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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

H pylori is a global human pathogen and is the major cause of gastritis and the gastritis-associated diseases: gastric ulcer, duodenal ulcer, gastric cancer, and primary gastric B-cell lymphoma (MALToma). Although several reliable diagnostic tests are widely available, the ideal regimen for treating the infection re-mains to be established. The current first-line or legacy triple therapy regimens fail in 20% to 40% of patients. Causes of treatment failure include antibiotic resistance, poor compliance, short (7-10 days) duration of therapy, and drug-related side effects. Fourteen-day triple therapy has an approximately 12% better cure rate than does 7-day therapy; therefore, shorter durations can no longer be recommended. Recent studies confirmed older observations that the success rate of legacy triple regimens (PPI plus two antibiotics) can be improved if the duration is extended to 14 days or if a third antibiotic is given. Sequential therapy (PPI plus amoxicillin followed by a PPI plus clarithromycin plus metronidazole) requires further evaluation although the concept appears very promising and therapy should probably replace the legacy triple therapies. More studies are needed to examine doses, durations, and the need for sequential administration of the drugs, which extends the duration to 14 days. Nonetheless, sequential quadruple therapy probably should replace the legacy triple therapies. Classic quadruple therapy contains bismuth, a PPI, 1500 mg of metronidazole, and 1500 mg of tetracycline. It provides the highest average eradication rates and in many regions should be considered as the initial approach. Confirmation of eradication using noninvasive diagnostic tests, such as a urea breath test or stool antigen assay, is now the standard of care. The diagnosis of latent or symptomatic H pylori like the diagnosis of latent or symptomatic syphilis, always should prompt treatment. Because of decreasing cure rates, new and improved therapies are needed.
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PMID:Helicobacter pylori diagnosis and management. 1688 64

A 6-year-old boy was hospitalized because of dark feces and facial pallor of 1 weeks duration. Other gastrointestinal symptoms, including vomiting and abdominal pain, were absent, but he felt dizziness when standing and fatigue on effort. Hematologic studies revealed iron-deficiency anemia, and endoscopy showed gastric erosions and a duodenal ulcer. All test results for Helicobacter pylori infection, including H. pylori antigen in stool, anti-H. pylori IgG immunoassay in serum, and the (13)C-urea breath test, were positive. Because an H. pylori-associated gastric ulcer had been diagnosed with endoscopy in the patients father 3 years earlier, father-son transmission was suspected. The patient was treated with triple-agent eradication therapy (proton pump inhibitor [lansoprazol], amoxicillin, and clarithromycin) for 2 weeks. One month after therapy was completed, eradication of H. pylori was confirmed by negative results on the stool antigen test. Peptic ulcer disease can occur in young children, as in this case. The stool antigen test kit is a useful and reliable method that can be used even in preschool children to diagnose H. pylori infection.
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PMID:Helicobacter pylori infection with a duodenal ulcer in a 6-year-old boy. 1710 82

One half of the world's population has Helicobacter pylori infection, with an estimated prevalence of 30 percent in North America. Although it is unclear whether eradication of H. pylori improves symptoms in patients with nonulcer dyspepsia, there is strong evidence that eradication of this bacteria improves healing and reduces the risk of recurrence or rebleeding in patients with duodenal or gastric ulcer. A "test-and-treat" strategy is recommended for most patients with undifferentiated dyspepsia. With this approach, patients undergo a noninvasive test for H. pylori infection and, if positive, are treated with eradication therapy. This strategy reduces the need for antisecretory medications as well as the number of endoscopies. The urea breath test or stool antigen test is recommended. Until recently, the recommended duration of therapy for H. pylori eradication was 10 to 14 days. Shorter courses of treatment (i.e., one to five days) have demonstrated eradication rates of 89 to 95 percent with the potential for greater patient compliance. A one-day treatment course consists of bismuth subsalicylate, amoxicillin, and metronidazole, all given four times with a one-time dose of lansoprazole. In children with documented H. pylori infection, however, all regimens should continue to be prescribed for seven to 14 days until short-course treatment is studied and its effectiveness has been established in this population.
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PMID:Update on Helicobacter pylori treatment. 1824 84

