• Diagnosis
• Eradication
• Gastric cancer
• Helicobacter pylori
• Infection

• Helicobacter Infections/diagnosis
• Helicobacter Infections/drug therapy
• Helicobacter Infections/epidemiology
• Helicobacter Infections/therapy
• Humans
• Helicobacter pylori
• Africa/epidemiology
• Consensus
• Prevalence

• Humans
• Helicobacter pylori
• Gastroenterology
• Peptic Ulcer/diagnosis
• Peptic Ulcer/therapy
• Metabolic Diseases
• Helicobacter Infections/diagnosis
• Helicobacter Infections/therapy

• Antiinflamatorios no esteroideos
• COX-2 selective inhibitors
• Complicaciones gastrointestinales
• Gastroprotección
• Gastroprotection
• Helicobacter pylori
• Inhibidores selectivos COX-2
• Non-steroidal anti-inflammatory drugs
• Peptic ulcer disease
• Upper gastrointestinal complications
• Úlcera péptica

• Humans
• Proton Pump Inhibitors/therapeutic use
• Helicobacter Infections/complications
• Helicobacter Infections/diagnosis
• Helicobacter Infections/drug therapy
• Peptic Ulcer/complications
• Peptic Ulcer/diagnosis
• Anti-Inflammatory Agents, Non-Steroidal/adverse effects
• Endoscopy, Digestive System
• Helicobacter pylori

• Anti-inflammatory agents
• Aspirin
• Helicobacter pylori
• Peptic ulcer
• non-steroidal

• Helicobacter Infections/complications
• Helicobacter Infections/diagnosis
• Helicobacter Infections/drug therapy
• Helicobacter pylori
• Humans
• Peptic Ulcer/chemically induced
• Peptic Ulcer/drug therapy
• Peptic Ulcer Hemorrhage
• Pharmaceutical Preparations

• Anti-inflammatory agents
• Peptic ulcer
• Primary prevention
• non-steroidal

• Anticoagulants
• Antiplatelet agent
• Guideline
• Non-steroidal anti-inflammatory agents
• Peptic ulcer

• Adult
• Anti-Inflammatory Agents, Non-Steroidal/therapeutic use
• Helicobacter Infections/drug therapy
• Helicobacter pylori
• Humans
• Peptic Ulcer/chemically induced
• Peptic Ulcer/drug therapy
• Pharmaceutical Preparations
• Practice Guidelines as Topic
• Proton Pump Inhibitors/therapeutic use

• Anti-inflammatory agents
• Anticoagulants
• Antiplatelet agent
• Guideline
• Peptic ulcer
• non-steroidal

• Anti-Inflammatory Agents/adverse effects
• Anti-Inflammatory Agents/therapeutic use
• Anticoagulants/adverse effects
• Anticoagulants/therapeutic use
• Cyclooxygenase 2 Inhibitors/therapeutic use
• Endoscopy, Gastrointestinal
• Helicobacter Infections/diagnosis
• Helicobacter Infections/drug therapy
• Hemorrhage/complications
• Hemorrhage/therapy
• Humans
• Peptic Ulcer/diagnosis
• Peptic Ulcer/etiology
• Peptic Ulcer/prevention & control
• Platelet Aggregation Inhibitors/adverse effects
• Platelet Aggregation Inhibitors/therapeutic use
• Proton Pump Inhibitors/therapeutic use

• Helicobacter pylori
• consensus
• endoscopy
• eradication
• gastric cancer
• gastric precancerous lesion
• level of evidence
• peptic ulcer
• proton-pump inhibitor

• Disease Management
• Epidemiological Monitoring
• Helicobacter Infections/complications
• Helicobacter Infections/diagnosis
• Helicobacter Infections/drug therapy
• Humans
• Mass Screening/methods
• Stomach Neoplasms/prevention & control
• Taiwan

Current knowledge about clinical and genetic risk factors for aspirin-induced gastric mucosal injury is not sufficient to prevent these gastric mucosal lesions.

We recruited aspirin takers as the exposed group and healthy volunteers as the control group. The exposed group was categorized into two subgroups such as subgroup A as gastric mucosal injury diagnosed by gastroscopy, including erosion, ulcer or bleeding of the esophagus, stomach, or duodenum; subgroup B as no injury of the gastric mucosa was detected by gastroscopy. Clinical information was collected, and 53 single nucleotide polymorphisms were evaluated.

