Factor In Peptic Ulcer Research Articles

Non-Helicobacter pylori Helicobacters, a Treatable Provocateur of Parkinson’s Disease: Hypothesis, Evidence and Species Specificity

Epidemiological and eradication trial evidence indicates that Helicobacter pylori, a major causative factor in peptic ulcer and gastric cancer, is a driver of the hypokinesia of Parkinson’s disease (PD). Psychological (cognitive impairment, depression and anxiety) and gastrointestinal (peptic ulceration and constipation) PD features can precede the symptomatic onset of motor features by decades. We hypothesise that the non-H. pylori Helicobacters (NHPH), which have farm, companion and wild animals as their main hosts, can have a role in PD aetiopathogenesis. In those occupationally at risk of NHPH infection, we address whether there is increased mortality with PD, or depression or suicide. Our systematic review gave evidence that occupational exposure to animals/their products is associated with excess mortality with PD. Indeed, whilst livestock farming increased the risk, crop farming decreased it. Moreover, excess mortality from non-Hodgkin lymphoma in livestock farmers is compatible with NHPH being causal. Our scoping review showed that farmers, veterinarians and abattoir workers have an increased risk of depression and suicide; whether their depression is associated with being down the pathway to PD and/or the presence of Helicobacter infection needs investigation. Regarding Helicobacter species specificity, the link between the presence of NHPH in gastric biopsy and PD was described using a ureA polymerase chain reaction (PCR) assay, targeting the most-commonly named NHPH, H. suis. We describe its redesign and optimisation as a probe-based PCR, confirming the exclusion of H. pylori but not H. suis specificity (additionally identifying 6 species of a 22-NHPH-species panel). The exploration of the zoonotic hypothesis requires a non-invasive pan-Helicobacter PCR screen, allowing the detection and molecular grouping of Helicobacter species.

Defining core patient descriptors for perforated peptic ulcer research: international Delphi.

Perforated peptic ulcer (PPU) remains a common condition globally with significant morbidity and mortality. Previous work has demonstrated variation in reporting of patient characteristics in PPU studies, making comparison of studies and outcomes difficult. The aim of this study was to standardize the reporting of patient characteristics, by creating a core descriptor set (CDS) of important descriptors that should be consistently reported in PPU research. Candidate descriptors were identified through systematic review and stakeholder proposals. An international Delphi exercise involving three survey rounds was undertaken to obtain consensus on key patient characteristics for future research. Participants rated items on a scale of 1-9 with respect to their importance. Items meeting a predetermined threshold (rated 7-9 by over 70 per cent of stakeholders) were included in the final set and ratified at a consensus meeting. Feedback was provided between rounds to allow refinement of ratings. Some 116 clinicians were recruited from 29 countries. A total of 63 descriptors were longlisted from the literature, and 27 were proposed by stakeholders. After three survey rounds and a consensus meeting, 27 descriptors were included in the CDS. These covered demographic variables and co-morbidities, risk factors for PPU, presentation and pathway factors, need for organ support, biochemical parameters, prognostic tools, perforation details, and surgical history. This study defines the core descriptive items for PPU research, which will allow more robust synthesis of studies.

Peptic ulcer disease among dyspeptic patients at endoscopy unit, University of Gondar hospital, Northwest Ethiopia

