Cause Of Duodenal Ulcer Research Articles

The cure rate of 10-day bismuth-containing quadruple therapy for Helicobacter pylori eradication is equivalent to 14-day: a systematic review and meta-analysis.

Helicobacter pylori (H. pylori) infection is a major cause of duodenal ulcers, gastric ulcers, and gastric cancer. However, the optimal duration for H. pylori eradication therapy remains controversial. Most studies have mainly focused on triple therapy, and there is insufficient research on bismuth-containing quadruple therapy. The aim of this study was to compare the clinical effect of the 10-day bismuth-containing quadruple treatment regimen with the 14-day regime in eradicating H. pylori. We searched PubMed, Embase, Web of Science, and the Cochrane Library for randomized controlled trials published in English until May 2022 according to the eligibility criteria. Summary risk ratios (RRs) and 95% confidence intervals (CIs) for eradication rates, adverse effects, and compliance were calculated for included studies. Four studies, involving 1173 patients, were eligible for inclusion. The eradication rate was similar in the 10-day treatment group and the 14-day treatment group in the intention-to-treat analysis (RR 0.97, 95% CI 0.93 to 1.01). Meanwhile, the incidence of adverse effects was lower in patients who received 10days of treatment than in those who received 14days of treatment and patients' compliance was almost the same between two groups. Compared to the 14-day bismuth-containing quadruple regimens, 10-day regimens had similar efficacy and lower incidence of adverse effects. Therefore, the 10-day regimen is safe and well-tolerated and should be recommended for H. pylori infection.

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2021 Ischemic Duodenal Ulceration After Thoracic Endovascular Aortic Repair (TEVAR)

INTRODUCTION: Ischemia is a rare cause of duodenal ulcers due to the redundant blood supply in the duodenum. Aortic surgery is a known, but rare, risk factor for mesenteric ischemia. Endovascular aortic repair is an increasingly common alternative to open surgery for select patients with aortic aneurysms, however post-procedural complications including endoleaks and graft migration can occur. Less commonly reported complications include bowel ischemia, with only a handful of reports detailing duodenal ulceration in the current literature. Here we present a case of ischemic duodenal ulceration following thoracic endovascular aortic repair (TEVAR). CASE DESCRIPTION/METHODS: An 82-year-old male on dual-antiplatelet therapy presented with complaints of lightheadedness, dyspnea, and melena. He had been discharged to skilled nursing three days earlier following thoracic endovascular aortic repair (TEVAR) for DeBakey type III aortic dissection distal to the left subclavian artery. His recovery was complicated by endovascular leak at the left subclavian artery, left renal artery dissection, and thrombosis of the superior mesenteric artery (SMA), which were treated with coiling and stenting of the left renal artery and SMA. Hemoglobin upon hospital return was 6.7 g/dL compared to 8.3 g/dL on initial discharge. Esophagogastroduodenoscopy revealed a large, near-circumferential Forrest IIc ulcer in the duodenum with concern for underlying ischemic etiology. Computed tomography angiography (CTA) of the chest and abdomen revealed a duodenal ulcer with associated mural thickening and fat stranding. CTA reconfiguration identified stenosis at the bifurcation of the common hepatic artery and stenosis of the celiac artery compared to post-TEVAR CTA images. These findings were confirmed with celiac angiography and repaired using drug coated balloon catheter percutaneous transluminal angioplasty to the common hepatic artery and balloon expandable stenting to the celiac artery. The patient’s hemoglobin stabilized post-operatively and he had complete symptom resolution. DISCUSSION: Upper intestinal ischemia is a rare but important cause of duodenal ulceration and hemorrhage following TEVAR, as demonstrated in this case. Bowel ischemia from TEVAR is more commonly seen when the distal aspect of the graft has celiac artery involvement. Early recognition of ischemic duodenal ulceration after TEVAR is of significant clinical importance, as treatment differs from other etiologies of duodenitis and early intervention lowers morbidity.