Among 385 participants, 234 were in the aspirin-exposed group. According to gastroscopy, 82 belonged to subgroup A, 91 belonged to subgroup B, and gastroscopic results of 61 participants were not available. Using the Chi-square test and logistic regression, we found that peptic ulcer history (odds ratio [OR] = 5.924, 95% confidence intervals [CI]: 2.115–16.592), dual anti-platelet medication (OR = 3.443, 95% CI: 1.154–10.271), current Helicobacter pylori infection (OR = 2.242, 95% CI: 1.032–4.870), male gender (OR = 2.211, 95% CI: 1.027–4.760), GG genotype of rs2243086 (OR = 4.516, 95% CI: 1.180–17.278), and AA genotype of rs1330344 (OR = 2.178, 95% CI: 1.016–4.669) were more frequent in subgroup A than subgroup B. In aspirin users who suffered from upper gastrointestinal bleeding, the frequency of the TT genotype of rs2238631 and TT genotype of rs2243100 was higher than in those without upper gastrointestinal bleeding.

Peptic ulcer history, dual anti-platelet medication, H. pylori current infection, and male gender were possible clinical risk factors for aspirin-induced gastric mucosal injury. GG genotype of rs2243086 and AA genotype of rs1330344 were possible genetic risk factors. TT genotype of rs2238631 and TT genotype of rs2243100 may be risk factors for upper gastrointestinal bleeding in aspirin users.

• Helicobacter pylori
• gastric cancer
• non-steroidal anti-inflammatory drugs
• peptic ulcer disease
• prevention
• screening
• vaccine

The interaction between nonsteroidal anti-inflammatory drugs (NSAIDs) and Helicobacter pylori remains controversial. We retrospectively investigated whether H. pylori infection exacerbates severe gastric mucosal injury among chronic NSAID users.

From January 2010 to December 2013, a total of 245 long-term NSAID (including low-dose aspirin) users who had undergone an esophagogastroduodenoscopy and had been evaluated for H. pylori infection were enrolled at Okayama University Hospital and Tsuyama Chuo Hospital. The degree of gastric mucosal injury was assessed according to the modified Lanza score (MLS). Severe gastric mucosal injury was defined as an MLS ≥4. Univariate and multivariate logistic regression analyses were performed.

In the univariate analysis, age ≥75 years (odds ratio [OR], 2.4; 95% confidence interval [CI], 1.3 to 4.2), H. pylori-positivity (OR, 2.0; 95% CI, 1.2 to 3.5), and the concomitant use of proton pump inhibitors (PPIs) (OR, 0.48; 95% CI, 0.26 to 0.86) were significantly associated with severe gastric mucosal injury. The multivariate analysis was adjusted by age and sex and demonstrated that H. pylori-positivity (OR, 1.8; 95% CI, 1.0 to 3.3) and the concomitant use of PPIs (OR, 0.53; 95% CI, 0.28 to 0.99) significantly contributed to severe gastric mucosal injury.

H. pylori infection exacerbates severe gastric mucosal injury among chronic NSAID users.

• Anti-inflammatory agents, non-steroidal
• Gastric mucosal injury
• Helicobacter pylori
• Proton pump inhibitors

• Ghana
• Helicobacter
• NSAIDs
• Peptic ulcer
• endoscopy

• Adult
• Aged
• Anti-Inflammatory Agents, Non-Steroidal/administration & dosage
• Anti-Inflammatory Agents, Non-Steroidal/adverse effects
• Aspirin/administration & dosage
• Aspirin/adverse effects
• Case-Control Studies
• Female
• Helicobacter Infections/complications
• Helicobacter pylori
• Humans
• Male
• Middle Aged
• Peptic Ulcer Hemorrhage/chemically induced
• Peptic Ulcer Hemorrhage/microbiology
• Prospective Studies
• Surveys and Questionnaires

• Adult
• Anti-Inflammatory Agents, Non-Steroidal/administration & dosage
• Anti-Inflammatory Agents, Non-Steroidal/adverse effects
• Aspirin/administration & dosage
• Aspirin/adverse effects
• Female
• Gastrointestinal Diseases/chemically induced
• Gastrointestinal Diseases/prevention & control
• Gastrointestinal Hemorrhage/chemically induced
• Gastrointestinal Hemorrhage/epidemiology
• Humans
• Male
• Middle Aged
• Preventive Health Services

