scholarly journals CagA Antibodies in Japanese Children with Nodular Gastritis or Peptic Ulcer Disease

2000 ◽  
Vol 38 (1) ◽  
pp. 68-70
Author(s):  
Seiichi Kato ◽  
Toshiro Sugiyama ◽  
Mineo Kudo ◽  
Kenji Ohnuma ◽  
Kyoko Ozawa ◽  
...  

ABSTRACT cagA + Helicobacter pylori strains have been linked to more severe gastric inflammation, peptic ulcer disease, and gastric cancer in adults, but there have been few studies of cagA in children. We examined the relationship between H. pylori cagA status and clinical status in Japanese children. Forty H. pylori -positive children were studied: 15 with nodular gastritis, 5 with gastric ulcers, and 20 with duodenal ulcers. H. pylori status was confirmed by biopsy-based tests and serum anti- H. pylori immunoglobulin G (IgG) antibody. As controls, 77 asymptomatic children with sera positive for anti- H. pylori IgG were enrolled. Levels of IgG antibodies to CagA in serum were measured by an antigen-specific enzyme-linked immunosorbent assay. In 16 patients with successful H. pylori eradication, posttreatment levels of CagA and H. pylori IgG antibodies also were studied. The CagA antibody seropositivities of asymptomatic controls (81.8%) and patients with nodular gastritis, gastric ulcers, and duodenal ulcers (80.0 to 95.0%) were not significantly different. Compared with pretreatment levels of CagA antibodies, posttreatment levels decreased progressively and significantly. We conclude that, as in Japanese adults, a high prevalence of cagA + H. pylori strains was found in Japanese children, and that there was no association with nodular gastritis or peptic ulcer disease. In the assessment of eradicative therapies, monitoring of serum anti-CagA antibodies does not appear to offer any direct benefit over monitoring of anti- H. pylori antibodies.

2007 ◽  
Vol 56 (1) ◽  
pp. 9-14 ◽  
Author(s):  
Rejane Mattar ◽  
Sergio Barbosa Marques ◽  
Maria do Socorro Monteiro ◽  
Anibal Ferreira dos Santos ◽  
Kiyoshi Iriya ◽  
...  

The purpose of this study was to verify whether the presence of any of the Helicobacter pylori cagPAI genes or segments – cagA, cagA promoter, cagE, cagM, tnpB, tnpA, cagT and the left end of the cag II (LEC) region – would be a useful marker for the risk of peptic ulcer disease development. H. pylori DNA extracted from positive urease tests of 150 peptic ulcer patients and 65 dyspeptic controls was analysed by PCR. Duodenal ulcers were present in 110, gastric ulcers in 23 and both gastric and duodenal ulcers in 17 patients. A significant association (P <0.001) was found between a conserved cagPAI and peptic ulcer disease (34 %). The positivity of the cagA gene varied according to the region of the gene that was amplified. The region near to the promoter was present in almost all of the H. pylori isolates (97.2 %). The segment from nt 1764 to 2083 and the extreme right end were frequently deleted in the isolates from the controls (P <0.01). The positivity of the promoter region of cagA and cagT, cagE, cagM and LEC showed a significant difference between the isolates from peptic ulcer patients and from the controls (P <0.01). Patients usually had moderate gastritis; however, the intensity of the active inflammation was higher in the peptic ulcer group (P <0.001). cagT, cagM, LEC and the right end terminus of the cagA-positive H. pylori isolates were associated with a 27-fold, 8-fold, 4-fold and 4-fold risk of peptic ulcer disease, respectively, and may be useful markers to identify individuals at higher risk of peptic ulcer disease development in Brazil.


PEDIATRICS ◽  
1988 ◽  
Vol 82 (3) ◽  
pp. 410-414
Author(s):  
Brendan Drumm ◽  
J. Marc Rhoads ◽  
David A. Stringer ◽  
Phillip M. Sherman ◽  
Lynda E. Ellis ◽  
...  

