Evaluation of the Gastric Microbiome in Patients with Chronic Superficial Gastritis and Intestinal Metaplasia / 中国医学科学杂志(英文版)

Objective To evaluate the gastric microbiome in patients with chronic superficial gastritis (CSG) and intestinal metaplasia (IM) and investigate the influence of Helicobacter pylori (H. pylori) on the gastric microbiome. Methods Gastric mucosa tissue samples were collected from 54 patients with CSG and IM, and the patients were classified into the following four groups based on the state of H. pylori infection and histology: H. pylori-negative CSG (n=24), H. pylori-positive CSG (n=14), H. pylori-negative IM (n=11), and H. pylori-positive IM (n=5). The gastric microbiome was analyzed by 16S rRNA gene sequencing. Results H. pylori strongly influenced the bacterial abundance and diversity regardless of CSG and IM. In H. pylori-positive subjects, the bacterial abundance and diversity were significantly lower than in H. pylori-negative subjects. The H. pylori-negative groups had similar bacterial composition and bacterial abundance. The H. pylori-positive groups also had similar bacterial composition but different bacterial relative abundance. The relative abundance of Neisseria, Streptococcus, Rothia, and Veillonella were richer in the I-HP group than in G-HP group, especially Neisseria (t=175.1, P<0.001). Conclusions The gastric microbial abundance and diversity are lower in H. pylori- infected patients regardless of CSG and IM. Compared to H. pylori-positive CSG group and H. pylori-positive IM, the relative abundance of Neisseria, Streptococcus, Rothia, and Veillonella is higher in H. pylori-positive patients with IM than in H. pylori-positive patients with CSG, especially Neisseria.

Morfología y repercusiones diagnóstico-terapéuticas de las lesiones preneoplásicas gástricas / Morphology and diagnostic determinants of gastric precancerous conditions

El carcinoma gástrico (CG) de tipo intestinal se origina en un epitelio displásico, que a su vez se desarrolla en medio de una atrofia gástrica (AG) y metaplasia intestinal (MI). La infección por Helicobacter pylori (HP) es la causa más frecuente de AG, causando una pangastritis atrófica multifocal. Entre otras condiciones que producen inflamación crónica de la mucosa gástrica se encuentran también la gastritis autoinmune y la anemia perniciosa. El marco conceptual sobre el cual descansa gran parte de la investigación actual y nuestra comprensión de los cambios que ocurren en la mucosa gástrica se debe a la denominada "cascada de Correa"; quien planteó que la mucosa gástrica crónicamente inflamada, da paso a la AG, que va adquiriendo focos de MI y en dicho epitelio se desarrollará finalmente una displasia (DIS). Se ha acuñado el término lesiones preneoplásicas gástricas (LPG), para referirse a: AG, MI y DIS.Después de la erradicación de HP, se ha demostrado una reducción general de la incidencia de CG; efecto que no es tan claro, cuando la pangastritis por HP ha evolucionado a AG extensa. De tal modo que el efecto de la erradicación de HP medido a través de EC, ha sido poco consistente. La AG grave diagnosticada por histología representa la condición de mayor riesgo. Por otra parte, la MI puede ser de tipo intestinal (delgado-entérica ó incompleta) y la colónica (colónica ó completa) considerándose a esta última, como la variedad de peor pronóstico. El diagnóstico histológico de este tipo de lesiones determina que quien las padece, debe someterse a vigilancia endoscópica. El objetivo de este manuscrito fue resumir la evidencia existente respecto de las LPG, en términos de su caracterización morfológica y sus repercusiones diagnóstico-terapéuticas (significado patológico, graduación del riesgo, vigilancia recomendada; y factores de riesgo).

Gastric carcinoma (GC) of intestinal type, originates from a dysplastic epithelium, which in turn develops in the midst of gastric atrophy (GA) and intestinal metaplasia (IM). Helicobacter pylori (HP) infection is the most frequent cause of GA, causing a multifocal atrophic pangastritis. Among other conditions that produce chronic inflammation of gastric mucosa are also autoimmune gastritis and pernicious anemia. The conceptual framework on which much of current research rests and our understanding of the changes that occur in the gastric mucosa is due to the so-called "Correa waterfall"; who stated that gastric mucosa chronically inflamed, gives way to the GA, which is acquiring foci of IM and in said epithelium a dysplasia (DIS) will eventually develop. The term precancerous conditions (PCC) of the gastric mucosa have been coined to refer to: GA, IM and DIS. After HP eradication, a general reduction in the incidence of GC has been demonstrated; effect that is not so clear, when pangastritis by HP has evolved to extensive GA. Thus, the effect of HP eradication measured through clinical trials has been inconsistent. Severe GA diagnosed represents the highest risk condition. On the other hand, IM can be enteric (grade I), enterocolic (grade II) or colonic (grade III); considering IM III as the variety with the worst prognosis. Histological diagnosis of gastric PCC, determines that the one who suffers them, must undergo endoscopic surveillance. The aim of this manuscript was to update morphological aspects and diagnostic-therapeutic scope of gastric PCC.

