Síndrome autoinmune tirogástrico (SAT): serie de casos / Thyrogastric syndrome: Case Series

Resumen Un porcentaje importante de pacientes con gastritis crónica atrófica corporal autoinmune, o gastritis tipo A, desarrollan enfermedad autoinmune tiroidea (enfermedad de Graves o de Hashimoto) y viceversa, situación conocida como síndrome autoinmune tirogástrico (SAT), pero no se conoce su prevalencia, por lo que puede pasarse sin el diagnóstico completo. El desarrollo de la gastritis atrófica limita la absorción de la vitamina B12, lo que lleva a alteraciones hematológicas, neurológicas y metabólicas, por tanto, es importante realizar las pruebas necesarias para su diagnóstico y seguir de cerca la evolución de los pacientes. La detección serológica de los autoanticuerpos contra la glándula tiroides y el cuerpo gástrico muestran la etiología autoinmune y un estado inflamatorio con daño tisular. Todo paciente con enfermedad autoinmune debe ser valorado para descartar la presencia de otras patologías de etiología inmunológica.

Abstract A significant percentage of patients with chronic autoimmune atrophic body gastritis (type A gastritis) develop thyroid autoimmune disease (Graves' disease or Hashimoto's disease) and vice versa. This situation is known as thyrogastric syndrome. Its prevalence is unknown, due to incomplete diagnoses. Since the development of atrophic gastritis limits the absorption of vitamin B12 leading to hematological, neurological and metabolic alterations, it is important to perform necessary diagnostic tests and to closely monitor the evolution of patients. Serological detection of autoantibodies against the thyroid gland and the gastric body show the autoimmune etiology and an inflammatory state with tissue damage. Every patient with autoimmune disease should be evaluated to rule out the presence of other pathologies of immunological etiology.

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.

Doença ulcerosa péptica: realmente é possível identificá-la por meio das características da dor epigástrica? / Peptic ulcer disease: is it really possible to identify it through the characteristics of epigastric pain?

OBJETIVO: Determinar se características da dor epigástrica são capazes de identificar pacientes com doença ulcerosa péptica. MÉTODOS: Estudo caso-controle, com coleta de dados de setembro de 2014 a junho de 2016. Foram incluídos pacientes com mais de 18 anos com dispepsia que realizaram endoscopia digestiva alta ambulatorialmente. Os pacientes foram abordados antes de realizar a endoscopia digestiva alta, verificando, em suas guias, a presença de dispepsia, tendo sido convidados a responder um questionário, e, posteriormente, o prontuário de cada entrevistado foi avaliado para verificação do diagnóstico, sendo, então, divididos entre o Grupo Doença Ulcerosa Péptica (casos), com 32 pacientes, e o Grupo Controle, com 44 pacientes com dispepsia atribuída a outras causas. RESULTADOS: Dos pacientes com dispepsia não ulcerosa, 52,27% caracterizaram a dor como em queimação, sendo 47,72% moderada e que piorava com alimentação. Dentre os demais sintomas, 45,45% relataram náuseas e 25% desconforto pós-prandial, com 52,27% relatando histórico familiar negativo de doença ulcerosa péptica. Em contrapartida, dos pacientes com doença ulcerosa péptica, 53,12% referiram dor em queimação e de moderada intensidade, e 50% relataram piora com alimentação. Dentre os demais sintomas, prevaleceram também náuseas (53,12%) e desconforto pós-prandial (40,62%). A maioria (81,25%) relatou histórico familiar de doença ulcerosa péptica. Observou-se diferença estatística em dor noturna, predominando na doença ulcerosa péptica (p=0,0225) e dor em cólica na dispepsia não ulcerosa (p=0,0308), assim como na ausência de histórico familiar entre os pacientes com dispepsia não ulcerosa (p=0,0195). CONCLUSÃO: A dispepsia relacionada à doença ulcerosa péptica relaciona-se, principalmente, à piora noturna, sendo que a intensidade da dor, a relação com alimentação e os sintomas associados não auxiliaram na diferenciação da dispepsia não ulcerosa, diferentemente do que a literatura tradicionalmente informa. (AU)

