12 months. In 80 patients stimulated measurements of gastrin (after ingestion of two beef cubes) and PGI (after injection of pentagastrin) were also performed. H. pylori-negative patients after therapy underwent a urea breath test at 6 and 12 months, and patients who had stimulated gastrin and PG concentration measured had also an endoscopy performed at 6 months. RESULTS: H. pylori was eradicated in 73% of patients. A histological improvement was observed 1 month after completing H. pylori eradication therapy, both at gastric antrum and body (P < 0.001), while a further improvement at antrum was demonstrated at 6 months (P < 0.01). With regard to the different cut-off points for decreased basal and stimulated measurements for diagnosing H. pylori eradication, the best results were obtained, respectively, with PGII (sensitivity of 90% and specificity of 76%) and PGI 30 min after stimulation (sensitivity and specificity of 82%), with an area under the ROC curve of 0.87 in both cases. In the multiple regressions analysis H. pylori status correlated with gastrin, PGI and PGII after therapy (P < 0.001), while histological lesions correlated only with gastrin levels (P < 0.05). A decrease in basal and stimulated serum parameters was demonstrated immediately after eradication (Wilcoxon test, P < 0.001), and an additional decrease (at 6 months) was observed just in PGI (Friedman test, P < 0.01). However, gastrin and PGII values remained unchanged after the first month post-eradication. Seven patients were reinfected with H. pylori during follow-up. Quantitation of basal and stimulated gastrin and PGI levels was not reliable as a reinfection marker. Regarding basal PGII, the parallelism was strong at 6 months (re-increase in all four reinfected patients), although only in one out of three with reinfection at 1 year did PGII rise at that stage. CONCLUSIONS: (1) Measurement of gastrin and PG levels (especially basal PGII values) is a useful non-invasive method to confirm H. pylori eradication after therapy. (2) H. pylori eradication is associated with a significant decrease in basal and stimulated gastrin levels and in basal PGII levels that is detected immediately (1 month) after finishing treatment, and remains unchanged for 1 year. However, the decrease in basal and stimulated PGI levels occurs progressively for 6 months, although such levels remain also unchanged afterwards. (3) Measurement of gastrin and PGI concentrations has a limited usefulness in the diagnosis of H. pylori reinfections after successful eradication, although PGII determination could be more useful in this situation.

Ampicillin-sulbactam and amoxicillin-clavulanate susceptibility testing of Escherichia coli isolates with different beta-lactam resistance phenotypes.

The activities of ampicillin-sulbactam and amoxicillin-clavulanate were studied with 100 selected clinical Escherichia coli isolates with different beta-lactam susceptibility phenotypes by standard agar dilution and disk diffusion techniques and with a commercial microdilution system (PASCO). A fixed ratio (2:1) and a fixed concentration (clavulanate, 2 and 4 micrograms/ml; sulbactam, 8 micrograms/ml) were used in the agar dilution technique. The resistance frequencies for amoxicillin-clavulanate with different techniques were as follows: fixed ratio agar dilution, 12%; fixed concentration 4-micrograms/ml agar dilution, 17%; fixed ratio microdilution, 9%; and disk diffusion, 9%. Marked discrepancies were found when these results were compared with those obtained with ampicillin-sulbactam (26 to 52% resistance), showing that susceptibility to amoxicillin-clavulanic acid cannot be predicted by testing the isolate against ampicillin-sulbactam. Interestingly, the discrimination between susceptible and intermediate isolates was better achieved with 4 micrograms of clavulanate per ml than with the fixed ratio. In contrast, amoxicillin susceptibility was not sufficiently restored when 2 micrograms of clavulanate per ml was used, particularly in moderate (mean beta-lactamase activity, 50.8 mU/mg of protein) and high-level (215 mU/mg) TEM-1 beta-lactamase producer isolates. Four micrograms of clavulanate per milliliter could be a reasonable alternative to the 2:1 fixed ratio, because most high-level beta-lactamase-hyperproducing isolates would be categorized as nonsusceptible, and low- and moderate-level beta-lactamase-producing isolates would be categorized as nonresistant. This approach cannot be applied to sulbactam, either with the fixed 2:1 ratio or with the 8-micrograms/ml fixed concentration, because many low-level beta-lactamase-producing isolates would be classified in the resistant category. These findings call for a review of breakpoints for beta-lactam-beta-lactamase inhibitors combinations.

Mutations in 23S rRNA in Helicobacter pylori conferring resistance to erythromycin do not always confer resistance to clarithromycin.