• 16891 Cancer Research UK
• British Heart Foundation

Previous reports clearly demonstrated that Helicobacter pylori (H. pylori) infection, nonsteroidal anti-inflammatory drugs (NSAID) or low dose aspirin (ASA) use significantly and independently increased the risk for the development of peptic ulcer disease. Today, the presence of H. pylori infection associated with low dose ASA and/or NSAID use in the same patient is becoming more frequent and therefore the potential interaction between these factors and the consequences of it has important implications. Whether NSAID intake in the presence of H. pylori infection may further increase the risk of peptic ulcer carried by the presence of only one risk factor is still a matter of debate. Studies on the interaction between the two risk factors yielded conflicting data and no consensus has been reached in the last years. In addition, the interaction between H. pylori infection and low-dose ASA remains even more controversial. In real clinical practice, we can find different clinical scenarios involving these three factors associated with the presence of different gastrointestinal and cardiovascular risk factors. These huge variety of possible combinations greatly hinder the decision making process of physicians.

• Nonsteroidal anti-inflammatory drugs
• Low dose aspirin
• Helicobacter pylori infection
• Helicobacter pylori eradication
• Peptic ulcer disease

• Animals
• Anti-Inflammatory Agents, Non-Steroidal/adverse effects
• Aspirin/adverse effects
• Cardiovascular Diseases/chemically induced
• Cardiovascular Diseases/microbiology
• Cardiovascular Diseases/mortality
• Helicobacter Infections/complications
• Helicobacter Infections/microbiology
• Helicobacter Infections/mortality
• Helicobacter pylori/pathogenicity
• Humans
• Peptic Ulcer/chemically induced
• Peptic Ulcer/microbiology
• Peptic Ulcer/mortality
• Prognosis
• Risk Assessment
• Risk Factors

• Helicobacter pylori
• adaptation
• diagnosis
• guideline
• treatment

In this post-hoc analysis of a randomized, double blind, placebo controlled trial, we measured the sensitivity and specificity of Helicobacter pylori IgG-antibody titer changes, hematoxylin and eosin (H&E) stains, immunohistochemical (IHC) stains and culture results in NSAID using patients, following H. pylori eradication therapy or placebo.

347 NSAID using patients who were H. pylori positive on serological testing for H. pylori IgG-antibodies were randomized for H. pylori eradication therapy or placebo. Three months after randomization, gastric mucosal biopsies were taken for H. pylori culture and histological examination. At 3 and 12 months, blood samples were taken for repeated serological testing. The gold standard for H. pylori infection was based on a positive culture or both a positive histological examination and a positive serological test. Sensitivity, specificity and receiver operating curves (ROC) were calculated.

H. pylori eradication therapy was successful in 91% of patients. Culture provided an overall sensitivity of 82%, and 73% after eradication, with a specificity of 100%. Histological examination with either H&E or IHC stains provided sensitivities and specificities between 93% and 100%. Adding IHC to H&E stains did not improve these results. The ROC curve for percent change in H. pylori IgG-antibody titers had good diagnostic power in identifying H. pylori negative patients, with an area under the ROC curve of 0.70 (95 % CI 0.59 to 0.79, P = 0.085) at 3 months and 0.83 (95% CI 0.76 to 0.89, P < 0.0001) at 12 months. A cut-off point of at least 21% decrease in H. pylori IgG-antibody titers at 3 months and 58% at 12 months provided a sensitivity of 64% and 87% and a specificity of 81% and 74% respectively, for successful eradication of H. pylori.

In NSAID using patients, following H. pylori eradication therapy or placebo, histological examination of gastric mucosal tissue biopsies provided good sensitivity and specificity ratios for evaluating success of H. pylori eradication therapy. A percentual H. pylori IgG-antibody titer change has better sensitivity and specificity than an absolute titer change or a predefined H. pylori IgG-antibody titer cut-off point for evaluating success of H. pylori eradication therapy.