To determine whether it is possible to identify Peptic Ulcer Disease through the characteristics of epigastric pain. METHODS: This is a case-control study with data collected between September 2014 and June 2016 including patients over 18 years of age with dyspepsia who underwent upper gastrointestinal endoscopy as outpatients. The patients were approached before the upper gastrointestinal endoscopy when their test requisition form indicated the presence of dyspepsia. The subjects were invited to answer a questionnaire and, afterwards, the records of all interviewees were evaluated to check for the diagnosis. Then, they were divided into a peptic ulcer disease group (cases), with 32 patients, and a control group, with 44 patients with dyspepsia from other causes. RESULTS: Among non-ulcer dyspepsia patients, 52.27% described the pain as a "burning pain", with 47.72% reporting it as moderate and aggravated by food intake. As for other symptoms, 45.45% of subjects reported nausea, and 25% reported postprandial discomfort; 52.27% had no family history of peptic ulcer disease. In contrast, 53.12% of peptic ulcer disease patients reported "burning" and moderate pain, and 50% said the pain was aggravated by eating. As for the other symptoms, nausea (53.12%) and postprandial discomfort (40.62%) prevailed; most of the patients (81.25%) had family history of peptic ulcer disease. There was a statistical difference in night pain, which was more prevalent in peptic ulcer disease (p=0.0225), and colicky pain, which was more frequent in nonulcer dyspepsia (p=0.0308), as well as absence of family history in non-ulcer dyspepsia patients (p=0.0195). CONCLUSION: Dyspepsia caused by peptic ulcer disease is mainly related to night worsening, and pain intensity, the relationship with food intake, and associated symptoms did not help differentiate nonulcer dyspepsia, differently from what the medical literature traditionally suggests. (AU)

Comparative proteomics analysis of chronic atrophic gastritis: changes of protein expression in chronic atrophic gastritis without Helicobacter pylori infection

Chronic atrophic gastritis (CAG) is a very common gastritis and one of the major precursor lesions of gastric cancer, one of the most common cancers worldwide. The molecular mechanism underlying CAG is unclear, but its elucidation is essential for the prevention and early detection of gastric cancer and appropriate intervention. A combination of two-dimensional gel electrophoresis and mass spectrometry was used in the present study to analyze the differentially expressed proteins. Samples from 21 patients (9 females and 12 males; mean age: 61.8 years) were used. We identified 18 differentially expressed proteins in CAG compared with matched normal mucosa. Eight proteins were up-regulated and 10 down-regulated in CAG when compared with the same amounts of proteins in individually matched normal gastric mucosa. Two novel proteins, proteasome activator subunit 1 (PSME1), which was down-regulated in CAG, and ribosomal protein S12 (RPS12), which was up-regulated in CAG, were further investigated. Their expression was validated by Western blot and RT-PCR in 15 CAG samples matched with normal mucosa. The expression level of RPS12 was significantly higher in CAG than in matched normal gastric mucosa (P < 0.05). In contrast, the expression level of PSME1 in CAG was significantly lower than in matched normal gastric mucosa (P < 0.05). This study clearly demonstrated that there are some changes in protein expression between CAG and normal mucosa. In these changes, down-regulation of PSME1 and up-regulation of RPS12 could be involved in the development of CAG. Thus, the differentially expressed proteins might play important roles in CAG as functional molecules.

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

The presence of Helicobacter Pylori in postmenopausal women is not a factor to the decrease of bone mineral density

BACKGROUND: Osteoporosis affects approximately 30 percent of postmenopausal women. Gastrectomy, pernicious anemia, and more recently Helicobacter pylori infection, have all been implicated in the pathogenesis of osteoporosis. A reduced parietal cell mass is a common feature in these conditions. AIM: To study a possible relationship between chronic gastritis, parietal cell density of the oxyntic mucosa and bone mineral density in postmenopausal women, as chronic gastritis, Helicobacter pylori infection and osteoporosis are frequently observed in the elderly. METHODS: Fifty postmenopausal women (61.7 ± 7 years) were submitted to gastroduodenal endoscopy and bone densitometry by dual energy X-ray absorptiometry. Glandular atrophy was evaluated objectively by the determination of parietal cell density. Helicobacter pylori infection was evaluated by histology, urease test and breath test with 13C. RESULTS: Thirty-two patients (64 percent) presented chronic multifocal gastritis, and 20 of them (40 percent) showed signs of gastric mucosa atrophy. Lumbar spine osteoporosis was found in 18 patients (36 percent). The parietal cell density in patients with and without osteoporosis was 948 ± 188 and 804 ± 203 cells/mm², respectively. Ten osteoporotic patients (55 percent) and 24 non-osteoporotic patients (75 percent) were infected by Helicobacter pylori. CONCLUSION: Postmenopausal women with osteoporosis presented a well-preserved parietal cell density in comparison with their counterparts without osteoporosis. Helicobacter pylori infection was not different between the two groups. We concluded that neither atrophic chronic gastritis nor Helicobacter pylori seem to be a reliable risk factor to osteoporosis in postmenopausal women.