La microbiota según la topografía gástrica en pacientes con bajo y con alto riesgo de cáncer gástrico en Nariño, Colombia / Microbiota according to gastric topography in patients with low or high risk of gastric cancer in Nariño, Colombia

Resumen Introducción. La inflamación del antro gástrico por Helicobacter pylori aumenta el riesgo de úlcera duodenal, y la del cuerpo gástrico puede producir gastritis atrófica e incrementar la probabilidad de cáncer gástrico. Estas reacciones inflamatorias diferenciadas según su localización, podrían explicarse por la composición de la microbiota gástrica asociada con H. pylori. Objetivo. Identificar y comparar la microbiota del antro y del cuerpo del estómago en individuos de dos poblaciones: una con alto riesgo y otra con bajo riesgo de cáncer gástrico en Nariño, Colombia. Materiales y métodos. Se incluyeron biopsias del cuerpo y el antro gástrico de pacientes con gastritis no atrófica o con gastritis atrófica y metaplasia. La microbiota se definió por secuenciación de la región V3-V4 del gen 16S del ARNr de H. pylori (illumina-MiSeq™). Las unidades taxonómicas operativas se clasificaron utilizando las bases de datos BLASTn y RDPII. Las diferencias entre las poblaciones microbianas del antro y del cuerpo gástrico se evaluaron mediante el análisis de varianza multivariado con base en permutaciones (Permutational Multivariate Analysis of Variance, PERMANOVA) y análisis multivariados. Resultados. La clase Epsilonproteobacteria representada por H. pylori fue más abundante en las biopsias del antro y del cuerpo de los individuos con gastritis no atrófica (>50 %), en tanto que, en los individuos con gastritis no atrófica, esta clase correspondió al 20 % con una mayor diversidad metagenómica. La infección por H. pylori disminuyó significativamente la diversidad metagenómica del antro (p=0,005), en comparación con la del cuerpo gástrico. Conclusiones. Los grupos bacterianos involucrados en la disbacteriosis pueden colonizar ambas regiones topográficas del estómago, independientemente de las reacciones sectorizadas de inflamación. La infección por H. pylori asociada con la microbiota gástrica está relacionada con su localización en el estómago, el tipo de lesión y el mayor o menor riesgo de cáncer gástrico, lo que sugiere su importancia en la disbacteriosis y la de esta en la enfermedad gástrica.

Abstract Introduction: Inflammation in the gastric antrum caused by Helicobacter pylori increases the risk of duodenal ulcer while inflammation in the body generates atrophic gastritis and increased risk of gastric cancer. These inflammatory responses according to gastric topography could be explained by the composition of the gastric microbiota associated with H. pylori. Objective: To identify and compare the microbiota of the gastric antrum and body of individuals from two populations, one with high risk and one with low risk of gastric cancer from Nariño, Colombia. Materials and methods: Biopsies of the gastric antrum and body of patients with non-atrophic gastritis or metaplastic atrophic gastritis were included. The microbiota was defined by sequencing the 16S rRNA gene, V3-V4 region, (illumina-MiSeq™). The operational taxonomic units were classified using the BLASTn and RDPII databases. The differences among microbial populations were evaluated with the PERMANOVA and multivariate analyses. Results: The Epsilonproteobacteria class represented by H. pylori was more abundant in the antrum and body biopsies of individuals with metaplastic atrophic gastritis (>50%) while in individuals with non-atrophic gastritis it was 20 % and had greater metagenomic diversity. Helicobacter pylori infection significantly decreases the metagenomic diversity of the gastric antrum (p=0.005) compared to that of the body. Conclusions: The bacterial groups involved in the dysbiosis can colonize both topographic regions of the stomach, regardless of the sectorized inflammation responses. Helicobacter pylori infection associated with the gastric microbiota is related to its localization in the stomach, the type of lesion, and the population at risk of gastric cancer, which suggests its importance in microbial dysbiosis and gastric disease.

