Expression of cytokeratins 7 and 20 in Helicobacter pylori-associated chronic gastritis in children.

Helicobacter pylori gastric infection induces structural changes in the gastric epithelium. Among them, variations in the expression of cytokeratins have been reported in adult patients. In the present study, we describe the expression of CK7 and CK20 in gastric samples taken from the antrum in three groups of pediatric patients: (A) Helicobacter pylori-associated chronic gastritis (mean age: 11.4 years); (B) previous H. pylori chronic gastritis patients (mean age: 9.4 years); and (C) controls (mean age: 8.8 years). In all, the presence of sulfomucins was assessed with Alcian blue-periodic acid-Schiff pH 1.0. Immunoreactivity was graded as absent (0), weak (1+), moderate (2+), or intense (3+), in accordance with the intensity of the staining, and its distribution as focal or diffuse. CK7 reactivity was 2+ either focal or diffuse in all group A biopsies. The reactivity was more evident in the cells at the neck of the glands, in the areas with more inflammatory infiltrates, decorating long vertical segments of epithelium. In groups B and C, CK7 reactivity was also focal and 1+ at the cells of the necks of the glands. However, group B presented longer vertical segments of positive cells as compared to group C, and shorter than those of group A. The deeper glandular structures were focally 1+ in both groups. CK20 expression was comparable in all three groups, depicting a 2+ diffuse reactivity at the surface epithelium and interposed pits with absence or focal reactivity at the neck and coiled gland areas. Ki-67 immunostaining paralleled that of the CK7. Staining for sulfated mucosubstances was positive in two of five cases of groups A and B, and in none of the cases of group C. We conclude that: (1) the long segments of CK7-positive glandular necks in H. pylori cases most probably indicate intense regenerative activity during active inflammation; (2) eradication of H. pylori does not warrant ad integrum restitution since long segments of Ki-67+, CK7+ cells at the germinative compartment of the glands (as well as cells with sulfomucins) were still recognizable in ex- H. pylori patients; (3) finally, differing from what happens in adults, children somehow manage to maintain fully differentiated CK20+ superficial epithelium while the H. pylori is in action.

The clinical and histological spectrum of esophagitis in pediatrics. Some keys to its links to gastritis.

UNLABELLED: The purpose of our study was to assess the clinical and histological spectrum of esophagitis, seeking possible links between esophagitis and gastritis particularly Helicobacter pylori-associated, in pediatric patients. MATERIAL AND METHODS: We retrospectively studied 66 sequential and 63 gastric biopsies from 66 patients fulfilling the histological diagnosis of "esophagitis". Cases were arranged in two groups: G1 (H. pylori negative): N = 44 (27 m; 17 f), mean age 7.3 y (range 7-9 m-18 y) and G2 (H. pylori positive): N = 22 (16 f; 6 m), mean age 12.8 y (range 7-16 y). RESULTS: The bases for performing endoscopy and biopsies were as follows: in G1 (N44) symptoms of gastroesophageal reflux (GER) in 24 cases and non-GER in 20 cases; in G2 (N = 22): symptoms of GER in 13 and non-GER in 9 cases. Esophageal endoscopic findings for G1 patients included: normal mucosa 39; esophagitis 3; congestive mucosa and esophagitis 1 each. Stomach endoscopic findings for G1 patients were normal mucosa 29; nodular antrum 7; congestive mucosa 4; ulceration 2; unknown 2. G2 children revealed nodular antrum 19; congestive antrum 2; normal mucosa 1. Histology of esophageal biopsies in G1 was esophagitis grade 1,35; grade 2,4; grade 3, 4, and grade 5, 1. G2 showed esophagitis grade 1,20, and grade 2,2. The histologic findings of the gastric biopsies were as follows: G1 (N = 41): normal mucosa 23; mild chronic gastritis 6; mucus depletion in the superficial 5; mild acute gastritis 3; hemorrhage 1; insufficient tissue 3. G2: chronic gastritis associated with H. pylori with or without follicular hyperplasia 21; mild gastritis 1.

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

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 scarring 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.

[Toxocariasis with liver involvement]. / Toxocariasis con afectación Hepática.

We are reporting 16 cases of toxocariasis found in a two year period. Mean age was 2 years and 9 months. Sex distribution was 1:1. Thirteen (81%) children presented pica, 8 (50%) had pets at home, 10 (62.5%) presented anemia and long standing fever, and all eosinophilic leukocytosis. Fundoscopy was normal in all. Toxocara antibodies (Through ELISA) were increased in all of them. High resolution ultrasonography revealed hypoechoic areas in the liver in 50% of the cases. Therapeutic response was good, the clinical signs and symptoms disappearing at the end of treatment. The eosinophilic leukocytosis, ELISA serum positivity for toxocara and ultrasound findings persisted approximately for a year. Toxocariasis is a common parasitosis in our setting. It must be regarded as the first diagnosis when confronted with eosinophilic leukocytosis and abnormal liver findings by ultrasound.

