Eradication of Helicobacter pylori decreases the expression of p53 and c-Myc oncogenes

Although it is fairly well accepted that Helicobacter pylori infection [H. pylori] plays a significant role in causing gastric cancer, the exact mechanisms involved in its pathogenesis are unclear and there is controversial data about the state of chronic gastritis and the precancerous lesion after treatment of H. pylori. This study was designed to investigate the relationship between H. pylori infection, the activity of chronic gastritis and oncogenes before and after treatment of H. pylori. Fifty-five of chronic gastritis cases were studied for H. pylori, activity of chronic gastritis, p53 and c-Myc expression. Positive H. pylori cases were re-evaluated again for the activity of gastritis, expression of p53 and c-Myc after treatment [6 months later]. Forty-five cases were positive for H. pylori. The activity of chronic gastritis correlated with H. pylori infection. p53 and c-Myc expression correlated positively with the grade of chronic gastritis. After treatment of H. pylori, the activity of gastritis decreased and the expression of both p53 and c-Myc decreased. H. pylori infection in the gastric mucosa may be implicated in the pathway of gastric carcinogenesis. It seems that H. pylori infection is responsible for early genomic instability even before any neoplastic changes and its eradication can reverse the sequence of inflammation and related atrophy, metaplasia, and genomic instability and, thus, may prevent gastric cancer development

Prevention of gastric cancer: a challenging but feasible task / Prevención del cáncer gástrico: una tarea difícil pero factible

Despite its declining incidence gastric cancer still ranks as the second most common malignancy of the digestive tract, accounting for 10% of cancer deaths worldwide. At the time of the diagnosis less than 15% of the patients are in the stage of early cancer, the only stage in which a definite cure of gastric cancer is possible. Therefore the challenges are either early detection or even better prevention of gastric cancer. H. pylori has become recognized as the major risk factor for gastric adenocarcinoma. Epidemiological, biological, histomorphologic, molecular-genetic, epidemiological evidence and more recently few clinical trails have shown that H. pylori eradication has the potential to prevent the development of gastric cancer. Currently, H. pylori eradication is an indication for the prevention of gastric cancer in patients and groups of individuals with strongly increased risk, but further investigations are still required before an implementation of a general and global policy to eradicate H. pylori for the prevention of gastric cancer can be instituted. At present time, the main challenge remains to find out at what point mucosal abnormalities are no longer reversible and gastric cancer development cannot be prevented despite H. pylori eradication.

A pesar de la disminución en su incidencia, aún hoy el cáncer gástrico se presenta como la segunda causa más común de muerte por enfermedad maligna del tubo digestivo, siendo responsable del 10% de las muertes por cáncer a nivel mundial. Al momento del diagnóstico menos del 15% de los pacientes se encuentran en la etapa de cáncer gástrico temprano, el único estadío en el cual es posible su curación. Por lo tanto, el desafío está en la detección temprana o aún mejor, en la prevención del cáncer gástrico. H. pylori ha sido reconocido como el factor de riesgo más importante para el desarrollo del adenocarcinoma de estómago. Evidencia epidemiológica, biológica, histológica, molecular y más recientemente algunos estudios clínicos han demostrado que la erradicación del H. pylori tiene el potencial de prevenir el desarrollo de lesiones premalignas y del cáncer gástrico. Actualmente la erradicación del H. pylori está indicada para la prevención del cáncer gástrico en pacientes y grupos de individuos con alto riesgo, pero futuras investigaciones son aún necesarias antes de que sea establecida una política global para la erradicación del H. pylori en la prevención del cáncer gástrico. Actualmente el mayor desafío radica en encontrar en qué punto los cambios en la mucosa gástrica se tornan irreversibles, siendo el cáncer gástrico no prevenible a pesar de la erradicación del H. pylori.