RACIONAL: A osteoporose afeta aproximadamente 30 por cento das mulheres na pós-menopausa. Gastrectomia, anemia perniciosa e mais recentemente, a infecção pelo H. pylori, têm sido implicados na patogênese da osteoporose. A diminuição da massa de células parietais constitui aspecto comum a estas condições. OBJETIVOS: Estudar possível relação entre gastrite crônica, densidade de células parietais da mucosa oxíntica e a densidade mineral óssea em mulheres na pós-menopausa. MÉTODOS: Cinqüenta mulheres na pós-menopausa (média de idade 61.7 ± 7 anos) foram submetidas a endoscopia digestiva alta e a densitometria óssea pela absorciometria com raio-X de dupla energia. A atrofia glandular foi avaliada, histologicamente e pela determinação da densidade das células parietais na mucosa do corpo gástrico. A infecção pelo H. pylori foi avaliada através da histologia, teste da urease e teste respiratório com C13. RESULTADOS: Trinta e dois pacientes (64 por cento) apresentaram gastrite crônica e 20 (40 por cento) deles apresentaram sinais de atrofia de mucosa gástrica através da análise histopatológica rotineira. Osteoporose da coluna lombar foi encontrada em 18 (36 por cento) pacientes. A densidade de células parietais em pacientes com e sem osteoporose foi 948 ± 188 e 804 ± 2003 células/mm², respectivamente. Dez pacientes (55 por cento) com osteoporose e 24 por cento (75 por cento) pacientes sem osteoporose estavam infectados pelo H. pylori. CONCLUSÃO:Mulheres na pós-menopausa com osteoporose apresentaram mucosa gástrica e população de células parietais mais conservadas em relação àquelas sem osteoporose. A infecção pelo H.pylori não foi estatisticamente diferente entre mulheres com e sem osteoporose, indicando que a infecção por esta bactéria, com ou sem atrofia da mucosa gástrica, não se constitui em fator de risco para osteoporose em mulheres na pós-menopausa.

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).

Modificaciones de las células enteroendocrinas en gastritis por Helicobacter pylori / Enteroendocrine cells modifications in Helicobacter pylori gastritis

Objetivo: Estudiar las modificaciones en número y distribución de las células entero endocrinas (CEE) en el antro gástrico de pacientes con infección por Helicobacter pylori (HP), para demostrar su participación en la respuesta inmune. Material y Método: Se utilizaron biopsias de antro gástrico de veintiseis (26) pacientes, entre 40 y 60 años de edad. Las muestras se colorearon con HE y giemsa modificado e inmunomarcaron con Cromogranina A. Cinco pacientes integraron el grupo control. Once pacientes mostraron gastritis crónica activa y los diez restantes gastritis atrófica multifocal (AMF), ambas asociadas a HP. Las CEE se cuantificaron refiriéndoselas cada 100 células epiteliales y se evaluó el patrón de distribución de las mismas. Resultados: En antros de pacientes controles (normales), la distribución de las CEE relacionadas fue uniforme con una media de 19,51 CEE/100. En los procesos inflamatorios, se detectó 12.01 CEE/100 en las gastritis crónicas y 6.31 CEE/100 en las AMF. Asimismo se observó una distribución irregular de las CEE relacionadas con áreas inflamatorias o con folículos linfoides. Conclusiones: La disminución de las CEE correspondería a una degranulación y luego debido a la agresión del HP, a la desaparición o inhibición de las stem cell hacia la línea endócrina. La persistencia de CEE en proximidad a las áreas de mayor infiltrado inflamatório, sugeriría su participación modulando esta respuesta, probablemente liberando péptidos que interactúan con linfócitos T, macrófagos y eosinófilos. Las CEE en el antro gástrico tendrían una intervención activa en la reacción inmune provocada por el HP.