Background. Two major causes of gastric ulcers are Helicobacter pylori (H. pylori) infection and nonsteroidal anti-inflammatory drug (NSAID) use. Aims. This study aimed to determine if there were different expressions of matrix metalloproteinases (MMPs) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) between H. pylori-infected and NSAID-related ulcers. Methods. The 126 gastric ulcer patients (H. pylori infected n = 46; NSAID related n = 30; combined with two factors n = 50) provided ulcer and nonulcer tissues for assessment of MMP-3, -7, and -9 and TIMP-1 expression by immunohistochemical staining. Results. Gastric ulcer tissues had significantly higher MMP-3, -7, and -9 and TIMP-1 expressions than nonulcer tissues (P < 0.05). H. pylori-infected gastric ulcers had even higher MMP-7, MMP-9, and TIMP-1 expressions in epithelial cells than NSAID-related gastric ulcers (P < 0.05). In patients with the two combined factors, gastric ulcers expressed similar proportions of antral ulcers and MMP-7 and MMP-9 intensities to NSAID-related gastric ulcers, but lower MMP-9 and TIMP-1 than H. pylori-infected gastric ulcers (P < 0.05). Conclusions. H. pylori-infected gastric ulcers express higher MMP-7, MMP-9, and TIMP-1 than NSAID-related ulcers. In patients with the two combined factors, ulcer location and MMP-7 and MMP-9 intensities are similar to NSAID use.

• Aged
• Anti-Inflammatory Agents, Non-Steroidal/adverse effects
• Biopsy
• Duodenal Ulcer/epidemiology
• Duodenal Ulcer/microbiology
• Duodenal Ulcer/pathology
• Endoscopy, Gastrointestinal
• Female
• Follow-Up Studies
• Gastric Mucosa/drug effects
• Gastric Mucosa/pathology
• Gastritis/epidemiology
• Gastritis/microbiology
• Gastritis/pathology
• Helicobacter Infections/epidemiology
• Helicobacter Infections/pathology
• Helicobacter pylori
• Humans
• Male
• Middle Aged
• Registries
• Rheumatic Diseases/drug therapy
• Rheumatic Diseases/epidemiology
• Risk Factors
• Time Factors

Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most widely prescribed medications in the World. A frequent complication of NSAID use is gastroduodenal bleeding. Risk factors for gastroduodenal bleeding while on NSAID therapy are age, prior peptic ulcer and co-medication with anti-platelet agents, anticoagulants, glucocorticosteroids and selective serotonin-reuptake inhibitors (SSRI). Prevention strategies for at-risk patients include the use of the lowest effective dose of NSAIDs, co-therapy with proton-pump inhibitors and/or the use of a COX-2 selective agent. Treatment of Helicobacter pylori infection is beneficial for primary prophylaxis of NSAID-induced gastroduodenal bleeding in NSAID-naive patients. For patients with cardiovascular risk factors requiring NSAIDs, naproxen should be selected. In very high risk patients for both gastrointestinal and cardiovascular complications NSAID therapy should be avoided altogether.

• NSAIDs
• gastroduodenal bleeding
• prevention strategies
• risk factors

AIM: To investigate the effect of celecoxib, a selective COX-2 inhibitor, on Helicobacter pylori (H. pylori) colonization-related factors and its mechanism.

METHODS: After co-incubation with celecoxib, morphology of H. pylori strain 26695 was observed under a transmission electron microscope. Flagella motility was assessed by stab agar motility test. Adherence of H. pylori to AGS cells was determined by enzyme linked immunosorbent assay. Levels of mRNA expression in flagellar genes (flaA, flaB), urease genes (ureA, ureB) and adhesin genes (babA, sabA, alpA, alpB, hpaA, hopZ) were measured by real-time polymerase chain reaction.

RESULTS: Separation and non-integrity of bacterial cell wall, rarefaction and asymmetry of cytoplasm, and even lysis of H. pylori were observed in the presence of celecoxib. When H. pylori strains were incubated in the presence of celecoxib, their flagellar motility and adherence to AGS cells were inhibited. The expression of ureA, ureB, babA, sabA, alpA, alpB, hpaA, hopZ was up-regulated while the expression of flaA, flaB was down-regulated in the presence of celecoxib.

CONCLUSION: Celecoxib inhibits flagellar motility and adherence of H. pylori to AGS cells, and destructs their normal structure in vitro.

• Helicobacter pylori
• Celecoxib
• Colonization
• Ultrastructure

• Anti-Inflammatory Agents, Non-Steroidal/administration & dosage
• Anti-Inflammatory Agents, Non-Steroidal/adverse effects
• Helicobacter Infections/complications
• Helicobacter Infections/therapy
• Helicobacter pylori
• Humans
• Peptic Ulcer/etiology
• Peptic Ulcer/prevention & control
• Time Factors