A report of two children with Helicobacter heilmannii gastritis and review of the literature.

An 11-year-old boy with epigastric abdominal pain and a 2 year-old girl with failure to thrive underwent esophagogastroduodenoscopy. Endoscopic biopsies from the gastric antrum of both children revealed corkscrew-like spiral bacteria, consistent with the diagnosis of Helicobacter heilmannii infection. H. heilmannii is a rare finding in children and is thought to be present in approximately 0.3% of patients undergoing upper endoscopy. Clinical presentation, gross and histologic appearance, and treatment regimens are discussed. The clinical and histologic features of previously reported cases of H. heilmannii gastritis in children living in the United States are reviewed in table form.     

Helicobacter pylori duodenal colonization in children

To investigate the prevalence and the significance of Helicobacter pylori duodenal colonization, endoscopic duodenal biopsies were performed in 168 children with chronic abdominal pain, gastroesophageal reflux, gastrointestinal bleeding, and malabsorption syndrome. Helicobacter pylori infection was detected in 68 children (40.4%): in 31 of them H. pylori was present in the gastric antrum, and in 37 in the duodenum also. Duodenitis was observed in 25 children with duodenal H. pylori ; gastric metaplasia in 3. Scanning electron microscopy revealed the presence of the micro-organism in 3/13 cases; the bacteria were located in the intercellular spaces and alterations of the epithelial surface were found. In conclusion, H. pylori gastritis in children is often associated with duodenal colonization which can cause duodenitis, and also without gastric metaplasia, which indicates a possible role of the micro-organism in the pathogenesis of the lesions.     

Gastroesophageal reflux disease and Helicobacter pylori infection in neurologically impaired children: inter-relations and therapeutic implications

BACKGROUND: The aim of this retrospective study was to assess the relationship between Helicobacter pylori infection and gastroesophageal reflux disease in a high-risk population of children. METHODS: Forty-three neurologically impaired pediatric patients with H. pylori had upper gastrointestinal endoscopy between 1990 and 2000. Infection was confirmed by positive H. pylori culture or by identification of organisms in gastric biopsy specimens (fundus, n = 2; antrum, n = 3). Reflux esophagitis was diagnosed by ulceration of the esophageal mucosa at endoscopy. Four to 6 weeks after the completion of antibiotic treatment of H. pylori, a second endoscopy was performed and the gross appearance of the esophagus was recorded. RESULTS: At the first endoscopy, esophagitis was noted in 14 of 43 patients. After treatment, H. pylori infection was eradicated in all 14 patients with esophagitis but in only 19 of 29 (66%) of those with normal esophagus (P = 0.01). Esophagitis was still present in 4 of 14 (29%) patients who had esophagitis at the first endoscopy. Persistent esophagitis was only related to the presence of esophagitis before treatment (P = 0.02). In 29 patients with a normal esophagus at the first endoscopy, only one case of esophagitis was observed after H. pylori eradication. CONCLUSION: The data suggest that treatment of H. pylori infection should be considered in children with concomitant GERD, and such treatment is unlikely to either induce or exacerbate peptic esophagitis.     

Helicobacter pylori in children and adolescents: increase of primary clarithromycin resistance, 1997-2000

BACKGROUND: The authors evaluate the prevalence of Helicobacter pylori resistance in 117 children and demonstrate the changes over a 4-year period. METHODS: In 117 children and adolescents, H. pylori-positive gastritis was revealed by diagnostic upper endoscopy. Biopsies from the antrum and body of the stomach were tested by histology, urease test, and culture. H. pylori was isolated using standard culture techniques, and susceptibility to amoxicillin, clarithromycin, and metronidazole was tested using the E-test (AB-Biodisk, Sweden). RESULTS: Endoscopy revealed gastric ulcers in 2 of 117 subjects, duodenal ulcers in 6 of 117, and erosive gastritis or duodenitis in 23 of 117. Almost all patients showed antral nodularity. Histology always showed chronic gastritis with different degrees of activity. During the 4-year study period, the authors noticed an increase of primary clarithromycin-resistant H. pylori strains, from 14.3% to 27.6% (mean, 20.3%). Metronidazole resistance varied between 5% and 25%. No resistance to amoxicillin was found. CONCLUSION: Eradication of H. pylori should take place only after testing of susceptibility. The general use of clarithromycin in children should be restricted to better-defined indications. Resistance to clarithromycin of H. pylori may also become a future problem for the treatment of adults.     