BackgroundDyspepsia is a common complaint in upper gastrointestinal disorders. It is described as predominant epigastric pain lasting for at least one month. Globally, peptic ulcer disease occurs in 3.5–32% of patients with dyspepsia. Helicobacter pylori (H. pylori) infection and non-steroidal anti-inflammatory drugs/aspirin use are the widely known risk factors for peptic ulcer disease. There was no recent document on H. pylori infection rate among patients with peptic ulcer disease in Ethiopia. This study aimed to determine magnitude and associated factors of peptic ulcer disease among dyspeptic patients in Northwest Ethiopia.MethodsAn institutional-based cross sectional study was conducted at the University of Gondar hospital, Northwest Ethiopia. A convenience sampling method was used to recruit 218 study subjects. A pre-designed semi-structured questionnaire was used to extract clinical information. Olympus flexible fiber-optic endoscope (Olympus, GIF-E 600, Olympus Corp., Hamburg, Germany) was used to confirm the presence of peptic ulcer disease. Diagnosis of active H. pylori infection was made using the fecal H. pylori Antigen 25 T Card Test (Anamol Lab., Pvt. Ltd., Palghar, India). The Data were entered into EPI Info version 4.6.0.2, and then exported to SPSS version 20 for analysis. Explanatory variables associated with peptic ulcer disease were analyzed by applying logistic regression model. P value < 0.05 was used to declare significant association.ResultA total of 218 dyspeptic patients who underwent upper gastrointestinal endoscopic evaluations were included in the study. The mean (+ SD) age of patients was 42 ± 16.4 years. Forty nine percent (95% CI 42.4–56.2) of dyspeptic patients had active H. pylori infection. Peptic ulcer disease was diagnosed in 35% (95% CI 31.4–39.2) of patients with dyspepsia. H. pylori infection (AOR = 6.298, 95% CI 2.965–13.378, P value < 0.001) and NSAIDs/ASA use (AOR = 6.252, 95% CI 2.925–13.362, P value < 0.001) were identified as risk factors for peptic ulcer disease.ConclusionMedical treatment of peptic ulcer disease should target treatment of H. pylori infection and cautious use of non-steroidal anti-inflammatory drugs/aspirin.

Interleukin-13 level accompanying with Helicobacter pylori gastric infection in Kirkuk city Abstract

Background: Helicobacter pylori recognized as the most common cause of chronic gastritis and an important pathogenic factor in peptic ulcer, after colonization and stomach mucus layers caused increase in the levels of anti-inflammatory cytokine such as IL-13.&#x0D; The aims of this study is compare of IL-13 levels among treated patients with H. Pylori gastric infection, patients with H. Pylori gastric infection without treatment and healthy person&#x0D; Materials and Methods: The study was conducted in Kirkuk city from the September 2020 to March 2020, ELISA test used for interleukin -13 with peptic ulcer diseases (PUD).&#x0D; Results: Elevated levels of IL-13 reported in patients with acute and chronic H. pylori gastric infection compared to control group (44.74+8.18). A moderate significant in IL-13 level determined in infected patients without treatment, previously treated patients (140.12+45.36 vs 105+22.71). While, there was a high significant difference when these two groups and compared with the control group (44.74+8.18)).&#x0D; Conclusion: IL-13 levels is highest in patients with H. pylori gastric infection in compare healthy person.

Determinants of Peptic Ulcer

Globally, peptic ulcer is a disease that is very common in an adult population with 10% prevalence.Patients with H.pylori infection has 3 to 4 folds higher risk of getting peptic ulcer.Objective: To find out the determinants of Peptic ulcer among the patients visiting Services HospitalLahore Methods: A Cross sectional study was carried out. Patients were selected through nonprobabilityconvenient sampling technique from Services Hospital, Lahore. Patients were assessedthrough pre-tested questionnaire. SPSS version 21.0 was used for analysis of data. The study wascarried out at Medical departments of Services Hospitals, Lahore during Dec-2017 to March-2018Results: The prevalence of peptic ulcer was higher in males i.e. 68%. 41% patients were 36-45 years ofage, 63% patients were from urban areas, 40% of patients were overweight, 32% patients weresecondary educated and 75% patients were having no knowledge about peptic ulcer. There wassignificant association of gender with consumption of fried food items and smoking Conclusions:Study concluded that, male gender, low educational status, work pressure, smoking, addiction of painkillers and intake of fried food items were the risk factors of peptic ulcer.