NICE recommends immediate referral for patients with dyspepsia and significant acute GI bleeding and urgent specialist referral for investigation if any of the following alarm symptoms are present: progressive difficulty swallowing; chronic GI bleeding; unintentional weight loss; persistent vomiting; abdominal mass; iron deficiency anaemia; suspicious findings on barium meal. Patients aged > 55 with unexplained and persistent dyspepsia, despite H. pylori testing and acid suppression therapy, should also be considered for endoscopy, as should those with previous gastric ulcer or surgery, continuing need for NSAIDs or raised risk of gastric cancer. Patients with uninvestigated dyspepsia should be managed by empirical treatment with a PPI or testing for and treating H. pylori if present. Testing by urea breath test, stool antigen test, or locally validated lab-based serology is suggested. H. pylori eradication is usually given as triple therapy, for seven days, involving a PPI, clarithromycin and either amoxicillin or metronidazole. It is important to take a thorough history and to enquire about any medication the patient is taking. Drugs that are common culprits for dyspepsia include: NSAIDs; calcium antagonists; bisphosphonates; steroids; theophyllines; nitrates. NSAIDs can also cause GI bleeding. Absence of dyspepsia in patients taking NSAIDs does not indicate a reduced risk of bleeding. Peptic ulcers fall into three categories: H. pylori associated ulcers; drug-induced ulcers (particularly NSAIDs); and ulcers in H. pylori-negative patients not taking causative medication. H. pylori is associated with both gastric and duodenal ulcer disease but it is in the duodenum where the closest relationship exists. In any 6-12 month period, 20-40% of healthy people, more commonly men, will experience symptoms of heartburn. Oesophageal reflux can progress to more serious disease such as erosive oesophagitis, stricture or Barrett's oesophagus.
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PMID:Managing dyspepsia in primary care. 1993 59

It has been reported that an active aloe polysaccharide isolated from Aloe barbadensis Miller exerted various pharmacological effects, such as anti-inflammatory, wound healing, anti-hepatitis, anti-gastric ulcer, and anti-tumorigenicity in animals. Adverse health effects of aloe are of concern in humans. Therefore, this study was conducted to investigate a tolerable upper intake level (UL) of active aloe or a maximal allowable daily intake (ADImax) of active aloe based on 4-wk oral toxicity investigation in ICR mice. An active aloe was daily administered to male and female ICR mice for 4 wk at different dose levels (0, 120, 600, 3000, or 15,000 mg/kg body weight [bw]). All animals were sacrificed at the end of the experiment and changes of body weight, food consumption, organ weights, and hematological and biochemical parameters were recorded. In this study, no changes in clinical signs, urinalysis, or hematological or biochemical analysis were observed. In females, a dose-dependent quantitative decrease in albumin (ALB) levels was observed, but it was not significant, due to wide interindividual variations. A significant decrease in male kidney weight was observed from the 120-mg/kg to the 15,000-mg/kg bw treatment groups, and blood urea nitrogen (BUN) levels were also quantitatively lower. A dose-dependent reduction in the body weight of females was also observed, which might be related to less food consumption. Based on the reduced kidney weights in males, the lowest-observed-adverse-effect level (LOAEL) of an active aloe was estimated to be 120 mg/kg bw in male ICR mice, and the UL or ADImax was 0.4 mg/kg bw/d [(120 mg/kg bw/d)/(100 for safety factor) x (3 for modifying factor)], or 24 mg for a 60-kg adult (24 mg x 200 = 4.8 g of aloe gel/d/adult), assuming that consumers utilize active aloe for a month. Data showed that an active aloe did not induce any remarkable subacute toxic effects, but decreased male kidney weights, which requires further investigation.
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PMID:Estimation of tolerable upper intake level (UL) of active aloe. 2007 18

