Gastritis autoinmune: diagnóstico y manejo de una entidad subdiagnosticada / Autoimmune gastritis: diagnosis and management of an underdiagnosed disease

Autoimmune gastritis (AIG) or chronic atrophic gastritis type A, is a chronic inflammatory disease that affects the body and fundus mucosa of the stomach. It is an underdiagnosed entity, whose clinical presentation has a broad spectrum, which may include asymptomatic patients; hematological manifestations such as iron deficiency anemia, vitamin B12 deficiency anemia (so called pernicious); non-specific digestive symptoms like dyspepsia; neurological and psychiatric manifestations. AIG is associated with other autoimmune diseases, mainly hypothyroidism ("Tyrogastric Syndrome") and type 1 diabetes. It is characterized by the development of anti-parietal cell and anti-intrinsic factor antibodies, decrease in pepsinogen I (PGI) level with low PGI/PGII ratio (< 3), and high level of gastrin. Endoscopic findings are not sufficient for the diagnosis of gastric atrophy. The use of the Sydney pathological report protocol and the OLGA/OLGIM system to evaluate the severity of gastritis have improved their diagnosis and the possibility to establish the risk of developing gastric neoplasms. The importance of its diagnosis and surveillance is based on the development of type 1 neuroendocrine gastric neoplasms, in addition to an increased risk of the incidence of gastric adenocarcinoma. Currently, an individualized endoscopic surveillance seems reasonable, with a minimum interval of 3 years.

La gastritis autoinmune (GAI) o gastritis crónica atrófica tipo A, es una enfermedad inflamatoria crónica que afecta la mucosa del cuerpo y fondo del estómago. La GAI es una entidad subdiagnosticada, cuya presentación clínica es de amplio espectro, puede incluir pacientes asintomáticos; manifestaciones hematológicas, tales como anemia ferropriva, anemia por déficit de vitamina B12 (anemia perniciosa); digestivas inespecíficas tipo dispepsia; neurológicas y psiquiátricas. La GAI está asociada a otras enfermedades autoinmunes, principalmente hipotiroidismo ("síndrome tirogástrico") y diabetes tipo 1. Se caracteriza por el desarrollo de anticuerpos anti células parietales y anti factor intrínseco, bajo nivel de pepsinógeno I (PGI) con una baja relación PGI/PGII (< 3), e hipergastrinemia. Los hallazgos endoscópicos no son suficientes para el diagnóstico de atrofia gástrica. El uso de protocolo de Sydney de reporte patológico y sistema OLGA/OLGIM para evaluar la severidad de gastritis han mejorado su diagnóstico y objetivado su riesgo de desarrollar neoplasias gástricas. La importancia de su diagnóstico y seguimiento está basada en el desarrollo de neoplasias gástricas neuroendocrinas tipo 1, además de un riesgo incrementado de la incidencia de adenocarcinoma gástrico, entre otros. Actualmente, parece razonable un seguimiento endoscópico individualizado, siendo un intervalo mínimo de 3 años.

Tratamiento en pacientes operados de estómago con ácidos biliares elevados y Helicobacter pylori positivo / Treatment in patients operated on of the stomach with elevated biliary acids and positive Helicobacter pylori