Mutations conferring resistance to erythromycin or clarithromycin in Helicobacter pylori were studied. Mutation A2142G was consistently associated with clarithromycin MIC of > 256 micrograms/ml, whereas mutants carrying A2143G had MICs ranging from < or = 0.016 to > 256 micrograms/ml, suggesting that additional factors account for the observed multiple levels of resistance to clarithromycin.

Allele-specific PCR method based on pncA and oxyR sequences for distinguishing Mycobacterium bovis from Mycobacterium tuberculosis: intraspecific M. bovis pncA sequence polymorphism.

An allele-specific amplification method based on two genetic polymorphisms to differentiate Mycobacterium tuberculosis from Mycobacterium bovis was tested. Based on the differences found at position 169 in the pncA genes from M. tuberculosis and M. bovis, a PCR system which was able to differentiate most of the 237 M. tuberculosis complex isolates tested in one of the two species was developed. All 121 M. tuberculosis strains showed the expected base (cytosine) at position 169. Most of the M. bovis isolates had a guanine at the cited position. Nevertheless, 18 of the 116 M. bovis isolates, all of them goat isolates, showed the pncA polymorphism specific to M. tuberculosis. These results suggest that goat M. bovis may be the nicotinamidase-missing link at the origin of the M. tuberculosis species. Based on the polymorphism found at position 285 in the oxyR gene, the same system was used to differentiate M. tuberculosis from M. bovis. In this case, DNAs from all 121 M. tuberculosis isolates had the expected base (guanine) at this position. In addition, all 116 M. bovis isolates, including those from goats, showed the identical polymorphism (adenine). The oxyR allele-specific amplification method can differentiate M. bovis from M. tuberculosis, is rapid (results can be obtained in less than 3 h), and is easy to perform.

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.

Usefulness of the combined IgG and IgA antibody determinations for serodiagnosis of Helicobacter pylori infection.

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.

Helicobacter pylori infection in a healthy population in Spain.

OBJECTIVE: To determine the seroprevalence of Helicobacter pylori infection in healthy individuals in Spain and its relationship with different epidemiological features. PATIENTS AND METHODS: The study was conducted on a large group of healthy individuals without ulcer disease antecedents or other gastrointestinal disease; moreover, information, was obtained on symptoms attributable to the gastrointestinal tract, smoking, alcohol consumption, non-steroidal anti-inflammatory drug (NSAID) use as well as the presence of peptic ulcer disease antecedents among first-degree relatives. The H. pylori infection status was ascertained by immunoglobulin G (IgG) antibody determination, using a quantitative enzyme-linked immunosorbent assay. RESULTS: Three hundred and eighty-one individuals (138 males and 243 females) were included in the study (mean age: 34.3 +/- 12.9 years; range: 5-77). Two hundred and two individuals (53%) were positive for H. pylori IgG antibodies. A consistent increase in H. pylori infection seroprevalence with increasing age was observed. No association was observed between H. pylori infection and consumption of alcohol, NSAID use or smoking. On the other hand, the presence of digestive symptoms and peptic ulcer disease antecedents among first-degree relatives were associated with a higher prevalence of infection in a given individual (P < 0.05). CONCLUSION: H. pylori infection seroprevalence in healthy individuals in Spain is similar to that in countries with high socio-economic standards and other Western countries. Digestive symptoms and previous antecedents of peptic ulcer disease in first-degree relatives were associated with a higher prevalence of Helicobacter pylori infection.

Beta-lactam stability in frozen microdilution PASCO MIC panels using strains with known resistance mechanisms as biosensors.

The stability of amoxicillin/clavulanate, piperacillin/tazobactam, cefepime, imipenem, and meropenem in PASCO (PASCO System, DIFCO Laboratories, Detroit, MI, USA) frozen microdilution susceptibility panels stored for 16 weeks at -20 degrees C and -70 degrees C was evaluated. The increase in MIC values for the five American-Type Culture Collection (ATCC) quality control strains for susceptibility testing recommended by the National Committee for Clinical Laboratory Standards (NCCLS) and for 13 strains with different well-characterized resistance mechanisms was indicative of bioactivity deterioration. The overall agreement (+/- 1 twofold dilution) at purchase between the MIC values of PASCO frozen microdilution susceptibility panels and the standard agar dilution method was 97.7%. Minimum inhibitory concentration values for the associations of amoxicillin/clavulanate and piperacillin/tazobactam remained unchanged for the study period at -70 degrees C. In contrast, a carbapenem bioactivity decrease was detected only with strains having well-characterized resistance mechanisms from the 12th week onwards. At -20 degrees C, antibiotic deterioration with these latter strains was observed earlier than with ATCC strains: the activity of meropenem and imipenem remained unchanged only for the first 2 weeks, while a loss of activity was detected for amoxicillin/clavulanate and piperacillin/tazobactam at the 7th and 10th week, respectively. Cefepime was highly stable both at -20 degrees C and -70 degrees C. Strains with well-characterized resistance mechanisms should be used in routine quality control studies of antibiotic stability for susceptibility testing panels during the storage period.