Peptic ulcer disease: a critical analysis of the current state of the problem

History of study of peptic ulcer, evolution of ideas about its etiology and pathogenesis are set out in this review. The precedingtheories of the formation of peptic ulcer and the current provisions explaining the development of this disease are described. Special attention is paid to the role of the bacterium Helicobacter pylori put forwardin the occurrence of peptic ulcer and the formation of its recurrence; the microbiological and genetic features of helicobacteria are described in detail, giving them unique pathogenic properties. The genetic, immune, psychogenic mechanisms of the pathogenesis of peptic ulcer are described, the significance of oxidative stress and local factors in the formation of the ulcerative defect of the mucous membrane is revealed. A thorough critical analysis of some of the provisions of the dominant theory of ulcerogenesisis carried out. The inconsistency of helicobacteria, which are considered the main etiological factor of peptic ulcer, to the requirements of the Koch Triad, is emphasized: this pathogen does not always provoke the development of erosive-ulcerative mucosal lesions and is frequently not detected in many patients with peptic ulcer. Own data illustrating the dysbiotic nature of the violation of the microbial landscape of the stomach, and not the prevalence of helicobacteria in patients with peptic ulcer, are presented. Clinical features of peptic ulcer disease are properly described. Statements of the Maastricht consensus are strongly criticized for contradicting the basic principles of evidence-based medicine and not allowing the use of clinical thinking, analysis and synthesis of evidence. There is a doubt about the feasibility of the eradication of helicobacteria using the systemic broad-spectrum antibiotics. The rationale for further comprehensive study of peptic ulcer and the development of new, more effective therapeutic agents is put forward.

INFILTRATIVE LUNG TUBERCULOSIS, PEPTIC ULCER DISEASE AND HIV INFECTION (COMORBIDITY AND MULTIMORBIDITY OF DISEASES)

Aim - to explore the features of comorbidity and multimorbidity of infiltrative pulmonary tuberculosis (IPT), peptic ulcer (PU), HIV infection in modern conditions. Materials and methods. The study involved 392 patients with IPT aged 20-44 years, HIV-positive with CD4 200500/pl, suffering from uncomplicated ulcer. Results. Peptic ulcer disease was diagnosed in 20.5% of patients with IPT and 19.5% patients with HIV infection in stage C2 and IPT, complaining of dyspepsia. The multimorbid combination of IPT, HIV infection and PU is characterized by: oligosymptomatic onset of tuberculosis; the clinical picture shows the dominance of asthenic syndrome, manifestations of gastric and intestinal dyspepsia, weight loss (2-4 times more frequently than in patients without HIV infection), less prominent destructive process in the lung tissue (2 times less than in patients without HIV infection). H.pylori is the aetiological factor of PU in 62.5% of patients with IPT and 58.7% patients with HIV infection in stage C2 and IPT. The combination of H.pylori-negative PU and IPT has significantly more unfavorable prognosis compared to comorbidity of H.pylori-positive peptic ulcer and IPT. Conclusion. Diagnosis of PU, HIV infection and H.pylori-status allows defining multiple categories of comorbidity (patients with IPT and dyspeptic syndrome, patients with IPT and H.pylori-associated peptic ulcer, patients with IPT and H.pylori-negative ulcer) and multimorbidity (HIV-infected patients with IPT and H.pylori-associated ulcer, HIV-infected patients with IPT and H.pylori-negative ulcer).

Effect of diet combined with exercise therapy on life quality of and nursing satisfac-tion of peptic ulcer patients

Objective To investigate the application effect of diet combined with exercise therapy in the nursing of peptic ulcer pa -tients.Methods A total of 100 cases of peptic ulcer patients treated in our hospital from 2011 October to 2012 April were randomly divided into the observation group and the control group .Two groups were given the same treatment , the control group was given routine health edu-cation, the observation group was given diet and exercise therapy based on the control group , short-term and long-term curative effects were compared between two groups.Results Health knowledge rate in the observation group was significantly higher than that in the control group with statistical significance （ P〈0.05 ） .The total effective rate in observation group was 94%and 92% in the control group had no statistical significance （ P〉0.05 ） .Life quality in social functioning , general health , mental health in the observation group was significant-ly higher than that in the control group with statistical significance （ P〈0.05 ） .Nursing satisfaction in the observation group was significant-ly higher than that in the control group , the recurrence rate was significantly lower than that in the control group with statistical significance （ P〈0.05 ） .Conclusions Diet combined with exercise therapy is beneficial to reduce the risk of recurrence of peptic ulcer factors , im-prove the life quality of patients , and reduce the recurrence rate. Key words: Diet; Exercise; Peptic ulcer; Life quality; Recurrence