It has been clearly established that Helicobacter pylori (H. pylori) infection plays a pivotal role in the pathogenesis of chronic gastritis, peptic ulcer, gastric adenocarcinoma, and gastric lymphoma MALT (mucosa-associated lymphoid tissue) in the general population, but data regarding the prevalence and the role of H. pylori infection in liver cirrhosis are conflicting. Most serological studies estimated a high prevalence of H. pylori infection in patients with liver cirrhosis; however, when other methods (urea breath test, histology, culture, rapid urease test) were used, the overall H. pylori prevalence was similar to that in controls. Although the prevalence of both gastric ulcer (GU) and duodenal ulcer (DU) is higher in cirrhotic patients than in general population, the relationship between H. pylori infection and peptic ulcer in cirrhosis remains controversial. Our data regarding peptic ulcer prevalence in cirrhotic patients are in agreement with previous studies that suggest an increased prevalence of both GU and DU. The incidence of bleeding peptic ulcer is high in cirrhotic patients and carries an increased risk of complications or death in these patients and therefore eradication of H. pylori infection might be as effective in preventing ulcer relapse and bleeding as it is in noncirrhotic ulcer patients. Hepatic encephalopathy is a frecquent complication of liver cirrhosis, and it is widely accepted that ammonia plays a major role in its pathogenesis. The ammonia production by H. pylori urease does not increase blood ammonia levels during cirrhosis, and eradication of H. pylori infection does not affect hepatic encephalopathy status.
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PMID:[Prevalence and role of Helicobacter pylori infection in some gastroduodenal and hepatic complications in cirrhotic patients]. 2020 58

This study aims to determine primary Helicobacter pylori resistance and its effect on eradication of the organism. Ninety-two patients with dyspeptic symptoms were enrolled. H. pylori was cultured and antibiotic sensitivity was determined by the Epsilometer test (Etest) for clarithromycin (CLR), amoxicillin (AMX) and metronidazole (MTR). 23S ribosomal RNA (rRNA) point mutations associated with clarithromycin resistance were also detected. Patients were treated with omeprazole (40 mg daily), CLR (500 mg) and AMX (1g twice a day) for 14 days. A 14C-urea breath test (14C-UBT) was repeated four weeks after completion of treatment to confirm eradication. Triple therapy failure was seen in 30 (33%) patients. The resistance rates were: CLR 33% (30/92), MTR 48% (44/92) and AMX 2% (2/92). Clarithromycin resistance (CLR-R) was present in the 16-39 age group in 21 (47%) (P = 0.007) compared to nine (19%) in the 40-79 age group. CLR resistance was seen in 30 H. pylori isolates, 20 (67%) from patients with non-ulcer dyspepsia (NUD), six (20%) with gastric ulcer (GU) and four (13%) with duodenal ulcer (DU). Triple therapy failure was associated with CLR-R in 28 (93%) (P < 0.001). CLR-R mutations were present in 30 (33%) and were associated with treatment failure in 27 (90%; P < 0.001). They were present in 20 (44%) isolates obtained from patients in the 16-39 age group (P = 0.018). Treatment failure was associated with A2142G mutation in 20 (67%; P < 0.001), A2143G mutation in 12 (40%; P < 0.001) and A2142C mutation in five (17%; P = 0.003). In conclusion, triple therapy failure was associated with CLR-R. Metronidazole resistance exceeded that of CLR, hence it cannot be substituted for CLR in a triple therapy.
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PMID:Antibiotic susceptibility patterns of Helicobacter pylori and triple therapy in a high-prevalence area. 2129 47