Endoscopic nodular gastritis: an endoscopic indicator of high-grade bacterial colonization and severe gastritis in children with Helicobacter pylori

OBJECTIVE: To investigate the significance of endoscopic nodular gastritis associated with Helicobacter pylori infection. METHODS: This prospective study included 185 children (50.8% boys) aged 1 to 12 years (mean, 6.9 +/- 3.0 years) who underwent upper intestinal endoscopy during evaluation of chronic abdominal pain. The authors assessed the endoscopic appearance of the stomach, noting those patients with endoscopic nodular gastritis. Urease activity of gastric mucosal biopsies was measured. With histologic examination, the presence and density of H. pylori organisms, the presence of follicular gastritis, the nature of inflammation, and the gastritis activity grade and overall gastritis score were assessed. RESULTS: H. pylori infection was identified in 50 children (27%). Endoscopic nodular gastritis was significantly associated with active chronic gastritis and follicular gastritis. Nodularity in the stomach showed a high specificity (98.5%) and positive predictive value (91.7%) for the diagnosis of H. pylori infection and was observed in 22 of 50 (44%) H. pylori-positive patients and in 2 of 135 (1.5%) H. pylori-negative patients. A significant association was observed between older age and the prevalence of this finding (P< 0.001). There was a significant increase in endoscopic nodular gastritis with increased H. pylori density and a positive correlation (Pearson coefficient = 0.97) with increased gastritis score on histologic examination. Increase in gastritis score was dependent on increased H. pylori density in patients with gastric nodularity; this finding was independent of age. CONCLUSIONS: Endoscopic findings of antral nodularity in children suggest the presence of H. pylori infection and follicular gastritis and may identify cases of severe gastritis and marked bacterial colonization.     

Nature and extent of gastric lesions in symptomatic Chilean children with Helicobacter pylori-associated gastritis

Chile has one of the highest rates of gastric cancer in the world and most children and adolescents in the country are colonized by Helicobacter pylori. This study assessed the nature and extent of the gastric lesions in 73 consecutive patients aged 5-17 y, referred for upper gastrointestinal endoscopy. Their H. pylori-associated gastric pathology was characterized and these data were compared with their sociodemographic status. Endoscopic assessment was normal in 43 patients while in 30 there was a variety of mucosal lesions. Sixty patients (83%) had histological chronic gastritis of the antrum and in 45 (63%) the lesions also involved the gastric corpus; 90% of patients with chronic gastritis were colonized by H. pylori. Although most of these patients had epithelial erosions and dedifferentiation of the pit epithelium, atrophy and metaplasia were not found. Patients' socioeconomic status was inversely correlated with their rate of colonization by H. pylori (p < 0.005), the frequency of gastric lesions on endoscopy (p < 0.01) and the frequency of involvement of antral and corpus mucosa by chronic gastritis (p < 0.002). This latter feature was positively correlated with age (p < 0.001). Conclusion: This study shows a high frequency of extensive lesions of H. pylori-associated chronic gastritis in young Chilean patients. This histological picture is consistent with the hypothesis of a H. pylori-associated progressive gastric pathology which may represent a major factor in the high local rate of gastric cancer.     

