Peptic Ulcer Disease in Children: Etiology, Clinical Findings, and Clinical Course

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.

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.


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.


1995 ◽  
Vol 16 (7) ◽  
pp. 257-265
Author(s):  
Adam G Mezoff ◽  
William F Balistreri

The term peptic ulcer disease describes a group of disorders, rather than a single pathologic process. It is recognized increasingly in children, often with long-term ramifications. In the past decade, management of patients who have peptic ulcer disease has changed dramatically. Antacid therapy has given way to treatment with histamine (H2) receptor antagonists, a new class of pharmacologic agents that has fostered a billion dollar industry. Other modalities of treatment have been developed as well, such as cytoprotective agents (sucralfate) and proton pump inhibitors (omeprazole), which are based on research into the pathophysiology of gastric acid disorders. In addition, the discovery of an infectious agent (Helicobacter pylori) that contributes to the formation of peptic ulcers has led to a reevaluation of the traditional approach to diagnosis and treatment of abdominal pain in children. Duodenal ulcers are defined as mucosal defects penetrating the mucosa, submucosa, and muscularis mucosa of the duodenum. Gastric ulcers are defined as mucosal defects that penetrate the muscularis mucosa of the stomach. Primary ulcers are those that have no known underlying cause. Secondary ulcers are associated with a known ulcerogenic event such as stress, burns, or ingestion of nonsteroidal anti-inflammatory medications. A discussion of peptic inflammation that typically does not cause ulceration, such as esophagitis, is beyond the scope of this review.


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.


2017 ◽  
Vol 56 (206) ◽  
Author(s):  
Mukesh Sharma Paudel ◽  
Sudhamshu KC ◽  
Amrendra Kumar Mandal ◽  
Nandu Silwal Poudyal ◽  
Ramila Shrestha ◽  
...  

Introduction: AUGIB is characterized by hematemesis or melena or both. Peptic ulcers and variceal bleed account for majority of cases. Use of proton pump inhibitors in current era is associated with a gradual reduction in burden of peptic ulcer disease. We conducted this study to look into the cause of AUGIB in our community.Methods: We studied 100 patients in one year period who presented to us with hematemesis or melena. The study was conducted in department of Gastroenterology, Bir hospital, Kathmandu. We identified the culprit lesions by upper gastrointestinal endoscopy.Results: The average age of patients with AUGIB was 51.6 years with 59 (59%) males. Duodenal ulcers are most common 29 (29%), followed by varices 23 (23%) and gastric ulcers 14 (14%). More than one lesion was identified in 38 (38%) patients. Patients with variceal bleed were more likely to present with hematemesis alone as compared to those with ulcer bleed (p=0.005). Variceal bleed patients presented earlier to the hospital (p=0.005), had lower MAP at presentation (p=0.0002), had lower hemoglobin level (p=0.0001) and higher serum creatinine level at presentation (p=0.001). Patients with variceal bleed were more likely to have consumed alcohol 20 (86.9%) and patients with ulcer bleed were more likely to be smokers 29 (67.4%) or consume tobacco 14 (32.5%) (p=0.006).Conclusions: Ulcer related bleeding is still the most common cause of AUGIB. Many patients with AUGIB have more than one lesions identified during upper gastrointestinal endoscopy.Keywords:  bleeding; endoscopy; peptic ulcer; upper gastrointestinal;varices. [PubMed]


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.


2009 ◽  
Vol 23 (9) ◽  
pp. 604-608 ◽  
Author(s):  
Marcel JM Groenen ◽  
Ernst J Kuipers ◽  
Bettina E Hansen ◽  
Rob J Th Ouwendijk

BACKGROUND/OBJECTIVES: As recently as 40 years ago, a decline in the incidence of peptic ulcers was observed. The discovery of Helicobacter pylori had a further major impact on the incidence of ulcer disease. Our aim was to evaluate the trends in the incidence and bleeding complications of ulcer disease in the Netherlands.METHODS: From a computerized endoscopy database of a district hospital, the data of all patients who underwent upper gastrointestinal endoscopy from 1996 to 2005 were analyzed. The incidence of duodenal and gastric ulcers, with and without complications, were compared over time.RESULTS: Overall, 20,006 upper gastrointestinal endoscopies were performed. Duodenal ulcers were diagnosed in 696 (3.5%) cases, with signs of bleeding in 158 (22.7%). Forty-five (6.5%) of these ulcers were classified as Forrest I and 113 (16.2%) as Forrest II. Gastric ulcers were diagnosed in 487 cases (2.4%), with signs of bleeding in 60 (12.3%). A Forrest 1 designation was diagnosed in 19 patients (3.9%) and Forrest 2 in 41 patients (8.4%). The incidence of gastric ulcers was stable over time, while the incidence of duodenal ulcers declined.CONCLUSIONS: The incidence of duodenal ulcer disease in the Dutch population is steadily decreasing over time. Test and treatment regimens for H pylori have possibly contributed to this decline. With a further decline in the prevalence of H pylori, the incidence of gastric ulcers is likely to exceed the incidence of duodenal ulcers in the very near future, revisiting a similar situation that was present at the beginning of the previous century.


Sign in / Sign up

Export Citation Format

Share Document