Endoscopic Characteristics Comparison of Helicobacter pylori and Orientia tsutsugamushi Infection

Background Aside from Helicobacter pylori, another cause for the development or worsening of gastrointestinal ulcers is scrub typhus, an acute febrile disease caused by Orientia tsutsugamushi. We aimed to compare the endoscopic characteristics of peptic ulcers caused by these infectious agents.Methods This retrospective case–control study involved patients who underwent upper gastrointestinal endoscopy at Chosun University Hospital in Korea.ResultsIn total, 141 patients with peptic ulcer were included in the study. Compared with patients with O. tsutsugamushi infection (n = 62; age, 63.8 ± 12.1 years; male sex, 42%), those with H. pylori infection (n = 79; age, 53.0 ± 14.8 years; male sex, 81%) were younger and more likely to be male (P < 0.001 for both). Patients with O. tsutsugamushi infection were more likely to have multiple lesions (40/62, 64.5% vs. 37/79, 46.8%; P = 0.042) and irregular-shaped lesions (27/62, 43.6% vs. 20/79, 25.3%; P = 0.031). Patients with H. pylori infection had higher incidence of hemorrhagic ulcers (26/79, 32.9% vs. 8/62, 12.9%; P = 0.007), and lesions occurred most often in the duodenum (43.0%), followed by the antrum (36.7%), body (34.2%), and angle (12.7%) of the stomach. In patients with O. tsutsugamushi infection, lesions occurred most often in the antrum (70.97%) of the stomach. In both groups, gastric ulcer lesions occurred most often in the antrum, followed by the body and angle of the stomach (36.7% vs. 70.97%, 34.2% vs. 22.6%, and 12.7% vs. 14.5% for gastric ulcers associated with H. pylori and O. tsutsugamushi infection, respectively). Patients with O. tsutsugamushiinfection had significantly higher incidence of ulcers on the antrum (70.97% vs. 36.7%, P < 0.001) and the greater curvature (45.2% vs. 24.0%, P = 0.012). Finally, 35.5% of patients with gastric ulcer caused by scrub typhus also had duodenal ulcer.Conclusion This is the first study to compare endoscopic features of peptic ulcers caused by H. pylori and O. tsutsugamushi. Peptic ulcers in patients with H. pylori infection occurred predominantly in the antrum/body/lesser curvature and presented with single, round/oval lesions, while ulcers in patients with scrub typhus occurred predominantly in the antrum/greater curvature and presented with multiple, irregular lesions. Scrub typhus should be considered as a cause of duodenal ulcer in scrub typhus-endemic areas.Disclosures All authors: No reported disclosures.

'The gut war': Functional somatic disorders in the UK during the Second World War.

Hospital admission and mortality statistics suggested that peptic ulcer reached a peak prevalence in the mid-1950s. During the Second World War, against this background of serious and common pathology, an epidemic of dyspepsia afflicted both service personnel and civilians alike. In the absence of reliable diagnostic techniques, physicians struggled to distinguish between life-threatening illness and mild, temporary disorders. This article explores the context in which non-ulcer stomach conditions flourished. At a time when fear was considered defeatist and overt psychological disorder attracted stigma, both soldiers and civilians exposed to frightening events may have unconsciously translated their distress into gastrointestinal disorders. While the nature of army food was initially identified as the cause of duodenal ulcer in servicemen, the pre-war idea that conscientious and anxious individuals were at high risk gathered support and fed into post-war beliefs that this was a stress-related illness. Diet continued to be employed as a means of management at a time when the nation was preoccupied by food because of the constraints imposed by rationing. The peptic ulcer phenomenon set much of the medical agenda for the war years and conflicted with the commonly held view that the British people had never been healthier.