The aim of this study was the detection of helicobacter pylori (HP) infection and estimation of the clinical validity and the accuracy of the 14C-urea breath test in the groups of patients studied. A total of 248 patients with gastric diseases were examined. There were 38 patients with gastric ulcer, 41 with duodenal ulcer, 43 with gastroduodenitis erosiva, 26 with hiatus hernia, 36 with gastric carcinoma and 64 patients with gastritis. There were 103 true positive (TP), 139 true negative (TN), 4 false negative (FN) and 2 false positive (FP) patients. There was no significant difference in the incidence of the HP infection between the groups of patients studied (p > 0.05). Sensitivity of the method was 96.3%, specificity 98.6%, positive predictive value 98.1%, negative predictive value 97.2% and accuracy 97.6%. Our results point out that the method is very accurate for the detection of HP infection.
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PMID:Helicobacter pylori infection in various groups of patients studied, estimated by 14C-urea breath test. 2163 May 53

A 75-year-old man underwent endoscopic hemostatic therapy for hemorrhagic gastric ulcer in September 2002. After healing of the gastric ulcer, he underwent Helicobacter pylori eradication therapy in February 2003. In August 2007, an irregular tumor was detected in the lower esophagus at annual checkup for gastric cancer screening using X-ray. Endoscopic examination showed that the lower margin of the tumor almost coincided with the esophagogastric junction and that a short segment of Barrett's epithelium existed near the tumor. Biopsies of the tumor showed moderately to poorly differentiated adenocarcinoma. Mild reflux esophagitis and minor hiatal hernia was also observed, and the previously treated gastric ulcer was not recurrent. Absence of H. pylori was confirmed by serum antibody and urea breath test. Surgical resection of the lower esophagus and proximal stomach was performed. The tumor invaded into the muscularis propria of the esophageal wall but had no evidence of lymph node metastasis. Based on macroscopic and pathological findings, the tumor was recognized as esophageal adenocarcinoma. Previous endoscopic examination did not detect any apparent signs of tumor in the esophagogastric junction. As far as we know, this is the first report documenting a newly developed esophageal adenocarcinoma after the successful eradication of H. pylori.
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PMID:Esophageal Adenocarcinoma Developing after Eradication of Helicobacter pylori. 2176 87

Biopsy of ulcer margin is routinely performed to exclude malignancy in patients with gastric ulcers, but its utility in diagnosing Helicobacter pylori infection has not yet been fully studied. A cohort of 50 patients with gastric ulcer was prospectively examined. Three tests including histology, rapid urease test, and urea breath test were performed in all patients for diagnosing H pylori infection. Six biopsied specimens from the margin of the gastric ulcer and 1 each specimen from antrum and body of non-ulcer part were obtained for histology using hematoxylin-eosin (H&E) stain. The criterion used for defining H pylori infection was a positive result in at least 2 of the 3 tests. H pylori infection was diagnosed in 27 (54%) of the patients. The diagnostic sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of the histological examination of the ulcer margin were 92.6%, 95.7%, 96.2%, 91.7%, and 94%, respectively. The addition of 1 specimen from the antrum or body or a combination of the 2 specimens did not increase the diagnostic yields of those for histological examination of ulcer margin alone. The diagnostic sensitivity, specificity, positive predictive value, negative predictive value, and accuracy for the rapid urease test were 96.3%, 100%, 100%, 95.8%, and 98%, respectively, and the corresponding values for the urea breath test were 88.9%, 87%, 88.9%, 87%, and 88%. We performed Giemsa stain for the 3 patients with false-negative and false-positive results of histological examination of ulcer margin using H&E stain, and all were positive for H pylori infection. In conclusion, histological examination of the ulcer margin using hematoxylin-eosin stain was quite accurate and useful for diagnosing H pylori infection in patients with gastric ulcers. A special stain is required when the diagnosis of H pylori infection is questionable on routine H&E staining.
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PMID:Histological examination of ulcer margin for diagnosing Helicobacter pylori infection in patients with gastric ulcers. 2298 83


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