The presence of Helicobacter Pylori in postmenopausal women is not a factor to the decrease of bone mineral density

BACKGROUND: Osteoporosis affects approximately 30 percent of postmenopausal women. Gastrectomy, pernicious anemia, and more recently Helicobacter pylori infection, have all been implicated in the pathogenesis of osteoporosis. A reduced parietal cell mass is a common feature in these conditions. AIM: To study a possible relationship between chronic gastritis, parietal cell density of the oxyntic mucosa and bone mineral density in postmenopausal women, as chronic gastritis, Helicobacter pylori infection and osteoporosis are frequently observed in the elderly. METHODS: Fifty postmenopausal women (61.7 ± 7 years) were submitted to gastroduodenal endoscopy and bone densitometry by dual energy X-ray absorptiometry. Glandular atrophy was evaluated objectively by the determination of parietal cell density. Helicobacter pylori infection was evaluated by histology, urease test and breath test with 13C. RESULTS: Thirty-two patients (64 percent) presented chronic multifocal gastritis, and 20 of them (40 percent) showed signs of gastric mucosa atrophy. Lumbar spine osteoporosis was found in 18 patients (36 percent). The parietal cell density in patients with and without osteoporosis was 948 ± 188 and 804 ± 203 cells/mm², respectively. Ten osteoporotic patients (55 percent) and 24 non-osteoporotic patients (75 percent) were infected by Helicobacter pylori. CONCLUSION: Postmenopausal women with osteoporosis presented a well-preserved parietal cell density in comparison with their counterparts without osteoporosis. Helicobacter pylori infection was not different between the two groups. We concluded that neither atrophic chronic gastritis nor Helicobacter pylori seem to be a reliable risk factor to osteoporosis in postmenopausal women.

RACIONAL: A osteoporose afeta aproximadamente 30 por cento das mulheres na pós-menopausa. Gastrectomia, anemia perniciosa e mais recentemente, a infecção pelo H. pylori, têm sido implicados na patogênese da osteoporose. A diminuição da massa de células parietais constitui aspecto comum a estas condições. OBJETIVOS: Estudar possível relação entre gastrite crônica, densidade de células parietais da mucosa oxíntica e a densidade mineral óssea em mulheres na pós-menopausa. MÉTODOS: Cinqüenta mulheres na pós-menopausa (média de idade 61.7 ± 7 anos) foram submetidas a endoscopia digestiva alta e a densitometria óssea pela absorciometria com raio-X de dupla energia. A atrofia glandular foi avaliada, histologicamente e pela determinação da densidade das células parietais na mucosa do corpo gástrico. A infecção pelo H. pylori foi avaliada através da histologia, teste da urease e teste respiratório com C13. RESULTADOS: Trinta e dois pacientes (64 por cento) apresentaram gastrite crônica e 20 (40 por cento) deles apresentaram sinais de atrofia de mucosa gástrica através da análise histopatológica rotineira. Osteoporose da coluna lombar foi encontrada em 18 (36 por cento) pacientes. A densidade de células parietais em pacientes com e sem osteoporose foi 948 ± 188 e 804 ± 2003 células/mm², respectivamente. Dez pacientes (55 por cento) com osteoporose e 24 por cento (75 por cento) pacientes sem osteoporose estavam infectados pelo H. pylori. CONCLUSÃO:Mulheres na pós-menopausa com osteoporose apresentaram mucosa gástrica e população de células parietais mais conservadas em relação àquelas sem osteoporose. A infecção pelo H.pylori não foi estatisticamente diferente entre mulheres com e sem osteoporose, indicando que a infecção por esta bactéria, com ou sem atrofia da mucosa gástrica, não se constitui em fator de risco para osteoporose em mulheres na pós-menopausa.