Helicobacter pylori infection in pediatrics. Present knowledge and practical problems

Helicobacter pylori (H. pylori) infection is acquired in childhood, earlier in developing countries, as a consequence the prevalence of infection is higher in developing countries (70%) than in developed countries (5-15%). H. pylori infection spreads from person-to-person, however the precise mode of transmission (oral-oral, fecal-oral or gastro-oral routes) is as yet, not known. Diagnosis of H. pylori infection can be performed with both invasive endoscopic-based tests, or non-invasive tests, mainly by measurement of IgG antibodies against the bacterium in serum samples or by measurement of 13CO2 in expired air (13C-urea breath test). In clinical practice endoscopy and biopsy is recommended before treatment to determine the presence and the degree of gastritis or ulcer. However, endoscopy is a complicated procedure in children and diagnosis of infection can be based on a non-invasive test. The association of H. pylori infection with recurrent abdominal pain seems evident in a subgroup of children with endoscopic features of gastritis, ulcer or hemorrhage. There is an increasing interest in the extraintestinal manifestations of H. pylori infection in children, i.e. iron-deficiency anemia, growth retardation and migraine, but this domain remains controversial. Since infection at a young age is believed to result in chronic atrophic gastritis and gastric cancer in adult life, it is logical to consider a future massive programme of eradication and immunization. Regimens suggested for H. pylori eradication are a combination of inhibitors of gastric acid secretion plus two antibiotics for 7-10 days.     

儿童CagA+幽门螺杆菌感染根治前后胃黏膜上皮细胞增殖、凋亡和P53蛋白水平表达的对比研究

目的研究幽门螺杆菌（Hp）感染胃黏膜上皮细胞增殖、凋亡和突变型P53蛋白水平的表达情况,以及Hp感染根除治疗前后胃黏膜上皮细胞增殖、凋亡指数变化。方法采用脱氧核糖核酸末端转移酶介导的缺口末端标记技术（TUNEL）以及PCNA免疫组织化学法对30例CagA^＋Hp感染患儿和30例Hp阴性患儿胃黏膜上皮细胞增殖、凋亡情况进行比较,同时对突变型P53基因蛋白的表达情况进行检测。CagA蛋白抗体的检测采用Western Blot2．1免疫印迹法。结果CagA^＋Hp感染组胃黏膜上皮细胞增殖指数为11．56％±4．21％,较Hp阴性组（5．85％±2．21％）高（t=7．57,P〈0．01）;凋亡指数CagA^＋Hp感染组（10．58％±5．31％）较Hp阴性组（2．86％±0．64％）高（t=8．096,P〈0．01）。30例CagA^＋Hp感染组有28例完成了三联药物的Hp根除治疗,2例失访,其中21例根除,7例未根除;21例cagA’Hp感染根除治疗后,胃黏膜上皮细胞增殖指数治疗前为（11．50％±4．11％）,治疗后为（6．30％±3．26％）（t=3．968,P〈0．01）。凋亡指数治疗前为（10．58％±4．02％）,治疗后为（3．74％±2．30％）（t=6．69,P〈0．01）。7例未根除治疗患儿胃黏膜上皮细胞增殖指数及凋亡指数变化无统计学意义。cagA’Hp感染组胃黏膜上皮细胞P53阳性表达率63％（19／30）;在P53阳性表达中,轻度2例,中度8例,重度9例。Hp阴性组胃黏膜上皮细胞P53阳性表达率16％（5／30）,均为轻度表达。CagA^＋Hp感染组P53阳性表达率高于Hp阴性感染组（X2=6．805,P〈0．01）。结论CagA^＋Hp感染可引起胃黏膜上皮细胞增殖、凋亡的变化,使黏膜增殖、凋亡动态失衡,黏膜的不稳定性增加,突变型P53基因蛋白异常表达可能参与此过程的调控。     

Inflammation of the gastric cardia in children with symptoms of acid peptic disease

