Th17 response and autophagy--main pathways implicated in the development of inflammatory bowel disease by genome-wide association studies.

Inflammatory bowel disease (IBD) is an entity that mainly includes ulcerative colitis (UC) and Crohn´s disease (CD). Improved health care, diet changes, and higher industrialization are associated with an increase in IBD prevalence. This supports the central role of environmental factors in the pathology of this disease. However, IBD also shows a relevant genetic component as shown by high heritability. Classic genetic studies showed relevant associations between IBD susceptibility and genes involved in the immune response. This is consistent with prior theories about IBD development. According to these, contact of the immune system with a high number of harmless antigens from the diet and the bacterial flora should originate tolerance while preserving response against pathogens. Failure to achieve this balance may originate the typical inflammatory response associated with IBD. Recently, genome-wide association studies (GWASs) have confirmed the implication of the immune system, particularly the Th17 immune response, previously associated to other autoimmune diseases, and of autophagy. In this paper, the mechanisms involved in these two relevant pathways and their potential role in the pathogenesis of IBD are reviewed.

High prevalence of virulence-associated genotypes in Helicobacter pylori clinical isolates in the Region del Maule, Chile.

The prevalence of Helicobacter pylori infection and the gastric cancer mortality rate in Chile are remarkably high. This study identified some virulence-associated genes in 78 H. pylori clinical isolates from dyspeptic patients from the Region del Maule, which is the region with the higher gastric cancer mortality rate in the country. The cagA, vacA and babA2 genes were detected in 94.9%, 100% and 97.4%, respectively. Two or more EPIYA C motifs were presented in 48.6% of cagA-positive strains, and this was associated with more severe histopathological findings in the gastric mucosa.

Respuesta Th17 y autofagia: principales vías implicadas en enfermedad inflamatoria intestinal por los estudios de asociación de genoma completo. Nuevos factores implicados en la susceptibilidad a enfermedad inflamatoria intestinal / Th17 response and autophagy - main pathways implicated in the development of inflammatory bowel disease by genome-wide association studies: new factors involved in inflammatory bowel disease susceptibility

La enfermedad inflamatoria intestinal (EII) es una entidad que engloba principalmente a la colitis ulcerosa (CU) y la enfermedad de Crohn (EC). Las mejoras sanitarias, cambios en la alimentación y una mayor industrialización se han asociado con mayor prevalencia de EII lo que demuestra la gran importancia de diferentes factores ambientales en la etiopatogenia de esta patología. Sin embargo, la EII presenta al mismo tiempo un importante componente genético según demuestra su alta heredabilidad. Los estudios genéticos clásicos mostraron asociaciones con genes implicados en la respuesta inmune, consecuentes con las teorías expuestas sobre el desarrollo de la enfermedad en las que el contacto del sistema inmune del sistema digestivo con gran número de antígenos inocuos de la flora y de la dieta debe originar tolerancia, manteniendo al mismo tiempo la respuesta frente a los patógenos. Un desequilibrio en este sistema originaría la respuesta inflamatoria típica de la EII. Recientemente, estudios de asociación de genoma completo (GWAS) han confirmado esta implicación del sistema inmune, particularmente de la respuesta inmune Th17, relacionada también con otras patologías autoinmunes. Otro proceso fuertemente implicado por estos estudios es el de la autofagia. En este artículo se revisan los mecanismos involucrados en estas dos vías y su posible relación con la patogenia de la EII

Inflammatory bowel disease (IBD) is an entity that mainle includes ulcerative colitis (UC) and Crohn’s disease (CD). Improved health care, diet changes, and higher industrialization are associated with an increase in IBD prevalence. This supports the central role of environmental factors in the pathology of this disease. However, IBD also shows a relevant genetic component as shown by high heritability. Classic genetic studies showed relevant associations between IBD susceptibility and genes involved in the immune response. This is consistent with prior theories about IBD development. According to these, contact of the immune system with a high number of harmless antigens from the diet and the bacterial flora should originate tolerance while preserving response against pathogens. Failure to achieve this balance may originate the typical inflammatory response associated with IBD. Recently, genome-wide association studies (GWASs) have confirmed the implication of the immune system, particularly the Th17 immune response, previously associated to other autoimmune diseases, and of autophagy. In this paper, the mechanisms involved in these two relevant pathways and their potential role in the pathogenesis of IBD are reviewed

[Eosinophilic pneumonia caused by mesalazine. Report of one case]. / Neumonía eosinofílica inducida por mesalazina. Caso clínico.

A 50 years old male with a diagnosis of ulcerative colitis treated with mesalazine, developed after 2 months of treatment, cough, fever and progressive dyspnea. Chest X ray examination and CT scan showed pulmonary infiltrates in the right upper lobe that subsequently involved both lower lobes. A biopsy, made through videothoracoscopy, showed an eosinophilic pneumonia. After the discontinuation of mesalazine and the use of glucocorticoids, the respiratory involvement resolved, and pulmonary infiltrates regressed. Mesalazine is widely used in the treatment of inflammatory bowel diseases. Pulmonary toxicity is an uncommon complication of mesalazine treatment. Nevertheless, this complication should be considered in patients that use it and develop respiratory symptoms.

Hepatotoxicidad por drogas: reporte de un caso y revisión de literatura / Drug-induced liver injury: a case report and literature review

La Hepatotoxicidad por drogas se define como una lesión hepática asociada a deterioro de la función de éste órgano, secundaria a exposición a una droga u otro agente no infeccioso. Es un cuadro infrecuente, pero puede determinar graves lesiones hepáticas y una mortalidad considerable si no se detecta a tiempo. Es labor del clínico mantener un alto Índice de sospecha al enfrentarse a un paciente con alteraciones hepáticas de reciente comienzo y uso concomitante de medicamentos. En el presente articulo se expone el caso clínico de un paciente masculino, 48 años de edad, con Depresión Severa en tratamiento con Sertralina, Clonazepam, Risperidona, Lamotrigna y Acido Valproico. Ingresó al Hospital de Talca con diagnostico de Síndrome Colestásico cuyo estudio demostró serología para VHB y VHC negativa y ecotomografía abdominal normal. Presentó buena respuesta clínica y de laboratorio a la suspensión de las drogas. El cuadro fue compatible con Hepatotoxicidad por drogas.