Effect of smoking on failure of H. pylori therapy and gastric histology in a high gastric cancer risk area of Colombia / Efecto del tabaquismo en la falla al tratamiento anti-H. pylori y en la histología gástrica en una zona de alto riesgo de cáncer gástrico en Colombia

It has been proposed that eradication of Helicobacter pylori infection is a sound strategy for gastric cancer prevention. Several factors including smoking have been associated to treatment failure rates. This study aimed to evaluate the smoking effect on the efficacy of H. pylori therapy, as well as on the histological parameters in the gastric mucosa from subjects from a high gastric cancer risk area. Two-hundred-sixty-four Colombian subjects with gastric precancerous lesions who participated in a chemoprevention trial, received anti- H. pylori treatment at baseline and had data recorded on cigarette use, were included in this study. A detailed histopathological assessment of the gastric mucosa was performed in biopsies taken before any intervention. H. pylori eradication was assessed in gastric biopsies at 36 months post-treatment. The overall eradication rate was 52.3%; rates of 41.3% and 57.1% were observed for active-smokers and non-smokers, respectively. Multivariate logistic regression analysis showed that smokers had a 2-fold higher probability of failure in Helicobacter pylori eradication than non-smokers (OR: 2.0; 95% CI: 1.01-3.95). At baseline, activesmokers had a higher score of intestinal metaplasia compared to non-smokers. In the corpus mucosa, active-smokers showed lower scores of H. pylori density, total inflammation, neutrophil infiltration, and mucus depletion than non-smokers. In the antrum, no significant differences were observed between active-smokers and non-smokers. In summary, in patients who smoked, H. pylori treatment was less effective. Smoking cessation may benefit H. pylori eradication rates.

La erradicación del Helicobacter pylori ha sido propuesta como medida promisoria en la prevención del cáncer gástrico. Varios factores, incluyendo el tabaquismo, se asocian con la falla del tratamiento. El objetivo de este estudio fue evaluar el efecto del tabaquismo en la eficacia del tratamiento anti-H. pylori y en la histología gástrica en residentes de una zona de alto riesgo de cáncer gástrico. Este estudio incluyó 264 sujetos colombianos con lesiones gástricas preneoplásicas que participaron en un estudio de quimioprevención, recibieron tratamiento anti-H. pylori al ingreso, y proveyeron información sobre tabaquismo. Se realizó un detallado análisis histopatológico en las biopsias colectadas al ingreso. La erradicación de la infección fue evaluada en las biopsias gástricas a los 36 meses post-tratamiento. El porcentaje general de erradicación fue de 52.3%, con proporciones de 41.3% y 57.1% en fumadores activos y no fumadores, respectivamente. El análisis de regresión logística múltiple mostró que el riesgo de presentar falla al tratamiento fue doble en fumadores en comparación con los no fumadores (OR: 2.0; 95% CI: 1.01-3.95). Los fumadores presentaron un mayor índice de metaplasia intestinal comparado con los no fumadores. En la mucosa del cuerpo gástrico los fumadores mostraron menores índices de colonización por H. pylori, inflamación total, infiltración de neutrófilos y depleción de moco que los no fumadores. En el antro no se observaron diferencias significacomtivas entre ambos grupos. En conclusión, el tratamiento anti-H. pylori fue menos efectivo en sujetos fumadores. La cesación del consumo de tabaco puede beneficiar las tasas de erradicación del H. pylori.

Relationship between Pepsinogen I/II Ratio and Age or Upper Gastrointestinal Diseases in Helicobacter pylori-positive and -negative Subjects / 대한소화기학회지

BACKGROUND/AIMS: Although previous reports suggested that pepsinogen (PG) I/II ratio was the index of gastric atrophy, PG I/II ratio was also related to other factors such as Helicobacter pylori (H. pylori) infection, various gastrointestinal diseases, and aging. The aim of this study was to evaluate the relationship between serum PG I/II ratio and age or upper gastro-intestinal diseases according to H. pylori infection status. METHODS: A total of 529 individuals (307 male; mean age, 57.2 years) were divided into 4 groups (94 gastric ulcers, 35 duodenal ulcers, 105 reflux esophagitis, and 295 atrophic gastritis) according to endoscopic diagnosis. H. pylori infection was determined by H. pylori IgG antibody (ELISA) and PG was measured by latex immunoassay. RESULTS: H. pylori infected patients showed markedly increased serum PG II levels (24.0+/-14.7 ng/mL vs. 13.8+/-16.6 ng/mL, p<0.001) and low PG I/II ratio (3.9+/-2.0 vs. 6.0+/-2.5, p<0.001) than non-infected subjects. In H. pylori infected patients, mean PG I/II ratios in the gastric ulcer and atrophic gastritis group were significantly lower than those of the duodenal ulcer and reflux esophagitis group (p<0.001, ANOVA, Turkey's multiples comparison test). The mean ratio of open type atrophic gastritis was lower than that of close type atrophic gastritis (3.0+/-1.4 vs. 3.8+/-1.7, p<0.005). PG I/II ratio gradually decreased with age in H. pylori-infected patients with atrophic gastritis (R(2)=0.9, p=0.005, linear regression analysis). CONCLUSION: Serum PG I/II ratio reflects H. pylori infection and gastric atrophy. In the presence of H. pylori infection, gastric atrophy progresses with age.