Investigation and analysis of pathogenic factors of peptic ulcer in internal medicine patients

目的 了解内科患者溃疡病发病因素,以探究相应的护理对策,为临床治疗、健康教育和临床护理提供相应的依据.方法 选取2008年1月至2010年1月在本院就诊的98例消化性溃疡患者为研究对象,分析患者溃疡病的发病因素.结果 通过分析患者各方面的特征发现,患者的溃疡病发病因素中情志因素所占比例为14.3%,饮食起居习惯所占比例为59.2%,环境因素所占比例为11.2%,社会心理因素所占比例为6.1%,体质因素所占比例为9.2%.结论 控制消化性溃疡患者的发病因素,积极采取有效的预防护理措施,能有效改善患者的生活质量。

Long Type dupA but Not Short Type dupA Associated With Peptic Ulcer Disease in Japan

Background and aims:Helicobacter pylori dupA (duodenal ulcer promoting) gene was reported as a virulence factor that induced duodenal ulcer and had a suppressive action on gastric cancer. However, the association of the dupA gene on clinical outcomes is different in different populations. Full-sequenced data of H. pylori showed that the length of the dupA gene is depends on the strain; Shi470 and G27 have approximately 600bp longer than that of other strains (e.g., strain J99) in the C-terminal region of the dupA gene. This suggests that the dupA gene has two genotypes: long and short type. In addition, previous studies indicated that some strains have a presence of the mutation (insertion or mutation) in the dupA gene, which created a premature stop codon . In this study, we aimed to examine the dupA genotypes (long type or short type), presence of the mutation, and examined the association with clinical outcomes in Japanese population. Methods: A total of 388 patients (97 with gastritis, 137 with duodenal ulcer [DU], 121 with gastric ulcer [GU], and 24 with gastric cancer [GC]) were included in this study. The status of the dupA genes was examined by polymerase chain reaction. The oligonucleotide primers for the dupA typing were designed according to the dupA gene sequence deposited in Genbank. First primers were designed to include the additional region of C-terminal of the dupA gene (long type dupA). Second primers were designed to include the conventional dupA gene (short type dupA). We also sequenced full-length dupA gene and evaluated the presence of mutation. Results: The prevalence of short type dupA gene alone was not significantly different among four groups (gastritis 14.4%, DU 8.0%, GU 6.5%, and GC 4.2%, respectively). Interestingly, the prevalence of the long type dupA gene in strains from DU was significantly higher than that from gastritis (19.7 v.s. 9.3%, p = 0.02). Those of GU, GC were also significantly higher than that of gastritis (25.8, 25.0 and 9.3%, p = 0.0001, p = 0.03, respectively). Full-length sequence of the dupA gene was completed in 33 strains. Among them, point mutation lead to stop codon was found in only one strain. Conclusions: The long type but not the short type dupA gene can be used as discriminating factor of peptic ulcer and gastric cancer from gastritis in Japan. These observations suggest that only strains that are intact dupA-positive might be involved in gastroduodenal diseases.

Higher Frequency of CagA EPIYA-C Phosphorylation Sites in H. pylori Strains From Relatives of Gastric Cancer Patients