OBJECTIVES: To assess the severity and causes of inflammation of the gastric cardia in children undergoing endoscopy for symptoms of acid peptic disease. STUDY DESIGN: Patients undergoing upper gastrointestinal endoscopy for symptoms of acid peptic disease had biopsies from gastric cardia, gastric, and esophageal sites, and 24-hour intraesophageal pH monitoring. Gastric cardia was defined at endoscopy as the anatomic zone from the squamocolumnar junction to 0.5 cm below it. Severity of gastric cardia inflammation was scored 0 to 9 according to densities of inflammatory cells and epithelial abnormalities in surface and pit epithelium. A score > or =2 was considered positive. RESULTS: Forty-seven children (median age, 6.5 years; range, 3-15) had Helicobacter pylori infection, gastroesophageal reflux disease (GERD), or both. In 22 patients, H pylori was detected in cardiac biopsies by rapid urease test and histology; it was detected also in the corpus and antrum in only seven of the 22. No patient had H pylori in gastric corpus/antrum without having the organism at the cardia as well. In 12 H pylori-positive patients, GERD was also diagnosed. Twenty-five patients had GERD and no H. pylori infection. Severity score was 3.8+/-0.8 in the H pylori group and 2.08+/-0.9 in the GERD alone group (P<.001); however, there was no difference in reflux index (24-hour % of gastroesophageal reflux) between the two groups. In neither group was correlation found between reflux index and severity score (H pylori, r=0.22; GERD alone, r=0.31; NS) nor between cardia inflammation and esophagitis grade (H pylori, r=0.37; GERD alone, r=0.22; NS). CONCLUSIONS: In children with symptoms of acid peptic disease, inflammation of the gastric cardia does occur. It is more severe when the cardiac zone is infected with H pylori than in its absence. Of major practical significance is the finding that the gastric cardia is a highly sensitive site for the detection of H pylori infection.     

Primary gastric Burkitt lymphoma in childhood: associated with Helicobacter pylori?

BACKGROUND: This retrospective study was designed to estimate the incidence of primary gastric non-Hodgkin lymphoma (NHL) in childhood and the possible association with Helicobacter pylori (H. pylori). PROCEDURE: We reviewed and analyzed the charts of 135 patients with NHL that were diagnosed and treated in a single oncology unit during the last 20 years. RESULTS: Only two patients, 5 and 12 years old, with primary gastric NHL were found. Upper gastroduodenal endoscopy detected an ulcer in the lesser curvature of the body of the stomach, in both cases. Endoscopy revealed a moderate chronic gastritis in the antrum of both patients that was H. pylori associated in one of them who also suffered from chronic gastritis. Biopsy specimens demonstrated infiltration by Burkitt lymphoma (BL). The two patients received chemotherapy for 6 months. Additionally, one of the two patients received a triple therapy regimen with bismuth, amoxicillin, and metronidazole for H. pylori. Fifteen and six years later they are in complete remission, free of symptoms. CONCLUSIONS: Primary gastric NHL in childhood is rare. It was found in fewer than 2% of our NHL patients. The temporal relationship between the H. pylori infection and BL suggest a causative link between these two events.     

Helicobacter pylori - dependent intragastric urea biodegradation in children: Diagnostic and pathogenetic importance

Abstract The objective of the present work was to study the relationship between intragastric urea hydrolysis generated by Helicobacter pylori urease and acid-peptic disease in childhood. Intragastric urease activity was examined by urea and ammonia concentration measurement in gastric juice in 91 children with upper abdominal complaints. Helicobacter pylori infection was detected from 70 (76.9%) of 91 patients, including all of the 15 subjects with peptic ulcer disease. Helicobacter pylori -related gastritis in children was associated with a decrease of urea and an increase of ammonia in gastric juice ( P < 0.001) in comparison with H. pylori-negative children. The gastritis score was correlated with the concentrations of urea and ammonia in the gastric juice of patients infected with H. pylori. There was a significant correlation between the histologically detected dissemination of organisms and gastric ammonia levels. Similar results were obtained concerning correlation between gastric juice ammonia and anti- H. pylori specific immunoglobulin G versus highly purified antigen of H. pylori containing urease. Present findings prove that H. pylori plays an essential role in the pathogenesis of gastritis and that ammonia is one of the main pathogenic factors of acid-peptic disease.     

