Factors related to gastric neuroendocrine tumors

Introduction and aims: An association between long-term use of proton pump inhibitors and the development of gastric neuroendocrine tumors has been reported, but it is still a subject of debate. The aims of the present study were to determine the presence of this association in a Mexican population and to identify the risk factors for developing gastric neuroendocrine tumors. Materials and methods: A case-control study was conducted, in which the cases were patients with a histopathologic diagnosis of gastric neuroendocrine tumor and the controls were patients evaluated through upper endoscopy. The controls were paired by age, sex, and endoscopic examination indication. Proton pump inhibitor use was considered prolonged when consumption was longer than 5 years. Results: Thirty-three patients with gastric neuroendocrine tumor and 66 controls were included in the study. Eighteen (54.5%) patients in the case group were women, as were 39 (59%) of the patients in the control group. The median age of the patients in the case group was 55 years (minimum-maximum range: 24-82) and it was 54 years (minimum-maximum range:18-85) in the control group. A greater number of patients in the gastric neuroendocrine tumor group presented with gastric atrophy (p<0.0001) and autoimmune atrophic gastritis (p = 0.0002), compared with the control group. No association between gastric neuroendocrine tumor and prolonged proton pump inhibitor use, sex, smoking, gastroesophageal reflux disease, Helicobacter pylori infection, diabetes mellitus, or autoimmune diseases was found in the univariate analysis. Conclusions: The results of our study showed no association between proton pump inhibitor use for more than 5 years and the development of gastric neuroendocrine tumor. The presence of gastric atrophy and autoimmune atrophic gastritis was associated with gastric neuroendocrine tumor development. Resumen: Introducción y objetivo: Se ha reportado una asociación entre el uso prolongado de inhibidores de la bomba de protones (IBP) y el desarrollo de tumores neuroendocrinos gástricos (TNE-G), la cual aún es controversial. El objetivo fue determinar esta asociación en nuestra población e identificar los factores de riesgo para el desarrollo de los TNE-G. Material y métodos: Estudio de casos y controles, se incluyeron pacientes con diagnóstico histopatológico de TNE-G, los controles fueron pacientes evaluados con endoscopia superior pareados por edad, sexo e indicación del estudio endoscópico. Se consideró uso prolongado de IBP cuando se utilizó por más de 5 años. Resultados: Se incluyeron en el estudio 33 pacientes con TNE-G y 66 controles. En el grupo de casos 18 (54.5%) son mujeres y en el grupo control 39 (59%). La mediana de edad es de 55 (rango mínimo-máximo: 24-82) años en el grupo de casos y 54 (rango mínimo-máximo: 18-85) años en el grupo control. En el grupo de los TNE-G se encontró una proporción mayor de pacientes con atrofia gástrica (p < 0.0001) y gastritis atrófica autoinmune (p = 0.0002) con respecto al grupo control. En el análisis univariado no se encontró asociación entre los TNE-G y el uso de IBP de forma prolongada, sexo, consumo de tabaco, enfermedad por reflujo gastroesofágico, infección por Helicobacter pylori, diabetes mellitus ni enfermedades autoinmunes. Conclusiones: No se encontró asociación entre el uso de IBP por más de 5 años y el desarrollo de TNE-G. La presencia de atrofia gástrica y gastritis atrófica autoinmune se asociaron al desarrollo de TNE-G. Keywords: Neuroendocrine tumors, Gastroenteropancreatic neuroendocrine tumors, Proton pump inhibitor, Atrophic gastritis, Palabras clave: Tumores neuroendocrinos, Tumores neuroendocrinos gastroenteropancreáticos, Inhibidor de la bomba de protones, Gastritis atrófic

Infections and systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that presents a protean spectrum of clinical manifestations, and may affect any organ. The typical course of SLE is insidious, slow, and progressive, with potential exacerbations and remissions, and even dramatically acute and rapidly fatal outcomes. Recently, infections have been shown to be highly associated with the onset and/or exacerbations of SLE, and their possible causative and/or protective role has been largely emphasized in the medical literature. However, the etiopathogenesis of SLE is still obscure and far from being completely elucidated. Among infections, particularly Epstein-Barr virus (EBV), parvovirus B19, retrovirus, and cytomegalovirus (CMV) infections might play a pivotal pathogenetic role. The multifaceted interactions between infections and autoimmunity reveal many possibilities for either causative or protective associations. Indeed, some infections, primarily protozoan infections, might confer protection from autoimmune processes, depending on the unique interaction between the microorganism and host. Further studies are needed in order to demonstrate that infectious agents might, indeed, be causative of SLE, and to address the potential clinical sequelae of infections in the field of autoimmunity