Background and aims:Helicobacter pylori dupA (duodenal ulcer promoting) gene was reported as a virulence factor that induced duodenal ulcer and had a suppressive action on gastric cancer. However, the association of the dupA gene on clinical outcomes is different in different populations. Full-sequenced data of H. pylori showed that the length of the dupA gene is depends on the strain; Shi470 and G27 have approximately 600bp longer than that of other strains (e.g., strain J99) in the C-terminal region of the dupA gene. This suggests that the dupA gene has two genotypes: long and short type. In addition, previous studies indicated that some strains have a presence of the mutation (insertion or mutation) in the dupA gene, which created a premature stop codon . In this study, we aimed to examine the dupA genotypes (long type or short type), presence of the mutation, and examined the association with clinical outcomes in Japanese population. Methods: A total of 388 patients (97 with gastritis, 137 with duodenal ulcer [DU], 121 with gastric ulcer [GU], and 24 with gastric cancer [GC]) were included in this study. The status of the dupA genes was examined by polymerase chain reaction. The oligonucleotide primers for the dupA typing were designed according to the dupA gene sequence deposited in Genbank. First primers were designed to include the additional region of C-terminal of the dupA gene (long type dupA). Second primers were designed to include the conventional dupA gene (short type dupA). We also sequenced full-length dupA gene and evaluated the presence of mutation. Results: The prevalence of short type dupA gene alone was not significantly different among four groups (gastritis 14.4%, DU 8.0%, GU 6.5%, and GC 4.2%, respectively). Interestingly, the prevalence of the long type dupA gene in strains from DU was significantly higher than that from gastritis (19.7 v.s. 9.3%, p = 0.02). Those of GU, GC were also significantly higher than that of gastritis (25.8, 25.0 and 9.3%, p = 0.0001, p = 0.03, respectively). Full-length sequence of the dupA gene was completed in 33 strains. Among them, point mutation lead to stop codon was found in only one strain. Conclusions: The long type but not the short type dupA gene can be used as discriminating factor of peptic ulcer and gastric cancer from gastritis in Japan. These observations suggest that only strains that are intact dupA-positive might be involved in gastroduodenal diseases.

Helicobacter pylori and NSAID-induced gastric ulcer in a Japanese population

A recent meta-analysis by Huang et al. clarified that Helicobacter pylori infection and nonsteroidal antiinflammatory drugs (NSAIDs) are important factors for peptic ulcer. The results showed that the risk for ulcer in NSAID(+)/H. pylori(+) patients was 61.1 fold higher when compared with NSAID(-)/H. pylori(-) patients. Some gastric ulcers detected in patients on NSAID therapy may actually be caused by H. pylori, but it is difficult to differentiate NSAID-induced gastric ulcer from H. pylori-induced gastric ulcer. Several studies have investigated the effects of H. pylori eradication on ulcer healing. One study reported that H. pylori eradication actually lowered the healing rate of gastric ulcers. Because there have been no studies finding that H. pylori eradication facilitates healing, H. pylori eradication is not recommended for NSAID users. Concerning the efficacy of H. pylori eradication in the prevention of NSAID-induced gastric ulcer, a meta-analysis concluded that among all patients on NSAID therapy, H. pylori eradication lowered the prevalence of ulcer, which was particularly marked in NSAID-naïve patients. When compared with those of proton pump inhibitors (PPIs), the preventative effects of H. pylori eradication were inferior. In Japan, national health insurance does not cover procedures that prevent or lower the risk for NSAID-induced ulcer. When administering NSAID to patients with risk factors, it is desirable to administer antiulcer agents.

Bisphosphonate Increases Risk of Peptic Ulcer in Rheumatoid Arthritis Patients On Long-Term Non-Steroidal Anti-Inflammatory Drug Therapy

Objective: Rheumatoid arthritis (RA) patients are at increased risk of developing peptic ulcer induced by non-steroidal anti-inflammatory drugs (NSAIDs). However, despite the recent introduction of a variety of new drugs for the treatment of RA patients, the impact of potential drug interactions on the development of ulceration has yet to be determined in a daily clinical setting. The aim of the present study was to estimate the potential risks for peptic ulcer presented by co-medication in Japanese RA outpatients on long-term NSAID treatment. Methods: Our hospital-based cohort study enrolled 196 consecutive RA outpatients on NSAID medication for at least three months. The incidence of peptic ulcer was determined by esophagogastroduodenoscopy (EGD) from February 2003 to June 2006. Potential risk factors for developing peptic ulcer were evaluated by univariate and multivariate analysis. Results: Peptic ulcer was found in 43 (21.9%) out of 196 RA outpatients on long-term NSAID treatment. Peptic ulcer incidence was 31% with bisphosphonate co-therapy and 17% without co-therapy. peptic ulcer incidence was only 5% in subjects with proton pump inhibitors (PPI) or prostaglandin E1 analogs (PG) co-therapy, 14% with histamine-H2 receptor antagonists (H2RA) co-therapy, and 28% without anti-ulcer agents. In multivariate logistic regression analysis, bisphosphonate co-therapy remained a significant risk factor for peptic ulcer (OR, 2.36 versus non-users; 95% CI, 1.12-4.97; P = 0.024). Other risk factors for ulcer development were advanced age greater than 60 years and smoking (OR, 2.58; 95% CI, 1.03-6.48; P = 0.043 and OR, 2.72; 95% CI, 1.13-5.54; P = 0.026, respectively.) Factors that significantly reduced the incidence of ulceration were H2RA and PPI/PG co-therapies (OR, 0.33; 95% CI, 0.12-0.88; P = 0.027 and 0.09; 95% CI, 0.01-0.86; P = 0.037, respectively.) Conclusions: Bisphosphonate co-therapy was found to be a significant risk factor in peptic ulcer, while standard-dose H2RA as well as PPI/PG co-therapies proved effective in preventing gastroduodenal injuries in Japanese RA patients on long-term NSAID treatment.