Treatment of Helicobacter pylori gastritis improves dyspeptic symptoms in children

BACKGROUND: In adults, the treatment of Helicobacter pylori infection is only recommended for patients with active gastric or duodenal ulcers. It is not known whether similar guidelines can be applied to children because the prevalence of peptic ulcer disease in childhood is estimated to be much lower than in adults. The purpose of this study was to determine whether treatment of H. pylori gastritis would improve symptoms of dyspepsia in children. METHODS: Sixteen patients (5 boys, 11 girls) aged 14 +/- 1.2 years who had symptoms of dyspepsia were evaluated using upper gastrointestinal endoscopy with biopsies to establish the diagnosis of H. pylori gastritis. They were treated for 2 weeks with clarithromycin, amoxicillin, and a proton pump inhibitor. Dyspepsia symptoms were evaluated by a questionnaire before and after treatment of the infection. The effect of H. pylori treatment on the total symptom score was analyzed with use of the Student t test. Values are presented as mean +/- SEM. RESULTS: All patients had antral nodularity and chronic active gastritis with spiral-shaped organisms but no evidence of peptic ulcer disease. Mean total symptom score decreased significantly at 2 to 4 weeks after treatment (12.6 +/- 0.9 vs. 2.1 +/- 0.5 P < 0.001), and it remained low (2.9 +/- 0.7) at follow-up 9.7 +/- 1.4 months (range, 2-24 months later). CONCLUSION: These results suggest that the treatment of H. pylori gastritis can improve dyspeptic symptoms in children.     

The role of Helicobacter pylori in abdominal pain in children]

Helicobacter pylori (H. pylori) colonizes the human stomach, especially during childhood. H. pylori gastritis, in the absence of duodenal ulcer, does not appear to be associated with specific symptoms. After eradication of H. pylori infection, abdominal pain is improved only in children with duodenal ulcer. Children with H. pylori gastritis cannot be distinguished from uninfected children on the basis of initial symptoms. However, although not demonstrated, a relationship between H. pylori and recurrent abdominal pain might exist since some studies showed that H. pylori-infected children present more frequent pain related to meals or ulcer-like symptoms. These discrepancies could be explained by the fact that H. pylori is probably not a frequent cause of recurrent abdominal pain. The use of refined clinical characteristics of abdominal pain could be of help identifying a subgroup of patients with abdominal pain in whom H. pylori infection needs to be sought and treated. Recent pediatric consensus conferences recommend testing for H. pylori infection by endoscopy only those patients presenting symptoms suggestive of an organic origin.     

Intraepithelial lymphocytes in duodenum from Brazilian adolescents with type 1 diabetes. Influence of Helicobacter pylori

Background: An increased number of intraepithelial lymphocytes (IELs) can be the only histological feature in early stages of celiac disease (CD). This is also presented in duodenum of patients with Helicobacter pylori -associated gastritis and in autoimmune diseases. Because CD is frequently associated with type 1 diabetes mellitus, we analyzed the density of IELs in the distal duodenum of non-celiac diabetic patients associated or not with H. pylori infection.
Methods: IEL density and the presence of H. pylori were determined in biopsies of the distal duodenum and gastric antrum and body obtained from Brazilian diabetic adolescents who were negative for anti-human tissue transglutaminase and anti-endomysial. The results were compared with the histological findings of gastric and duodenal biopsies obtained from non-diabetic older children and adolescents.
Results: H. pylori was detected in 33.3% of diabetic patients and in 56.7% of the control group. No association was observed between the presence of H. pylori and an increased lymphocyte density in the distal duodenum in either group. Diabetic patients presented a duodenal IEL density similar to that of the control group. Lymphocytic gastritis was not identified in any of the biopsies analyzed.
Conclusions: The density of IELs in the distal duodenum of diabetic adolescents did not differ from that observed in older children and adolescents without this autoimmune disease. H. pylori infection, which is frequent among adolescents from developing countries, did not modify lymphocyte density in the distal duodenum in the absence of lymphocytic gastritis.     

