Atrofia gástrica en niños: Características clínicas, endoscópicas y anatopatológicas

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Abstract

La atrofia gástrica en niños es rara, existen pocos datos sobre la prevalencia de atrofia gástrica o metaplasia intestinal en estas edades. Objetivo: investigar y describir las características clínicas, endoscópicas y anatopatológicas de pacientes pediátricos con gastritis crónica que tenían reporte de atrofia gástrica, para identificar factores etiológicos asociados a esta patología. Pacientes, Materiales Y Métodos: Se revisaron las historias clínicas de los pacientes atendidos en la Unidad desde 1994 a 2006, con reporte de biopsia con gastritis crónica y atrofia gástrica. Resultados: 23 niños con gastritis crónica y atrofia gástrica, una prevalencia general de 0,98%; con respecto a pacientes infectados con H. pylori la prevalencia de atrofia gástrica fue de 1,20% y en los no infectados de 0,71%. Se determino que la bacteria se identifico con más frecuencia en las biopsias, con una diferencia significativa con respecto al grupo de gastritis crónica y atrofia gástrica sin infección (p = 0.0001); la presencia de cúmulos linfoides, fue mas frecuente entre infectados (p = 0.0001). La atrofia gástrica focal leve se detectó en el 86,95% (20/23), 2 atrofia moderada y una severa. Se encontró que la atrofia gástrica focal leve fue más reportada en gastritis crónica moderada (p = 0.0004). Discusión: existe atrofia gástrica en niños con un predomino entre los infectados con H pylori. Se debe seguir un programa de vigilancia endoscópica para determinar la frecuencia de los cambios histológicos en la edad pediátrica, las estrategias de prevención y su consideración en el desarrollo de lesiones neoplásicas.

Translated abstract

Gastric atrophy in children is rare, few data exists about atrophy and metaplasia prevalence at these ages. Aims: To investigate and describe clinical, endoscopic and histological characteristics in pediatric patients with chronic gastritis who had gastric atrophy in order to identify etiologic factors asociated with this patology. Patients, Materials And Methods: clinical histories of patients attended in the unit from 1994 to 2006, with report of chronic gastritis, were reviewed. Results: 23 children with chronic gastritis and gastric atrophy, with a general prevalence of 0, 98%. In patients with Helicobacter pylori infection, the prevalence of gastric atrophy was 1, 20% and in non infected patients was 0, 71%. It was determined that the bacteria was identified more frequently in biopsies with chronic gastritis and atrophy with infection with a significative difference (p=0, 0001). The presence of limphoid cumulus was more frecuent among infected patients (p=0, 0001). Mild gastric atrophy was detected in 86, 95% (20/23), 2 moderate atrophy and one severe atrophy. It was found that mild gastric atrophy was reported in mayor number in moderate chronic gastritis (p=0, 0004). Discussion: Gastric atrophy exists in children with a predominance among Helicobacter pylori infected children. There has to be an endoscopic vigilance program to determine the frecuency of histologic changes in pediatric ages, prevention strategies and its consideration in the development of neoplasic lesions.

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Most cited references 27

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Helicobacter pylori infection, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer and early gastric cancer.

N Yamada-Fowler, Min Wen, Takeshi Matsuhisa … (2005)