Effects of nonsteroidal anti-inflammatory drugs on Helicobacter pylori-infected gastric mucosae of mice: apoptosis, cell proliferation, and inflammatory activity.

Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) are two well-known important causative factors of gastric damage. While H. pylori increases apoptosis and the proliferation of gastric epithelial cells and is an important factor in peptic ulcer and gastric cancer, NSAIDs induce cell apoptosis and have antineoplastic effects. We investigated the effects of NSAIDs (a nonselective cyclooxygenase [COX] inhibitor [indomethacin] and a selective COX-2 inhibitor [NS-398]) on the apoptosis and proliferation of gastric epithelial cells and gastric inflammation in H. pylori-infected mice. C57BL/6 mice were sacrificed 8 weeks after H. pylori SS1 inoculation. Indomethacin (2 mg/kg) or NS-398 (10 mg/kg) was administered subcutaneously once daily for 10 days before sacrifice. The following were assessed: gastric inflammatory activity, gastric COX protein expression by Western blotting; gastric prostaglandin E(2) levels by enzyme immunoassay, apoptosis by terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling, and cell proliferation by Ki67 immunostaining. Compared to the controls, H. pylori infection and/or NSAID treatment increased COX-1 and COX-2 protein expression. Gastric prostaglandin E(2) levels, apoptotic index, cell proliferation index, neutrophil activity, and the degree of chronic inflammation were all increased by H. pylori infection, and these effects were significantly decreased by indomethacin treatment. However, NS-398 treatment after H. pylori infection did not induce a significant reduction, although it did result in a tendency to decrease. These results show that NSAIDs can reverse the increased apoptosis and proliferation of epithelial cells and inflammatory activity in the stomachs of H. pylori-infected mice and that, like COX-2 activation, COX-1 induction contributes to the change of gastric mucosal cell turnover and inflammation induced by H. pylori infection.

Impact of Non-steroidal Anti-inflammatory Drug and Aspirin Use on the Prevalence of Dyspepsia and Uncomplicated Peptic Ulcer Disease