Relationship between Pepsinogen I/II Ratio and Age or Upper Gastrointestinal Diseases in Helicobacter pylori-positive and -negative Subjects / 대한소화기학회지

BACKGROUND/AIMS: Although previous reports suggested that pepsinogen (PG) I/II ratio was the index of gastric atrophy, PG I/II ratio was also related to other factors such as Helicobacter pylori (H. pylori) infection, various gastrointestinal diseases, and aging. The aim of this study was to evaluate the relationship between serum PG I/II ratio and age or upper gastro-intestinal diseases according to H. pylori infection status. METHODS: A total of 529 individuals (307 male; mean age, 57.2 years) were divided into 4 groups (94 gastric ulcers, 35 duodenal ulcers, 105 reflux esophagitis, and 295 atrophic gastritis) according to endoscopic diagnosis. H. pylori infection was determined by H. pylori IgG antibody (ELISA) and PG was measured by latex immunoassay. RESULTS: H. pylori infected patients showed markedly increased serum PG II levels (24.0+/-14.7 ng/mL vs. 13.8+/-16.6 ng/mL, p<0.001) and low PG I/II ratio (3.9+/-2.0 vs. 6.0+/-2.5, p<0.001) than non-infected subjects. In H. pylori infected patients, mean PG I/II ratios in the gastric ulcer and atrophic gastritis group were significantly lower than those of the duodenal ulcer and reflux esophagitis group (p<0.001, ANOVA, Turkey's multiples comparison test). The mean ratio of open type atrophic gastritis was lower than that of close type atrophic gastritis (3.0+/-1.4 vs. 3.8+/-1.7, p<0.005). PG I/II ratio gradually decreased with age in H. pylori-infected patients with atrophic gastritis (R(2)=0.9, p=0.005, linear regression analysis). CONCLUSION: Serum PG I/II ratio reflects H. pylori infection and gastric atrophy. In the presence of H. pylori infection, gastric atrophy progresses with age.

Inhibición de la actividad proteolítica de Helicobacter pylori por suero inmune de ratón / Inhibition of the proteolytic activity of Helicobacter pylori by mouse immune serum

The proteolytic activity (PA) of some microorganisms is an important pathogenic factor during tissue invasion. However, its role in Helicobacter pylori infection is not clear. Due to the importance of the immunological response to inhibit pathogenic factors of microorganisms, this study aims to establish an in vitro system to detect inhibitory antibodies to the PA of H. pylori in mouse serum. We obtained mouse sera from animals immunized by oral and intraperitoneal inoculations with the raw bacterial extract (BE) of H. pylori, in which we had previously detected PA. The degradation of azocasein subtract for BE was inhibited in 49.23 and 22.6 using 5 micrograms/ml of serum proteins (SP) from oral and intraperitoneal inoculation, respectively. However, when using more than 25 micrograms/ml of SP of immune serum, PA was inhibited in a similar way than with control serum. In conclusion we present a methodology for the detection of inhibitory antibodies to PA of H. pylori in the serum of the immunized mouse.

Factores geográficos socioeconómicos en la orientación de patología gastroduodenal asociada a la infección por helicobacter pylori / Geographic and socioeconomic factors in the orientation of Helicobacter pylory-associated gastroduodenal pathology