Upper gastrointestinal disease, Helicobacter pylori and recurrent abdominal pain

Over a 5-y period, 396 children complaining of recurrent abdominal pain (RAP) underwent upper gastrointestinal endoscopy in order to identify any underlying organic pathology and determine the prevalence of Helicobacter pylori (H. pylori) infection. Histologically confirmed mucosal inflammation was found in 338 out of 396 children (85.4%); in 113 of 396 patients (28.5%), H. pylori was identified on the gastric mucosa. Significant discriminating factors between H. pylori positive and negative children with RAP included age (mean age for positive 11 y vs. 8.1 y for negative, p < 0.01) and gender (male gender predominance in the H. pylori positive, p < 0.001). No significant difference was found between H. pylori positive and negative groups regarding incidence and character of the presenting symptoms. All H. pylori positive children (100%) had abnormal histology compared with 225 out of 283 negative ones (79.5%). Histologically confirmed gastritis was the most prominent finding in H. pylori positive children compared with H. pylori negative (98.2% vs. 19%, p < 0.001). Conversely, oesophagitis was more common in H. pylori negative children (47.7% vs. 27.4%, p < 0.001). The incidence of peptic ulcer was higher in H. pylori infected patients than in the H. pylori negative group (5.3% vs. 1%, p < 0.05). Our data suggest that gastrointestinal pathology is more common than previously thought in children with RAP, while H. pylori infection is a relatively important factor in the etiology of upper gastrointestinal inflammation in RAP syndrome.     

Management and response to treatment of Helicobacter pylori gastritis.

Gastritis associated with Helicobacter pylori was present in gastric biopsies from 24/95 (25%) children and adolescents undergoing endoscopy for recurrent abdominal pain and upper gastrointestinal symptoms. H pylori associated gastritis occurred mainly in older children (8-16 years) and was significantly associated with low socioeconomic class and a family history of peptic ulcer disease. Antral nodularity was a common endoscopic finding in H pylori positive children. Eighteen children, all over 5 years of age, were treated with tripotassium dicitratobismuthate (De-Nol) for two months and ampicillin for two weeks. In 12 children follow up gastric biopsies were obtained six weeks after completion of treatment. In 9/12 (75%) children H pylori was eradicated, and gastritis improved.     

Immunohistochemical detection of Helicobacter pylori infection in gastric biopsies of urea breath test-positive and -negative pediatric patients

Helicobacter pylori (H. pylori) is a common cause of gastritis in both children and adults, and its incidence increases every year. The aims of this study were to evaluate the histopathologic features of H. pylori gastritis and to compare immunohistochemical with histochemical [hematoxylin-eosin (HE) and Giemsa] staining of gastric biopsy specimens for the detection of H. pylori infection from urea breath test (UBT) (-) and UBT (+) children. Seventy-eight gastric biopsies from pediatric patients who were administered UBT were included in this study. Gastric biopsy specimens were evaluated histopathologically and graded according to the Sydney system. HE, Giemsa and immunohistochemical staining was performed for the identification of H. pylori. The frequency of H. pylori gastritis was higher in the antrum than corpus. All biopsies with H. pylori colonization showed chronic inflammation with activity. By using immunohistochemical method, coccoid forms of H. pylori and spiral bacteria with low density were observed easily. With histochemical staining, 1/10 (10%) UBT (-) biopsies were H. pylori (+), while with immunohistochemical staining, 3 of the biopsies from UBT (-) patients were found to be H. pylori (+). Biopsies from 65 of 78 (83.3%) UBT (+) patients were H. pylori (+) with histochemical staining, but only 53 of these biopsies were found to be H. pylori (+) immunohistochemically. We conclude that immunohistochemical staining is more specific than histochemical staining and UBT for the detection of H. pylori infection.     

