ABSTRACT
Resumen Con la introducción de la manometría esofágica de alta resolución se revelaron patrones no identificados previamente de la función esofágica. De igual forma, este método diagnóstico adiciona patrones de presión topográfica de la presión esofágica, lo que lleva al desarrollo de nuevas herramientas para el análisis y clasificación de desórdenes motores esofágicos. En la actualidad, la clasificación de Chicago 3.0 es la herramienta de análisis de los diferentes trastornos motores esofágicos. En Colombia, cada día se ve el crecimiento en la realización de este estudio. El artículo propone hacer una revisión de cómo realizar e interpretar una manometría esofágica de alta resolución y clasificar los diferentes trastornos de la motilidad esofágica según la última actualización de la clasificación de Chicago 3.0.
Abstract The introduction of high resolution esophageal manometry has led to the revelation of previously unidentified patterns of esophageal function. Similarly, this diagnostic method has revealed topographic patterns of esophageal pressure which has led to the development of new tools for analysis and classification of esophageal motility disorders. Currently, the Chicago 3.0 classification has become a tool for analysis of the various esophageal motility disorders. In Colombia, the use of this study is spreading and growing. This article reviews of how to perform and interpret high resolution esophageal manometry and shows how to classify esophageal motility disorders according to the latest update of Chicago 3.0.
Subject(s)
Esophageal Achalasia , Manometry , Gastrointestinal MotilityABSTRACT
AIM: Rifaximin is a non-absorbed antibiotic relative of rifampicin. The location of effect and staphylococcal resistance are two recent potential concerns with rifaximin. In this study we evaluate the location of effect of rifaximin as well as the development of staphylococcal rifampicin resistance. METHODS: Rats were divided into three groups. Group 1 gavaged for 10 days with PBS, group 2 gavaged with rifaximin for 10 days, and group 3 gavaged with rifaximin for 10 days and housed for 30 days. In each group, stool was collected daily for quantitative culture of Staphylococcus spp. and coliforms. After euthanasia luminal bacterial counts were determined at multiple gut locations by qPCR. Rifampicin susceptibility was tested on Staphylococcus pre and post rifaximin. RESULTS: At baseline, rats had a median of 2.90 × 10(6) cfu/ml Staphylococcus spp. in stool. After 10 days of rifaximin, this dropped to 1.20 × 10(5) cfu/ml (P < 0.01). With coliform counts, rats had a median of 1.86 × 10(4) cfu/ml at baseline which dropped to 2.2 × 10(3) cfu/ml (P < 0.01) after rifaximin. After cessation of rifaximin, coliform counts recovered within 3 days. When examining the total bacterial counts by qPCR, rifaximin reduced small bowel bacterial levels, but not colon. This reduction was sustained for 30 days. No colonies of Staphylococcus became resistant and only one colony was intermediate. The mean inhibitory concentration for rifampicin was not different before and after rifaximin. CONCLUSION: Staphylococcal spp. fail to demonstrate resistance to rifampicin after rifaximin. The transient reductions in stool coliform counts recover while rifaximin appears to produce durable reductions in duodenal bacteria.