It is highly probable that nutritionally-related geographic and socioeconomic factors may modulate the conversion of early stages of Helicobacter pylori-associated chronic active gastritis (chronic superficial gastritis [CSG] and chronic deep gastritis [CDG]) to chronic atrophic gastritis (CAG). The factors would be diets low in antioxidant vitamins and other micronutrients. In regions of the world and population groups with high socioeconomic level in which these modulating factors are absent, chronic active gastritis tends to stay in its early stages of CSG or CDG and to predispose to duodenal ulcer. On the contrary, in regions and population groups with low socioeconomic level in which the modulating factors are present, the frequency of CAG increases markedly. When CAG becomes severe and diffuse, hypochlorhydria ensues. Hypochlorhydria decreases the predisposition to duodenal ulcer, while CAG, a precancerous lesion, predisposes to gastric cancer of the intestinal type. The real role of the modulating factors already mentioned could be elucidated doing a multicentric study to determine endoscopically and histologically, in large series of dyspeptic patients from various regions of the world and with different socioeconomic levels, prevalence rates of duodenal ulcer, gastric ulcer, gastric cancer, Helicobacter pylori-associated CAG and intestinal metaplasia of the gastric mucosa, and to correlate these prevalence rates with blood levels of antioxidant capacity and related micronutrients. Latin America, because of its diversity in regions, geographic characteristics and population socioeconomic levels, seems to be the ideal place to conduct a study of that type. If the study could be performed, it would undoubtedly constitute an important contribution to a better understanding of Helicobacter pylori-associated gastroduodenal pathology.

Role of Helicobacter pylori in gastric carcinoma.

BACKGROUND. Helicobacter pylori infection has recently been incriminated in the pathogenesis of gastric carcinoma and chronic atrophic gastritis and intestinal metaplasia are considered to be precursors of this condition. Although the incidence of Helicobacter pylori infection in India is high that of gastric carcinoma is low. We, therefore, decided to examine the association between Helicobacter pylori, intestinal metaplasia and gastric carcinoma in a prospective study. METHODS. Fifty patients with carcinoma of the stomach and 50 with non-ulcer dyspepsia underwent upper gastro-intestinal endoscopy and had biopsies from the antrum, body and carcinomatous tissue. In 12 cases of gastric carcinoma, tissue was obtained from resected specimens at operation. The types of gastritis, intestinal metaplasia and presence of Helicobacter pylori were assessed by staining with haematoxylin and eosin, periodic acid-Schiff reagent with alcian blue and Warthin-Starry stains. RESULTS. The incidence of chronic atrophic gastritis, intestinal metaplasia and Helicobacter pylori were 82%, 36% and 38% in patients with carcinoma and 86%, 4% and 68% in those with non-ulcer dyspepsia. Helicobacter pylori positivity was significantly higher (p < 0.05) and intestinal metaplasia significantly lower (p < 0.001) in patients with non-ulcer dyspepsia than in those with carcinoma. Of the 50 cases with carcinoma, 28 were of the intestinal and 22 of the diffuse type. The incidence of chronic atrophic gastritis, intestinal metaplasia and Helicobacter pylori in the intestinal type of carcinoma was 71%, 46% and 39% while in the diffuse type it was 32%, 23% and 36%. The incidence of Helicobacter pylori infection did not differ significantly in the two types of carcinoma. CONCLUSIONS. We have found that although Helicobacter pylori infection and chronic atrophic gastritis are common in Indians, the incidence of intestinal metaplasia is low. Helicobacter pylori infection was equally common in both the intestinal and diffuse type of gastric carcinomas. Our findings, therefore, cast doubt on the role of Helicobacter pylori infection in gastric carcinogenesis.

Reflujo gastroesofágico en pacientes con gastritis y Helicobacter pylori

Se presentan 60 pacientes con síntomas consistentes con reflujo gastroesofágico (RGE) y gastritis crónica. Los síntomas más importantes encontrados fueron: pirosis 98.3 por ciento, regurgitación 93.8 por ciento, faringitis a repetición 83.3 por ciento, laringitis frecuente 80 por ciento, disfagia 80 por ciento, disfonía 78.3 por ciento, dolor epigástrico 98.3 por ciento, dispepsia 90 por ciento. todos los pacientes (100 por ciento) presentaron una gastritis crónica antral con 51.6 por ciento de tipo crónica superficial y 48.4 por ciento crónica atrófica. solamente seis pacientes (9.6 por ciento) tenían algún tipo de metaplasia. De los pacientes con gastritis crónica antral, 18 (30 por ciento) tenían Helicobacter pylori en las biopsias de antro. Veintidós pacientes (36.6 por ciento) presentaron una esofagitis péptica demostrada histológicamente pero ninguno mostró Helicobacter. Se discute la estrecha relación encontrada entre reflujo gastroesofágico y gastritis antral y su posible fisiopatología, así como la falta de correlacción entre el reflujo y la presencia delHelicobacter en el esófago.