The records of all children with peptic ulcer disease at the Hospital for Sick Children were retrospectively evaluated, excluding neonates, throughout a 5-year period. Only cases with a definite ulcer crater identified either at endoscopy or at surgery were included. There were 36 patients, 20 boys and 16 girls. Duodenal ulcers were more common than gastric ulcers (2.8:1). Ages ranged from 3 months to 17 years, with a mean age of 10 years. Patients were reviewed with respect to etiology of peptic ulcer disease, age when first examined, initial symptoms, and clinical course. Patients were divided into two groups, those with primary (n = 19) and those with secondary (n = 17) peptic ulcer disease. All peptic ulcers in patients younger than 10 years of age were secondary in nature. Secondary ulcers occurred generally in association with a severe underlying illness (11/17), and many ulcers necessitated emergency surgery because of perforation and/or severe hemorrhage (8/17). None of these patients had chronic or recurrent symptoms. In contrast, in children with primary peptic ulcer disease, initial symptoms were more benign. Most patients had abdominal pain and only one required emergency surgery. Children with primary duodenal ulcer disease had a high incidence of recurrent symptoms (67%), however, with surgery for intractable disease necessitated in 40%. Single-contrast barium meals were found to be unreliable in establishing a diagnosis of peptic ulcer disease, particularly cases of gastric ulcer disease.


2020 ◽  
pp. 2849-2861
Author(s):  
Joseph Sung

Helicobacter pylori infection, use of nonsteroidal anti-inflammatory drugs (NSAIDs) including aspirin, and smoking are the most important causes of peptic ulcer disease. Peptic ulcer disease is characterized by a history of waxing and waning symptoms of localized, dull, aching pain in the upper abdomen. Bleeding is the most common complication; free perforation of the stomach or duodenum into the peritoneal cavity is uncommon but serious. The diagnosis of peptic ulcer disease is made by endoscopy, which offers an opportunity for biopsy of gastric ulcers (which may be malignant) and reveals important prognostic indicators in patients with bleeding ulcers. A single daily dose of a proton pump inhibitor gives quick relief of symptoms and effective healing of peptic ulcers in 4 to 6 weeks. The management of patients with upper gastrointestinal haemorrhage requires a multidisciplinary medical and surgical approach. Early risk stratification based on clinical and endoscopic criteria allows delivery of appropriate care, with endoscopic intervention now widely accepted as the first line of therapy. This should be followed by administration of a high dose of an intravenous proton pump inhibitor to further reduce recurrent bleeding. Treatment of H. pylori is a cure for peptic ulcer disease in most patients. This usually requires at least two antimicrobial agents, with the most popular triple therapy combining a proton pump inhibitor with any two of amoxicillin, metronidazole, and clarithromycin for 7 to 14 days. Eradication of H. pylori infection, avoidance of high-dose NSAIDs or aspirin, and the maintenance use of proton pump inhibitors in high-risk individuals are the best ways to prevent recurrence of ulcer and ulcer complications.


2018 ◽  
Vol 5 (4) ◽  
pp. 1315
Author(s):  
Mrutyunjay I. Uppin ◽  
Kapildev K. Hannurkar

Background: Prevalence of Helicobacter pylori (H. pylori) emerges throughout the world and instigates peptic ulcer disease (PUD). The study was conducted with the aim to determine the prevalence of H. pylori in patients with PUD undergoing upper gastrointestinal endoscopy.Methods: This prospective study was conducted on 150 cases of PUD from August 2009 to February 2011. Endoscopy was done in all cases. Biopsy was done and sent for histopathological examination and rapid urease test for confirmation of presence of H. pylori.Results: Out of 150 patients with mean age of 45.76 years, 109 patients were diagnosed to have been infected with Helicobacter pylori (72.66%). Out of 89 patients with gastric ulcer, 61 patients were infected with Helicobacter pylori (68.53%). Forty two out of 51 patients (82.35%) with duodenal ulcers and 06 of 10 patients (60%) with carcinoma of stomach were positive for H. pylori. The remaining patients were found to be negative for the H. pylori infection.Conclusions: The findings of the study conclude that H. pylori was consistently associated with PUD.


2020 ◽  
Vol 3 (2) ◽  
pp. 30-32
Author(s):  
Rahul Charpot ◽  
Jaydeep M Gadhavi

Background: To establish the occurrence of peptic ulcer disease amid the Subjects with abdominal pain at tertiary care institute of Gujarat. Subjects and Methods: present research was performed at the Department of Surgery, tertiary care institute of Gujarat, for the period of one year in 200 patients with abdominal pain and diagnosed with peptic ulcer disease. Information was composed utilizing pre-designed questionnaire. Results:The majorities of participants was females, most were aged between 18 to 25 years. Around 97% had pain in the epigastric region. Gastric ulcers preponderate for 65% patients in current research, except refused during the later existence of the epoch, as the occurrence of duodenal ulcers stayed stable, however amplified rather the later phase. Conclusion: An extensive diversity of subjects with abdominal pain was documented amid the subjects. On the other hand, the socio-economic situation and educational levels of the Subjects with the illness were below par.