[Which factors influence the success of the classical triple therapy in the eradication of Helicobacter pylori?]. / De qué factores depende el éxito de la triple terapia "clásica" en la erradicación de Helicobacter pylori?

AIM: To study different factors influencing the success of classic triple therapy in Helicobacter pylori eradication. METHODS: Fifty-seven duodenal ulcer patients infected with H. pylori were prospectively studied. At endoscopy biopsy specimens were taken from the gastric antrum and body (H & E, Gram stain, and culture). Classic triple therapy was administered (bismuth, tetracyclin, metronidazole). Patients were investigated endoscopically one month after completing therapy, and repeated biopsy specimens from the antrum and body were also obtained. RESULTS: H. pylori eradication was achieved in 42 patients (74%). In multiple logistic regression analysis metronidazole susceptibility (regr. coef. = 3.4; OR = 29.3) and previous therapy with omeprazol plus amoxycillin (regr. coef. = -1.7; OR = 0.18) were the only variables which correlated with success in H. pylori eradication (chi 2 model = 21; p < 0.001). Additional variables (age, sex, smoking, histologic lesion and ulcer history) were no correlated with H. pylori infection. H. pylori was susceptible to metronidazole in 36 patients (79%). Eradication rates for metronidazole-susceptible and metronidazole-resistant H. pylori isolates were 87% and 25%, respectively (p < 0.001). When previous therapy with omeprazole plus amoxycillin had been administered the eradication rate was lower (61%) than in patients without previous therapy (82%). CONCLUSION: Success of classic triple therapy in H. pylori eradication is higher when the organism is metronidazole-susceptible, and lower when previous therapy with omeprazole plus amoxycillin has been administered. This factor, although not fully elucidated, lends no support to choosing triple therapy when eradicating therapy with omeprazole plus amoxycillin fails.

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.

[What factors influence healing of duodenal ulcer when Helicobacter pylori eradication treatment is used?]. / De qué factores depende la cicatrización ulcerosa duodenal cuando empleamos un tratamiento erradicador de Helicobacter pylori?

AIM: To study the influence of various factors on duodenal ulcer healing, specially the success or failure of Helicobacter pylori eradication. METHODS: One-hundred and nine patients with duodenal ulcer and H. pylori infection were studied. At endoscopy biopsies were obtained from the gastric antrum and body, and processed by microbiological (Gram stain and culture) and histological methods (haematoxylin-eosin); also, a 13C breath test was performed. A <> triple therapy (bismuth, tetracycline, metronidazole) or omeprazole plus amoxicillin was administered. Endoscopy and breath test were repeated one month after completing therapy. Eradication was defined as the absence of H. pylori by all diagnostic methods. RESULTS: H. pylori eradication was achieved in 60 patients (55%). In the multivariate analysis H. pylori eradication was the only variable which correlated with ulcer healing (regr. coef. = 2.4; OR = 10.6). Additional variables (age, sex, smoking, time of evolution, ulcer size, and type of therapy) were not significantly correlated. Ulcer healing was achieved in 92% of patients after H. pylori eradication, and in 51% of therapy failures (p < 0.001). CONCLUSION: H. pylori eradication accelerates ulcer healing, which represents an additional argument for employing eradicating therapy in patients with duodenal ulcer disease.

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.

[Basal levels of blood pepsinogen I and Helicobacter pylori infection in patients with duodenal ulcer and normal endoscopy]. / Niveles basales de pepsinógeno I sérico e infección por Helicobacter pylori en pacientes con úlcera duodenal y endoscopia normal.

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.

[Is measurement of basal levels of serum pepsinogen II useful in proving the eradication of Helicobacter pylori by treatment?]. / Es útil la determinación de las concentraciones basales de pepsinógeno II sserico para comprobar la erradicación de Helicobacter pylori con el tratamiento?