Sulfomucins in Helicobacter pylori-associated chronic gastritis in children: is this incipient intestinal metaplasia?

BACKGROUND: Little is known about early stages of intestinal metaplastic in chronic gastritis. The purpose of this study was to determine the presence of sulfated mucosubstances hence most probably intestinal metaplasia, in isolated cells of surface gastric pits, and glands in pediatric patients with Helicobacter pylori-associated chronic gastritis. METHODS: Participants were nine patients (nine different biopsies; mean age 11.5 years, range 3-16 years) with sulfomucin-containing cells evident in the gastric biopsy specimen. Eight of the patients were selected from a group of 15 patients with histologically documented H. pylori-associated chronic gastritis in whom the utility of the Sydney system was being tested. RESULTS: Symptoms and endoscopic findings of H. pylori-associated chronic gastritis were the same regardless of the presence or absence of sulfomucin-containing cells. On hematoxylin and eosin stained tissues, neither intestinal metaplasia nor atrophy was apparent. However, periodic acid-Schiff (PAS)-alcian blue (pH 1.0) stain revealed the presence of sulfated mucosubstances in isolated cells of gastric pits and glands in the nine patients. CONCLUSIONS: This finding may represent a "minimal" form of incomplete intestinal metaplasia (type III). Because the nine patients had been untreated, the change is probably reversible. Two follow-up biopsies in patients in whom H. pylori had been treated and eradicated showed absence of sulfated mucins. Although these findings cannot be regarded as fully developed type III intestinal metaplasia, it is possible that left untreated, the alteration may persist and evolve into some other complication. This conclusion justifies follow-up of these patients.

Assessment of the Sydney System in Helicobacter pylori-associated gastritis in children.

OBJECTIVE: The aim of our study was to establish the usefulness of the Sydney System in grading H. pylori-associated chronic gastritis in biopsies from pediatric patients. STUDY DESIGN: Fifteen children (average age: 10.8 years) with histologically-proven gastritis were studied. Classification and grading of gastritis were performed according to the analogue visual scales described in the updated version of the Sydney System. A chart was specially designed to record the morphological grading in this study. Altogether, we studied 79 gastric biopsies. RESULTS: Neutrophilic infiltrates were absent in 27 biopsies, mild in 35, and moderate in 17. This feature was not marked in any of the biopsies. Mononuclear infiltrates were mild in 38 biopsies, moderate in 36, and marked in 5. Density of H. pylori was mild in 39 biopsies, moderate in 27, and marked in 2. In three post-treatment biopsies belonging to the same patient, no H. pylori was observed. Additional 8 biopsies (7 from the body and 1 from the antrum) showed no H. pylori, although organisms were simultaneously present in other stomach sites. Lymphoid follicles were present in 19/79 biopsies. Intestinal metaplasia was not seen on slides stained with hematoxylin-eosin (HE). However, the Alcian blue-PAS stain revealed isolated positive cells in 8 out of 15 patients. None of the gastric biopsies showed mucosal atrophy. CONCLUSION: The results show that the Sydney System is applicable for pediatric patients in case of H. pylori-associated gastritis. However, the number of biopsies recommended in the Sydney System seems excessive for this age group.

[Clinico-endoscopic spectrum of gastritis associated with Helicobacter pylori in pediatrics]. / El espectro clínico-endoscopico de la gastritis asociada a Helicobacter pylori en pediatría.

In order to gain further knowledge about the clinical and endoscopic features of chronic gastritis (CG) associated with Helicobacter pylori (H py) we retrospectively analyzed 81 pediatric cases. All were biopsy-proven. The cases were divided in two groups: Group (1988-1992) included 21 cases. These represented the early stage of clinical recognition of the disease. Group 2(1993-1995) comprised 60 cases and represents the stage in which the disease was mandatory. Mean number of cases/year was 4.2 and 20 for group 1 and 2, respectively. Recurrent abdominal pain (RAP) was the most frequent clinical symptom (74/81; 91%), followed by upper digestive tract hemorrhage (UDTG) (34/81; 41.9%). The combination gastroesophageal reflux (GER) and esophagitis (E) was found in 52/81 (64.2%) of the children. Endoscopically, granularity of the mucosa was more frequently found in cases with RAP (47/74), GER (28/36) and E, while a smooth mucosa predominated in patients with UDTH (23/34). Our findings strongly suggest that symptomatic CG with H py in children expresses peculiar clinical and endoscopic features. Since RAP was present in 91% of the cases it appears adequate to include this disease in the differential diagnosis of it. These clinical manifestations have not been previously linked to CG with H py. Better understanding of the clinical and endoscopic spectrum of CG with H py results in adequate treatments and possibly prevention of gastric (and esophageal) diseases found in adults.