Background: Non-steroidal anti-inflammatory drug and aspirin (here collectively called NSAIDs) use is the second most common aetiologic factor for peptic ulcer disease and a major factor for peptic ulcer complications. The role of NSAIDs in the pathogenesis of uncomplicated peptic ulcer is less well understood and the interaction between NSAIDs and Helicobacter pylori infection on ulcer development is controversial. The aim of the present study was to examine the role of NSAIDs in the occurrence and clinical features of uncomplicated peptic ulcer disease. Methods: A total of 1091 consecutive patients referred for open-access upper gastrointestinal endoscopy by general practitioners (GPs) were enrolled. The use of NSAIDs was gathered from a structured questionnaire completed by the patients and from patient files by GPs. The exclusion criteria were previous H. pylori eradication and gastric surgery, as well as symptoms and/or signs suggestive of acute gastrointestinal bleeding. Results: Of the whole study group (n = 1091), 76 (7%) patients had a peptic ulcer. Thirty patients had an NSAID-use-associated peptic ulcer and 46 patients a non-NSAID-use peptic ulcer. Of patients with chronic gastritis (n = 599), 71% were H. pylori-positive and 108 used NSAIDs. Of those with chronic gastritis, 23 had an NSAID-use-associated peptic ulcer and 38 a non-NSAID ulcer. Of patients with normal gastric histology (n = 492), 75 patients used NSAIDs, 7 had an NSAID ulcer and 8 a non-NSAID ulcer. The only independent risk factor for peptic ulcer in patients using NSAIDs was H. pylori infection (odds ratio (OR) 3.1, 95% confidence interval (CI) 1.3-7.3), whereas dyspepsia (OR 1.0, 95% CI 0.4-2.4), male sex (OR 1.4, 95% CI 0.6-3.4), age (OR 1.0 per decade, 95% CI 0.8-1.3) and anaemia (OR 2.9, 95% CI 0.9-8.7) were not risk factors. In patients not using NSAIDs, independent risk factors for peptic ulcer were dyspepsia (OR 4.3, 95% CI 2.1-8.8), male sex (OR 2.0, 95% CI 1.1-2.8), age (OR 1.2 per decade, 95% CI 1.0-1.5), anaemia (OR 6.2, 95% CI 2.6-14.9) and H. pylori infection (OR 7.5, 95% CI 3.4-16.6). When comparing patients using NSAIDs or not, the OR of patients on NSAIDs for peptic ulcer was 2.7 (95% CI 1.5-5.0) among patients with chronic H. pylori gastritis (n = 424) and 5.3 (95% CI 1.8-15.0) among patients with normal gastric mucosa (n = 492). Conclusions: The use of NSAIDs increases the risk of peptic ulcer 3- and 5-fold in H. pylori-positive and H. pylori-negative patients, respectively. Dyspepsia is a poor predictor of peptic ulcer among patients using NSAIDs, and serologic H. pylori testing and treatment for chronic NSAID users is recommended.

Effects of Helicobacter pylori infection on Zollinger-Ellison syndrome.

Both Zollinger-Ellison syndrome (ZES) and Helicobacter pylori infection are major etiologic factors for peptic ulcer. The aim of this study was to investigate the effect of H. pylori infection on ZES with special reference to acid secretion. Sixteen patients with ZES were selected (median age, 59 years; range, 39-66 years; M/F, 9/7), and H. pylori status, ulcer location, gastric acid secretion, serum pepsinogen (PG) I and II concentrations, and PG I/II ratio were determined. The seroprevalence of H. pylori infection was 50%, whereas active H. pylori infection was seen in only 25% of the patients. Thirteen patients had duodenal ulcer (DU), 1 had gastric ulcer (GU), and 2 had both GU and DU. DU was seen in both H. pylori-positive and H. pylori-negative patients, whereas GU was found only in H. pylori-positive patients. Both basal and maximal acid outputs were significantly lower in H. pylori-positive patients than in H. pylori-negative patients (P< 0.05). Moreover, both serum PG I and the PG I/II ratio were significantly lower in H. pylori-positive patients than in H. pylori-negative patients. These results indicate that ZES is an independent risk factor for DU, but H. pylori infection may play some role in the development of GU in ZES. In patients with ZES, H. pylori infection may reduce both hypersecretion from parietal cells and PG I secretion from chief cells, and hyperacidity of the stomach in ZES may have eradicated H. pylori in some patients.

A Bismuth Salt Inhibits Herpes Simplex Virus

Bismuth has been shown not only to heal peptic ulcers but also to reduce recurrence. Helicobacter pylori (H pylori) plays an important role in the pathogenesis of peptic ulcers, and since bismuth has a bactericidal effect on this organism, the beneficial effect of bismuth on peptic ulcer disease has been attributed to the effect on H pylori . However, not all pathophysiological changes found in patients with duodenal ulcer disease can be explained by H pylori infection, and bismuth has only a weak bactericidal effect on H pylori . Infection with Herpes simplex virus (HSV) in autonomic ganglion cells has also been suggested as an etiological factor of peptic ulcer. In the present study we accordingly examined the effect of bismuth on the growth of HSV and compared it with that on H pylori . Ammonium bismuth citrate trihydrate (ABC) inhibited completely the growth of H pylori at the concentration of 32 mg/l and HSV-1 and HSV-2 at the concentrations of 2000 mg/l and 1000 mg/l, respectively. Since bismuth after oral ingestion is concentrated or even precipitated at the base of peptic ulcers, an effective concentration of bismuth with regard to HSV may also be obtained. Keywords : bismuth, duodenal ulcer disease, Herpes simplex virus, Helicobacter pylori , pathogenesis.