Author(s):  
Aran Sivakumar ◽  
Benjamin Stubbs

Peptic ulcer disease (PUD) is defined as a disruption in the innermost lining of the gastrointestinal tract, due to the secretion of gastric acid or pepsin. The disruption is in the gastric epithelial layer, specifically the muscularis mucosae. PUD normally affects the stomach along with the first and second parts of the duodenum, although it is not limited to these areas. Typically, gastric ulcers induce upper abdominal pain within 30 minutes of eating, whereas duodenal ulcers cause discomfort much later. Endoscopic and histological investigations are the key to early identification and treatment of patients with PUD, with testing for Helicobacter pylori necessary in those patients suspected of having PUD. In this article we will be looking at the aetiology, pathophysiology and management of PUD.


2018 ◽  
Author(s):  
Edward A Lew

Peptic ulcers are defects or breaks in the inner lining of the gastrointestinal (GI) tract. Although the pathogenesis is multifactorial they tend to arise when there is an imbalance between protective and aggressive factors, such as when GI mucosal defense mechanisms are impaired in the presence of gastric acid and pepsin. Peptic ulcers extend through the mucosa and the muscularis mucosae, a thin layer of smooth muscle separating the mucosa from the deeper submucosa, muscularis propria, and serosa. Peptic ulcer disease affects up to 10% of men and 4% of women in Western countries at some time in their lives. This chapter discusses the pathogenesis of peptic ulcer disease and the etiologic contribution of Helicobacter pylori infection, nonsteroidal anti-inflammatory drugs, and gastrinoma or other hypersecretory states. Also addressed are rare and unusual causes for ulcers and GI bleeding. A section on the diagnosis of peptic ulcers discusses clinical manifestations, physical examination findings, laboratory and imaging studies, and surgical diagnosis. Differential diagnosis is also reviewed. Tests to establish the etiology of peptic ulcer disease include endoscopy, quantitative serologic tests, the urea breath test, and the fecal antigen test. Discussed separately are treatments for uncomplicated duodenal ulcers, uncomplicated gastric ulcers, intractable duodenal or gastric ulcers, complicated peptic ulcers (bleeding ulcers, acute stress ulcers, perforated ulcers, obstructing ulcers, fistulizing ulcers, and Cameron ulcers), H. pylori ulcers, and gastric cancer. Figures illustrate the etiopathogenesis of peptic ulcers, prevalence of H. pylori infection in duodenal and gastric ulcer patients compared with normal controls, the approach to a patient with new and undiagnosed ulcerlike symptoms refractory to antisecretory therapy, an upper GI series showing an uncomplicated duodenal ulcer, a chest x-ray showing pneumoperitoneum from a perforated duodenal ulcer, gastric biopsy samples showing H. pylori organisms, and the approach to treatment and follow-up in patients with either complicated or uncomplicated duodenal or gastric ulcer. Tables list differential diagnoses of peptic ulcer disease, commonly used regimens to eradicate H. pylori, additional antimicrobial agents with activity against H. pylori, and FDA-approved antisecretory drugs for active peptic ulcer disease. This chapter contains 76 references.


2020 ◽  
Author(s):  
Edward A Lew

Peptic ulcers are defects or breaks in the inner lining of the gastrointestinal (GI) tract. Although the pathogenesis is multifactorial they tend to arise when there is an imbalance between protective and aggressive factors, such as when GI mucosal defense mechanisms are impaired in the presence of gastric acid and pepsin. Peptic ulcers extend through the mucosa and the muscularis mucosae, a thin layer of smooth muscle separating the mucosa from the deeper submucosa, muscularis propria, and serosa. Peptic ulcer disease affects up to 10% of men and 4% of women in Western countries at some time in their lives. This chapter discusses the pathogenesis of peptic ulcer disease and the etiologic contribution of Helicobacter pylori infection, nonsteroidal anti-inflammatory drugs, and gastrinoma or other hypersecretory states. Also addressed are rare and unusual causes for ulcers and GI bleeding. A section on the diagnosis of peptic ulcers discusses clinical manifestations, physical examination findings, laboratory and imaging studies, and surgical diagnosis. Differential diagnosis is also reviewed. Tests to establish the etiology of peptic ulcer disease include endoscopy, quantitative serologic tests, the urea breath test, and the fecal antigen test. Discussed separately are treatments for uncomplicated duodenal ulcers, uncomplicated gastric ulcers, intractable duodenal or gastric ulcers, complicated peptic ulcers (bleeding ulcers, acute stress ulcers, perforated ulcers, obstructing ulcers, fistulizing ulcers, and Cameron ulcers), H. pylori ulcers, and gastric cancer. Figures illustrate the etiopathogenesis of peptic ulcers, prevalence of H. pylori infection in duodenal and gastric ulcer patients compared with normal controls, the approach to a patient with new and undiagnosed ulcerlike symptoms refractory to antisecretory therapy, an upper GI series showing an uncomplicated duodenal ulcer, a chest x-ray showing pneumoperitoneum from a perforated duodenal ulcer, gastric biopsy samples showing H. pylori organisms, and the approach to treatment and follow-up in patients with either complicated or uncomplicated duodenal or gastric ulcer. Tables list differential diagnoses of peptic ulcer disease, commonly used regimens to eradicate H. pylori, additional antimicrobial agents with activity against H. pylori, and FDA-approved antisecretory drugs for active peptic ulcer disease. This chapter contains 5 figures, 6 tables and 78 references.