幽门螺杆菌感染与儿童胃炎关系探讨

为进一步研究幽门螺杆菌（Helicobacter pylori,H.pylori)感染与儿童胃炎的关系，对我科1998年至2000年间500例3岁－15岁儿童胃镜活检组织进行组织学和H.pylori观察，按Sydney胃炎标准对病变分级，分析和探讨H.pylori感染与儿童胃炎发展变化的关系。结果表明：40.4%的儿童胃炎与H.pylori感染有关；而且炎症的程度、淋巴滤泡的形成、嗜酸细胞增多及幽门腺萎缩明显高于无H.pylori感染的儿童胃炎。提示上海地区儿童胃炎有很高的H.pylori感染率，H.pylori感染与儿童胃炎关系密切，儿童H.pylori胃炎的胃粘膜病理变化比非H.pylori感染者严重。     

Can pre-neoplastic lesions be detected in gastric biopsies of children with Helicobacter pylori infection?

BACKGROUND: Active gastritis, gastric mucosal atrophy and intestinal metaplasia are lesions associated with Helicobacter pylori infection. Atrophy and intestinal metaplasia are only seen in adults. OBJECTIVES: We describe pediatric patients with atrophy and metaplasia, and compare the inflammatory response in these patients to controls. METHODS: As part of a multicenter study of pediatric H. pylori infection, gastric biopsy specimens obtained during diagnostic upper endoscopy of 19 H. pylori-infected children and 45 uninfected controls were reviewed and graded by using the updated Sydney system. The inflammatory response was characterized using immunohistochemistry for T lymphocytes, B lymphocytes, and macrophages, and TUNEL assay for apoptosis. RESULTS: Histology of H. pylori-infected and control biopsy specimens showed active gastritis in 32% and 2% respectively (P = 0.002). Mild intestinal metaplasia was found in 4 H. pylori-infected children, in two of whom it appeared to be accompanied by atrophy. Specimens from patients with H. pylori infection contained increased numbers of B lymphocytes in lymphoid nodules, and apoptosis in the superficial epithelium and inflammatory cells. T lymphocytes and macrophages appeared in similar numbers in specimens from controls and infected patients. CONCLUSIONS: We describe intestinal metaplasia associated with H. pylori infection in children. Since atrophy usually precedes intestinal metaplasia in adults, we suggest that atrophy exists in children. High numbers of B lymphocytes and apoptosis in the surface epithelium are seen in patients with H. pylori infection and may be related to the development of atrophy and intestinal metaplasia.     

Parietal cell antibodies and Helicobacter pylori in children

BACKGROUND: Gastric autoantibodies are common in Helicobacter pylori-infected adults, and the presence of these antibodies is associated with atrophic gastritis. The role of H. pylori in the autoimmune type of atrophic gastritis is unresolved, and it is not known at what stage the autoantibodies appear in serum during H. pylori infection. Therefore, we screened children with and without H. pylori infection for gastric parietal cell antibodies. METHODS: Seventy-one children with H. pylori infection verified by examination of gastric biopsy specimens (mean age, 9.4 years), 8 children with positive serology but negative histology for H. pylori (mean age, 11.6 years), and 130 children with negative serology for H. pylori (mean age, 7.7 years) were screened for the presence of gastric parietal cell antibodies in serum by indirect immunofluorescence. In addition, 61 children with celiac disease (mean age, 7.1 years) were screened for gastric parietal cell antibodies and H. pylori antibodies. RESULTS: None of the children with H. pylori infection had gastric parietal cell antibodies in serum. Only three positive parietal cell antibody reactions were found: a 14-year-old boy with positive serology for H. pylori but no other signs of infection (titer 5000), a 14-year-old girl with tuberculosis (titer 1250, seronegative for H. pylori) and a 10-year-old girl with insulin-dependent diabetes mellitus (titer 6250, seronegative for H. pylori). CONCLUSIONS: Although gastric autoantibodies are often found in adults with chronic H. pylori gastritis, it seems that H. pylori-infected children are not positive for gastric parietal cell antibodies. It remains to be studied in which H. pylori infections and at what stages gastric autoantibodies appear.