Nonsteroidal Anti-Inflammatory Drug-Associated Upper Gastrointestinal Lesions in Rheumatoid Arthritis Patients: Relationships to Gastric Histology, Helicobacter pylori Infection, and Other Risk Factors for Peptic Ulcer

Background: Nonsteroidal anti-inflammatory drugs (NSAIDs) are risk factors for peptic ulcer in rheumatoid arthritis (RA) patients, but the contribution of reactive gastritis, concomitant Helicobacter pylori infection, or RA activity to NSAID ulcer pathogenesis is unknown. Methods: Ninety-six RA patients taking NSAIDs and dyspeptic sex- and age-matched control patients without NSAID use or an RA diagnosis were enrolled in the study. Results: Gastric ulcer (GU) was detected in 29 (30%) RA patients and 3 control patients (P < 0.001). Sixteen RA patients and no control patient had an H. pylori-negative GU. The GUs of the RA patients were mainly located in the prepyloric region (28%) and antrum (62%). Nine of the 29 RA patients (31%) with GU had more than 1 ulcer. Erosive gastropathy was detected in 34 (71% H. pylori-negative) RA patients and in 13 (62% H. pylori-negative) control subjects (P < 0.001). Chronic gastritis was observed in 65 RA patients (48% H. pylori-negative) and in 58 control subjects (43% H. pylori-negative) (NS), whereas reactive gastritis was found in only 2 RA patients and in none of the controls. Corticosteroid use was the only independent risk factor for GU: odds ratio was 6.8 (95% confidence interval, 1.3-36.0). The prevalences of duodenal ulcer or esophagitis were not increased in RA patients. Conclusions: RA patients using NSAIDs continuously are at a greatly increased risk of developing both H. pylori-negative and -positive GUs, and corticosteroid use is an independent risk factor for ulcer development. Most RA patients have chronic gastritis, whereas reactive gastritis is rarely associated with continuous NSAID use in RA patients.

H. pylori a major aetiological factor in peptic ulcer - further confirmation

H. pylori a major aetiological factor in peptic ulcer - further confirmation

Phenylthiocarbamide taste sensitivity in chronic peptic ulcer

Ability to taste phenylthiocarbamide is genetically determined and has been investigated as a possible genetic marker for disease. This study examined phenylthiocarbamide taste sensitivity in gastric and duodenal ulcer disease. The study sample included 164 patients with gastric ulcer, 134 with duodenal ulcer, and 299 community controls. Eight concentrations of phenylthiocarbamide in distilled water were obtained by binary serial dilution. The lowest concentration distinguished by taste from distilled water defined taste threshold. Bimodality of threshold distributions distinguished nontasters from tasters. Comparisons of patients with controls gave odds ratios of nontaste in gastric ulcer and duodenal ulcer of, respectively, 0.7 (P > 0.1) and 1.3 (P > 0.3). The power of detecting at least a twofold difference between patients and controls in the odds of nontaste was 80%. Nontaste was more common in duodenal than in gastric ulcer patients (odds ratio = 2.0, P = 0.02). Taste sensitivity was unassociated with other genetic factors related to ulcer—ABO blood group, secretor status, and serum pepsinogen 1 level. The difference between gastric and duodenal ulcer patients in the ability to taste phenylthiocarbamide may be genetic; however, this study's inability, despite substantial power, to detect at least a twofold difference between patients and controls suggests that if phenylthiocarbamide taste sensitivity is a genetic factor in peptic ulcer, the relationship is weak.