Review article: Helicobacter pylori‐negative duodenal ulcer disease

Helicobacter pylori infection rates in duodenal ulcer (DU) patients may be lower than previously estimated. To review the real prevalence of H. pylori-negative DUs and its possible causes. Bibliographical searches in MEDLINE looking for the terms 'H. pylori' and 'duodenal ulcer'. Mean prevalence of H. pylori infection in DU disease, calculated from studies published during the last 10 years including a total of 16 080 patients, was 81%, and this figure was lower (77%) when only the last 5 years were considered. Associations with H. pylori-negative DU were: (1) False negative results of diagnostic methods, (2) NSAID use (21% in studies with <90% infection rate), (3) Complicated DU (bleeding, obstruction, perforation), (4) Smoking, (5) Isolated H. pylori duodenal colonization, (6) Older age, (7) Gastric hypersecretion, (8) Diseases of the duodenal mucosa, (9) Helicobacter'heilmanii' infection and (10) Concomitant diseases. In patients with H. pylori-negative DU disease, one should carefully confirm that the assessment of H. pylori status is reliable. In truly H. pylori-negative patients, the most common single cause of DU is, by far, the use of NSAIDs. Ulcers not associated with H. pylori, NSAIDs or other obvious causes should, for the present, be viewed as 'idiopathic'. True idiopathic DU disease only exceptionally exists.

Testing the substrate flexibility of Helicobacter pylori's pseudaminic acid biosynthetic pathway

Helicobacter pylori infection is the leading cause of duodenal ulcers and gastric cancer worldwide. We are developing an antibiotic strategy based on the presence of the unique sugar pseudaminic acid (PseNAc) on H. pylori but not on human cells. PseNAc is essential for formation of functional flagella on H. pylori, and H. pylori that lack the ability to make PseNAc are avirulent. In our two‐step strategy, we will (1) hijack H. pylori's PseNAc biosynthetic pathway with azidosugars, then (2) covalently deliver therapeutic compounds to azide‐covered H. pylori via Staudinger ligation to perturb the pathogens. For this strategy to be viable, H. pylori's PseNAc biosynthetic pathway must be permissive of azide‐containing substrates. Here we set out to examine the substrate flexibility of PseNAc biosynthetic enzymes by comparing in vitro kinetic data of natural versus azide‐containing substrates. We present our initial data expressing PseNAc biosynthetic enzymes, preparing azide‐containing substrates, and testing the substrate flexibility of the PseNAc biosynthetic pathway in vitro. Support was provided by the James Stacy Coles Foundation, HHMI, and Dreyfus Foundation.

Helicobacter pylorivirulence factors in duodenal ulceration: A primary cause or a secondary infection causing chronicity

Reports from countries with a high prevalence of Helicobacter pylori (H pylori) infection do not show a proportionately high prevalence of duodenal ulceration, suggesting the possibility that H pylori cannot be a primary cause of duodenal ulceration. It has been mooted that this discrepancy might be explained by variations in the prevalence of virulence factors in different populations. The aim of this paper is to determine whether the published literature gives support to this possibility. The relevant literature was reviewed and analyzed separately for countries with a high and low prevalence of H pylori infection and virulence factors. Although virulent strains of H pylori were significantly more often present in patients with duodenal ulcer than without the disease in countries with a low prevalence of H pylori infection in the population, there was no difference in the prevalence of virulence factors between duodenal ulcer, non - ulcer dyspepsia or normal subjects in many countries, where the prevalence of both H pylori infection and of virulence factors was high. In these countries, the presence of virulence factors was not predictive the clinical outcome. To explain the association between virulence factors and duodenal ulcer in countries where H pylori prevalence is low, only two papers were found that give little support to the usual model proposed, namely that organisms with the virulence factors are more likely than those without them to initiate a duodenal ulcer. We offer an alternative hypothesis that suggests virulence factors are more likely to interfere with the healing of a previously produced ulcer. The presence of virulence factors only correlates with the prevalence of duodenal ulcer in countries where the prevalence of H pylori is low. There is very little evidence that virulence factors initiate duodenal ulceration, but they may be related to failure of the ulcer to heal.