Alteraciones genéticas en gastritis crónica: Estudio de inestabilidad microsatelital y pérdida de la heterocigocidad / Genetic changes in chronic gastritis: study of microsatellite instability and loss of heterozygosity

Background: Multifocal chronic gastritis, associated to intestinal metaplasia, is considered a preneoplastic lesion, closely associated to intestinal type gastric cancer. Aim: To study the frequency of microsatellite instability (MSI) and loss of heterozygosity (LOH) in areas of chronic gastritis and intestinal metaplasia in gastric biopsies of patients without cancer. Material and methods: Gastric biopsy samples from 34 patients without cancer (22 with multifocal atrophic gastritis and 12 with diffuse antral gastritis), were studied. Glands from areas of chonic gastritis and intestinal metaplasia and lymphocytes, were collected using laser microdissection of paraffin embedded samples. The analysis of 15 mono and dinucleotide microsatellites was used to assess LOH and MSI. Results: LOH and MSI were found in some of the markers in 55% (12/22) and 59% (13/22) of cases with intestinal metaplasia, respectively. Only one of 12 areas with diffuse atrophic gastritis had MSI and a different area had LOH (p <0.05 or less, when compared with areas of multifocal atrophic gastritis). Three areas of normal epithelium in patients with multifocal atrophic gastritis, also had alterations. Most of these alterations were concordant with adjacent areas with intestinal metaplasia. Conclusions: LOH and MSI was found in areas of intestinal metaplasia in more than half of the studied cases and in few areas of atrophic gastritis without intestinal metaplasia. These findings suggest that genotypic alterations may precede phenotypic modifications and that intestinal metaplasia is a preneoplastic lesion (Rev Méd Chile 2003; 131: 1365-74).

Infección intrabucal por helicobacter en paciente de sexo masculino / Intraoral infection by helycobacter in a male patient

El Helicobacter Pylori es una bacteria espiralada Gram negativa anaerobia que coloniza la mucosa gástrica. Algunos investigadores sugieren que la cavidad oral es reservorio del Helicobacter pylori, teniendo implicancia en la reinfección. Objetivo. Determinar si el Helicobacter pylori puede ser agente etiológico del ardor lingual y halitosis. Presentación del caso. Paciente varón de 35 años consulta por halitosis y ardor bucal, acompañado de epigastralgia. Presenta hiperplasia de papilas filiformes en dorso lingual con exámen micológico negativo. La biopsia gástrica demostró una gastritis crónica en actividad por Helicobacter pylori. Se realizó la biopsia parcial del área lingual afectada para estudio histopatológico y determinación del Helicobacter pylori con Biología Molecular. Resultados. Histológicamente, la lesión lingual presentaba acantosis, papilomatosis e hiperqueratosis, identificándose con técnica de Giemsa bacterias espiraladas compatibles con Helicobacter pylori adheridas a la superficie de las células epiteliales. La técnica de PCR permitió detectar la presencia del ADN del Helicobacter pylori. Mediante tratamiento antibiótico local se logró la remisión de la sintomatología. Conclusión: Los resultados obtenidos sugieren un rol etiológico para el Helicobacter pylori en esta patología. Creemos necesario ampliar el tamaño de la población con efecto de dilucidar si el Helicobacter pylori está relacionado etiológicamente del ardor lingual y halitosis

Helicobacter pylori and associated histopathological changes in gastric biopsies of patients with leprosy.

Two antral biopsies each from 104 patients of leprosy and 100 controls were studied to find out the prevalence of H. pylori and associated histopathological changes. Sections were stained with hematoxylene and eosin, AB/PAS (Ph 2.5) and Loeffler's methylene blue stains. Infection by H. pylori, inflammation and atrophy were found to be significantly more in leprosy patients as compared to controls (p < 0.01, < 0.005 and < 0.02 respectively). On comparing the histopathological changes in various subgroups of leprosy, H. pylori, inflammation and activity showed a statistically decreasing trend from tuberculoid to lepromatous subgroups (p < 0.05, < 0.001, < 0.01 respectively). Atrophy showed a significant increasing trend from tuberculoid to lepromatous group (< 0.001), it is concluded that despite a low prevalence of H. pylori and associated gastritis in patients with lepromatous leprosy, gastric epithelial damage is more marked due to altered immune response.

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.