To evaluate the histological features of gastric mucosa, including Helicobacter pylori infection in patients with early gastric cancer and endoscopically found superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer. The biopsy specimens were taken from the antrum, corpus and upper angulus of all the patients. Giemsa staining, improved toluidine-blue staining, and H pylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylin-eosin staining was used for the histological diagnosis of gastric mucosa inflammation, gastric glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. The overall prevalence of H pylori infection in superficial gastritis was 28.7%, in erosive gastritis 57.7%, in gastric erosion 63.3%, in gastric ulcer 80.8%, in early gastric cancer 52.4%. There was significant difference (P<0.05), except for the difference between early gastric cancer and erosive gastritis. H pylori infection rate in antrum, corpus, angulus of patients with superficial gastritis was 25.9%, 26.2%, 25.2%, respectively; in patients with erosive gastritis 46.9%, 53.5%, 49.0%, respectively; in patients with gastric erosion 52.4%, 61.5%, 52.4%, respectively; in patients with gastric ulcer 52.4%, 61.5%, 52.4%, respectively; in patients with early gastric cancer 35.0%, 50.7%, 34.6%, respectively. No significant difference was found among the different site biopsies in superficial gastritis, but in the other diseases the detected rates were higher in corpus biopsy (P<0.05). The grades of mononuclear cell infiltration and polymorphonuclear cell infiltration, in early gastric cancer patients, were significantly higher than that in superficial gastritis patients, lower than that in gastric erosion and gastric ulcer patients (P<0.01); however, there was no significant difference compared with erosive gastritis. The grades of mucosa glandular atrophy and intestinal metaplasia were significantly highest in early gastric cancer, lower in gastric ulcer, the next were erosive gastritis, gastric erosion, the lowest in superficial gastritis (P<0.01). Furthermore, 53.3% and 51.4% showed glandular atrophy and intestinal metaplasia in angular biopsy specimens, respectively; but only 40.3% and 39.9% were identified in antral biopsy, and 14.1% and 13.6% in corpus biopsy; therefore, the angulus was more reliable for the diagnosis of glandular atrophy and intestinal metaplasia compared with antrum and corpus (P<0.01). The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pylori-positivity was 50.7%, 34.1%; of erosive gastritis 76.1%, 63.0%; of gastric erosion 84.8%, 87.8%; of gastric ulcer 80.6%, 90.9%; and of early gastric cancer 85.5%, 85.3%, respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pylori-negativity was 9.9%, 6.9%; of erosive gastritis 42.5%, 42.1%; of gastric erosion 51.1%, 61.9%; of gastric ulcer 29.8%, 25.5%; and of early gastric cancer 84.0%, 86.0%, respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis, erosive gastritis, gastric erosion, and gastric ulcer patients with H pylori positivity was significantly higher than those with H pylori negativity (P<0.01); however, there was no significant difference in patients with early gastric cancer with or without H pylori infection. The progression of the gastric pre-cancerous lesions, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis and gastric ulcer was strongly related to H pylori infection. In depth studies are needed to evaluate whether eradication of H pylori infection will really diminish the risk of gastric cancer.

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Atrophic gastritis in young children and adolescents.

H Cardona, M. Mazen Jamal, O Ricuarte … (2005)

Helicobacter pylori associated gastric cancer arises via a multistage process, with atrophic gastritis being the precursor lesion. Helicobacter pylori is typically acquired in childhood, yet little is known of the prevalence of atrophic gastritis in childhood. To study atrophic gastritis among children from countries with high gastric cancer incidence. Sections from topographically mapped gastric biopsy specimens from children undergoing clinically indicated endoscopy in Korea and Colombia were evaluated using visual analogue scales. Atrophy was defined as loss of normal glandular components, including replacement with fibrosis, intestinal metaplasia (IM), and/or pseudopyloric metaplasia of the corpus (identified by the presence of pepsinogen I in mucosa that was topographically corpus but phenotypically antrum). One hundred and seventy three children, 58 from Korea (median age, 14 years) and 115 from Colombia (median age, 13 years), were studied. Helicobacter pylori was present in 85% of Colombian children versus 17% of Korean children (p<0.01). Atrophic mucosa near the antrum-corpus border was present in 16% of children, primarily as pseudopyloric metaplasia (31%, IM; 63%, pseudopyloric metaplasia; 6%, both). The median age of children with corpus atrophy was 15 (range, 7-17) years. Gastric atrophy occurs in H pylori infected children living in countries with high gastric cancer incidence. Identification and characterisation of the natural history of H pylori gastritis requires targeted biopsies to include the lesser and greater curve of the corpus, starting just proximal to the anatomical antrum-corpus junction, in addition to biopsies targeting the antrum and cardia.

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Does gastric atrophy exist in children

Georges Dimitrov (2006)

Several clinical reports confirmed that gastric atrophy is a pathology not only limited to adult patients. In pediatrics, it is most often described in association with a H pylori infection but this bacteria does not seem to be the only etiological factor of this preneoplastic state in children. The frequency of gastric atrophy and intestinal metaplasia in children are unknown because they are not systematically sought during upper gastrointestinal endoscopy. The lack of specific histological classification of childrenos gastropathies makes their diagnosis difficult for pathologists. Based on our knowledge to date, we think that it is necessary to describe, in detail, the natural course of this lesion during childhood. A close and prolonged clinical and endoscopic follow-up is important for children with gastric atrophy.