1936 ◽  
Vol 32 (8) ◽  
pp. 909-916
Author(s):  
Ya. I. Daikhovsky

If until now the views of most authors still diverge on the pathogenesis of gastric ulcers, then there is complete unanimity in assessing the role of the nervous system in the development and course of gastric ulcers and duodenal ulcers, stomach ulcers and duodenal ulcers have long ceased to be considered as local disease, it is a manifestation of a disease of the whole organism with the localization of the process in the stomach or duodenal ulcer, which finds its expression in the term peptic ulcer disease. This view, firmly established in medicine, on stomach and duodenal ulcers is impossible, of course, not consider when it comes to treating this suffering.


PEDIATRICS ◽  
1995 ◽  
Vol 96 (2) ◽  
pp. 211-215
Author(s):  
Sonny K. F. Chong ◽  
Qinyuan Lou ◽  
Mark A. Asnicar ◽  
Sarah E. Zimmerman ◽  
Joseph M. Croffie ◽  
...  

Objective. To determine the role of Helicobacter pylori infection in children with recurrent abdominal pain and the usefulness of serologic tests in screening H pylori infection and monitoring treatment of H pylori-associated gastritis. Methods. During a 3 year period, we investigated the presence of serum immunoglobulin G (IgG) antibody to H pylori in 456 children using the high-molecular-weight cell-associated protein H pylori enzyme immunoassay kit. Among the 456 children studied, 218 (age range, 3 to 18 years; mean age, 9.5 years) had symptoms of recurrent abdominal pain (RAP syndrome) with or without vomiting, and the remaining 238 (age range, 3 to 18 years; mean age, 9.8 years) had no RAP (non-RAP syndrome). We performed upper gastrointestinal endoscopy on 111 consecutive children of the 218 with RAP syndrome and obtained mucosal biopsies for culture, histologic analysis, CLO test (Delta West, Perth, Australia), and H pylori detection by polymerase chain reaction. Results. Thirty-eight (17.4%) of 218 children in the RAP group and 25 (10.5%) of 238 children in the non-RAP group were seropositive for H pylori. Of the 111 children endoscoped, 95 were found to be negative, and 12 were positive by all five assays. Specimens from 2 children were negative by culture and the CLO test but positive by the other three assays. Specimens from 1 child were negative by histologic analysis but positive by all other tests. The remaining child was positive for anti-H pylori IgG but negative by all of the other four assays. Upper gastrointestinal endoscopy detected 14 children with peptic ulcer disease (9 duodenal ulcer and 5 gastric ulcer) and 12 with antral nodular gastritis. Only 4 of the 14 diagnosed with peptic ulcer were H pylori positive by all five assays, whereas all 12 children with antral nodular gastritis were H pylori positive. Nine of the 12 H pylori-positive children were treated with a combination of bismuth subsalicylate, amoxicillin, and metronidazole for 2 weeks. Sera obtained at 2, 4, and 6 months after treatment from all 9 children showed a decrease in anti-H pylori IgG titer. Three H pylori-infected children who did not receive any treatment served as control children, and their IgG levels remained elevated or increased over time. Conclusion. The results from our study indicate that screening for the serum IgG antibody to H pylori is a practical method for diagnosing H pylori infection in children, and that serial measurements of the H pylori IgG antibody are useful for monitoring treatment of H pylori because of its high sensitivity and ease of performance. Only 4 of the 14 children diagnosed with peptic ulcer disease were confirmed to be infected with H pylori, whereas all 12 children with antral nodular gastritis were found to be infected by H pylori. These observations suggest that H pylori infection is more frequently associated with gastritis than with peptic ulcer disease in children, and that H pylori gastritis is a cause of RAP syndrome in children.


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