Se realizó un estudio del tipo experimental, no ciego y aleatorizado, constituido por 30 pacientes adultos de uno y otro sexos con diagnóstico de gastritis crónica alcalina por reflujo duodenogástrico, en resecados de estómago (Billroth I, Billroth II), mediante endoscopia superior, con ácidos biliares totales elevados y Helicobacter pylori positivo. Estos pacientes se distribuyeron en 2 grupos de tratamiento durante 8 semanas. El grupo A, de 15 pacientes, recibió tratamiento con: subcitrato de bismuto coloidal (Q-ulcer), metronidazol y tetraciclina, más ranitidina como antihistamínico H2. El grupo B, de 15 pacientes, se le administró celulosa microcristalina (Microcel). Ambos grupos recibieron metoclopramida como fármaco procinético durante todo el tratamiento. Los índices de erradicación de la infección por H. pylori fueron del 46,7 por ciento para el grupo A y del 42,9 por ciento para el grupo B. La concentración de ácidos biliares totales al final del tratamiento disminuyó en el 53,3por ciento de los pacientes del grupo A y en el 71,4 por ciento de los pacientes del grupo B. La concentración de ácidos biliares totales en el remanente gástrico al final del tratamiento, no influyó en la evaluación clínica, endoscópica e histológica de los pacientes en ambos esquemas de tratamiento. No se presentaron efectos adversos secundarios en los pacientes del grupo A y 1 paciente (6,6 por ciento) del grupo B abandonó el estudio al empeorar su cuadro clínico, el cual fue intervenido quirúrgicamente, por lo que se considera fracaso del tratamiento. Se concluye que estos esquemas terapéuticos no fueron eficaces.

A non-blind randomized experimental study was undertaken. It included 30 adults of both sexes with diagnosis of alkaline chronic gastritis due to duodenogastric reflux, in stomach resections (Billroth I, Billroth II), by upper endoscopy, with elevated total biliary acids and positive Helicobacter pylori. These patients were divided into 2 groups of treatment during 8 weeks. The group A was composed of 15 patients and received treatment with colloidal bismuth subcitrate (Q-ulcer), metronidazole and tetracycline, plus ranitidine as H2 antihistaminic. The group B was made up of 15 patients and it was administered microcrystalline cellulose (Microcel). Metoclopramide was given to both groups as a prokinetic drug during the whole treatment. The indexes for the eradication of H. pylori infection were 46.7 percent for group A, and 42.9 percent for group B. The concentration of total biliary acids at the end of the treatment decreased in 53.3 percent of the patients from group A and in 71.4 percent in group B. The concentration of total biliary acids in the gastric residue at the end of the treatment did not influence on the clinical, endoscopic and histological evaluation of the patients in both treatment schemes. No adverse secondary effects were observed in the patients from group A. One patient (6.6 percent) from group B left the study because its clinical picture got worse. He underwent surgery and it was considered a failure of the treatment. It was concluded that these therapeutic schemes were not efficient.

Cirurgia laparoscópica no diagnóstico de gastrite crônica atrófica seguida de tratamento clínico em cadela: relato de caso / Laparoscopic surgery in the diagnosis of atrophic gastritis in a dog followed by clinical treatment: case report

Descrevem-se o diagnóstico e o tratamento de um caso de gastrite atrófica crônica, em uma cadela sem raça definida, de dois anos de idade. A paciente apresentava como principal sintomatologia vômito crônico. O hemograma, a urinálise e as avaliações bioquímicas séricas não revelaram alterações significativas. Os exames radiológicos e ultra-sonográficos abdominais também não foram sugestivos de alterações. Realizaram-se inspeção da cavidade peritoneal, gastrotomia, gastroscopia, gastrectomia para biopsia e gastrorrafia intracorpórea videolaparoscópicas. Constatou-se ausência de rugosidades estomacais. Ao exame histológico, observou-se atrofia das células principais e parietais da mucosa gástrica. O quadro clínico permitiu o diagnóstico de gastrite crônica atrófica. O animal foi medicado com terapia imunossupressora e apresentou remissão completa dos sinais clínicos

This report describes a case of chronic atrophic gastritis. A two-year-old female mongrel dog showed chronic emesis. The complete blood count serum chemistry and urinalysis values were within the normal limits. Radiographs revealed no alterations. Abdominal evaluation, gastrotomy, gastroscopy, gastrectomy and intracorporeal stomach suture were done by laparoscopic approach. Absence of gastric villous was noticed through laparoscopic biopsy. The microscopic analysis reveled parietal and principal gastric mucosal cells atrophy, which, associated with clinical signs, allowed the chronic atrophic gastritis diagnosis. The animal was treated and clinical signs complete remission was observed