Atrofia focal con cicatrices estrelladas en niños con gastritis crónica asociada con Helicobacter pylori. Gastritis atrófica inicial? / Focal atrophy with stellate scars in children with chronic gastritis associated to Helicobacter pylori. Is this early atrophic gastritis?

Background: Atrophic gastritis has not been described in children in the setting of Helicobacter pylori infection. Methods: Gastric biopsies of six children (7 to 11 years old) with history of HpCG and recent therapeutic eradication of H. pylori, were reviewed. In the 6 H. pylori was documented with histology, culture, direct visualization and/or serology before treatment. Cases were compared with five biopsies of age-matched patients showing none of the above-mentioned clinical data. All the biopsies were formalin-fixed, paraffin embedded and stained with hematoxilin-eosin, Masson trichrome and reticulin stain. Results: The biopsies of the six treated patients showed variable-in-size stellate-shaped spots of glandular loss replaced by dense connective tissue with few inflammatory cells. The fibrous tissue showed a central area of scaring and radially oriented spikes extending to adjacent interglandular tissue, more evident with the Masson trichrome stain. Density of inflammatory cells in the lamina propria was variable. H. pylori organisms were consistently absent. On the reticulin stain the atrophic areas showed coarser and compacted reticulin. Stellate scars were not present in the five controls. Conclusions: Small foci with fibrous scars may be found in children with long standing HpCG, perhaps as an early sequel of it. We hypothesize that if the chronic gastritis-gastric atrophy process is a continuum, these stellate scars may be representing the very beginning of the multifocal atrophic gastritis usually seen in adult patients.

Factores geográficos socioeconómicos en la orientación de patología gastroduodenal asociada a la infección por helicobacter pylori / Geographic and socioeconomic factors in the orientation of Helicobacter pylory-associated gastroduodenal pathology

It is highly probable that nutritionally-related geographic and socioeconomic factors may modulate the conversion of early stages of Helicobacter pylori-associated chronic active gastritis (chronic superficial gastritis [CSG] and chronic deep gastritis [CDG]) to chronic atrophic gastritis (CAG). The factors would be diets low in antioxidant vitamins and other micronutrients. In regions of the world and population groups with high socioeconomic level in which these modulating factors are absent, chronic active gastritis tends to stay in its early stages of CSG or CDG and to predispose to duodenal ulcer. On the contrary, in regions and population groups with low socioeconomic level in which the modulating factors are present, the frequency of CAG increases markedly. When CAG becomes severe and diffuse, hypochlorhydria ensues. Hypochlorhydria decreases the predisposition to duodenal ulcer, while CAG, a precancerous lesion, predisposes to gastric cancer of the intestinal type. The real role of the modulating factors already mentioned could be elucidated doing a multicentric study to determine endoscopically and histologically, in large series of dyspeptic patients from various regions of the world and with different socioeconomic levels, prevalence rates of duodenal ulcer, gastric ulcer, gastric cancer, Helicobacter pylori-associated CAG and intestinal metaplasia of the gastric mucosa, and to correlate these prevalence rates with blood levels of antioxidant capacity and related micronutrients. Latin America, because of its diversity in regions, geographic characteristics and population socioeconomic levels, seems to be the ideal place to conduct a study of that type. If the study could be performed, it would undoubtedly constitute an important contribution to a better understanding of Helicobacter pylori-associated gastroduodenal pathology.

Gastritis crónica

La gastritis crónica, enfermedad multifactorial, es muy frecuente en el mundo. La gastritis atrófica multifocal es la de mayor incidencia en poblaciones con alto riesgo de cáncer y úlceras gástricos: ésta no suele ser reversible, como si lo son la de reflujo o la antral difusa. Se insiste en una unificación, por parte de patólogos y otros especialistas, de la terminología, nomenclatura y clasificación empleadas para evitar confusiones. Implícitas incluso en el nuevo sistema de Sidney.

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.