BACKGROUND: The aim of this study was to demonstrate the influence of the eradication of Helicobacter pylori on the basal concentrations of serum pepsinogen II in patients with duodenal ulcer. METHODS: Thirty-two patients with active duodenal ulcer were prospectively studied. A triple therapy was used consisting in bismuth, metronidazole and tetracycline. At the time of initial endoscopy and in those performed 5 months later on completion of the treatment, biopsies of the gastric mucosa were taken for histologic and microbiologic studies, and the basal concentrations of serum pepsinogen II are also determined. RESULTS: The eradication of H. pylori was accompanied by a significant pathologic improvement (p < 0.001) in both the antrum and the gastric body. On eradication of H. pylori, the basal pepsinogen II value (m +/- SD) decreased from 9.2 +/- 2.7 ng/ml to 6.4 +/- 1.7 ng/ml after treatment (p < 0.001). However, when eradication was not achieved, these values increased (11.8 ng/ml) with respect to the initial determination (9.3 ng/ml) (p < 0.05). The area under the ROC curve was 0.99 (SE 0.01) with a sensitivity of 92% and specificity of 100% with respect to the diagnosis of infection eradication (cut off point of the decrease of pepsinogen levels O). CONCLUSIONS: The eradication of Helicobacter pylori in patients with duodenal ulcer is associated with a significant decrease in the basal concentrations of serum pepsinogen II measured 5 months after completion of treatment. The verification of this decrease constitutes a useful, inexpensive non invasive method to prove the eradication of H. pylori with treatment.

[The importance of obtaining biopsies of the gastric body in the follow-up after eradicating treatment of Helicobacter pylori]. / Importancia de la obtencion de biopsias del cuerpo gástrico en el seguimiento después del tratamiento erradicador de Helicobacter pylori.

BACKGROUND: The aim of the present was to study the usefulness of performing biopsies of the gastric body in addition to those normally obtained of the antrum in the control of the eradication of Helicobacter pylori after treatment. METHODS: Sixty-four patients with duodenal ulcer and infection by H. pylori were prospectively studied. Two therapeutic schedules were used: amoxycillin/clavulanic associated with omeprazole (n = 32) and the classical triple therapy (bismuth, metronidazole, tetracycline) (n = 32). At the time of initial endoscopy and one month after completion of the treatment biopsies of the antrum and gastric body were taken for histologic (hematoxylin-eosin) and microbiologic (Gram and culture) studies. A patient was considered to have H. pylori infection when its presence was demonstrated by histologic or microbiologic methods in either of the localizations. RESULTS: The eradication of H. pylori was globally achieved in 64% (n = 41) of the cases. In the patients in whom eradication was not achieved (n = 23), H. pylori was detected only in the antrum in 70% (30% false negatives) while this was seen in the gastric body in 96% of the cases (p < 0.05). CONCLUSIONS: Carrying-out biopsies of only the antrum after eradicating H. pylori treatment is associated with a high percentage of false negative diagnosis of infection. Therefore, additional biopsies of the gastric body are recommended.

[Prevalence of Helicobacter pylori infection in gastrectomy and vagotomy]. / Prevalencia de la infección por Helicobacter pylori en la gastrectomía y en la vagotomía.

OBJECTIVE: To report the prevalence of Helicobacter pylori infection in patients undergoing gastrectomy or vagotomy plus pyloroplasty because of peptic ulcer disease. METHODS: Eighty-five patients were studied (mean age = 61 years; 85% males) who had undergone gastric surgery: Billroth I gastrectomy (n = 25), Billroth II (n = 51) and vagotomy plus pyloroplasty (n = 9). During endoscopy biopsy specimens were obtained from fundus and both sides of anastomosis for histological (hematoxylin-eosin) and microbiological (Gram stain and culture) investigations. RESULTS: The overall percentage of Helicobacter pylori infection was 43.6% (Billroth I = 40%; Billroth II = 37%; vagotomy = 89%) and no differences were observed between both types of surgical reconstruction. However, differences were indeed observed (p < 0.01) when comparing percentages of infection between patients undergoing gastrectomy and vagotomy. Among infected gastrectomized patients H. pylori was detected in fundus in 93% of cases, whereas the recovery rate from anastomotic mouth biopsies was only 72% (p < 0.05). CONCLUSIONS: The prevalence of H. pylori infection in gastrectomized patients (Billroth I and II) was low regarding the cause of surgery (peptic ulcer disease), and no differences were observed between both types of surgical reconstruction. The prevalence of infection after vagotomy and pyloroplasty was significantly higher. Among infected gastrectomized patients, H. pylori was detected more frequently in gastric fundus compared with biopsy specimens obtained from the anastomotic mouth.