IDENTIFICATION OF HELICOBACTER PYLORI INFECTION IN ‎PATIENTS WITH UPPER GASTROINTESTINAL DISEASES, ‎AND ITS ANTIMICROBIAL SENSITIVITY

H.pylori is the cause of duodenal ulcer, and a lot of other gastrointestinal diseases, the aim of this study ‎was to see the extent of this microorganism in our patients and to study its antimicrobial sensitivity. The ‎study included 283 patients(148 males and 135 females) with upper gastrointestinal complaints including ‎dyspepsia, heartburn, bleeding, and malabsorption to evaluate the presence of Helicobacter pylori ‎‎(H.pylori) infection using rapid urease test (RUT) and culture to see there sensitivity to different ‎antibiotics.‎ ‎ The study revealed that 199 patients (70.3%) have positive RUT compared to 218 patients (77.0%) ‎showed positive culture results. The positive culture results were confirmed by positive results of ‎biochemical tests (oxidase, catalase and urease).‎ ‎ Antibiotic sensitivity testing was performed in 28 cultures of H. pylori, and the results showed that 26 ‎cultures ( 92.9%) were sensitive to amoxycillin, followed by clarithromycin, rifampicin and cephalexin with ‎figures of 23 (82.1%), 22 (78.6%) and 21 (75.0%) respectively. Whereas, 16 cultures (57.1%) were ‎resistant to metronidazole, 15 (53.4%) to erythromycin and 9 (32.1%) to both cephalothin and ‎tetracycline.‎ ‎ It is concluded that, H.pylori infection is a predominant etiological factor of upper gastrointestinal ‎diseases, Also, RUT represent simple, convenient and reliable mean for the rapid diagnosis of H.Pylori ‎infection. Antibiotic sensitivity was the highest with amoxycillin and clarithromycin while the most ‎resistant antibiotic strains were encountered with metronidazole

Gastric juice epidermal growth factor concentration and Helicobacter pylori in patients with duodenal ulcer.

The level of epidermal growth factor (EGF) was measured in the basal and maximally stimulated gastric juice of 20 control subjects and 20 patients each with duodenal ulcer and non-ulcer dyspepsia. Basal gastric juice was analysed for ammonia and urea concentrations, and the [ammonia]3/[urea] ratio was used to show Helicobacter pylori status, as was the [13C]urea breath test in nine controls. There was complete concordance in the nine controls between the two methods for determining H. pylori status. Twenty-five subjects were H. pylori positive (seven with duodenal ulcer, nine with non-ulcer dyspepsia, nine controls) and 35 H. pylori negative (13, 11 and 11 respectively). In H. pylori-positive subjects, the median EGF concentrations in the stimulated secretion of patients with duodenal ulcer and without (non-ulcer dyspepsia and controls combined) were 46.7 and 18.0 ng/ml (P < 0.001), and in H. pylori-negative subjects were 40.0 and 26.5 ng/ml respectively (P < 0.01). There was no difference in EGF concentration between controls and subjects with non-ulcer dyspepsia irrespective of H. pylori status. Lack of EGF is unlikely to be a cause of duodenal ulcer. The increased EGF concentration in patients with ulcer bore no relationship to the H. pylori status of the individual. If this bacterium causes duodenal ulcer, it is not via a reduction in EGF concentration.

Diagnostic tests for childhood Helicobacter pylori Infection: Invasive, Noninvasive or Both?

Diagnostic tests for childhood Helicobacter pylori Infection: Invasive, Noninvasive or Both?

Possible absence of Helicobacter pylori in the early stages of duodenal ulceration.

Helicobacter pylori is thought to be a cause of duodenal ulceration, but there is some evidence that it is found less often in early than in later disease. To assess the presence of H. pylori in patients undergoing endoscopy for dyspepsia, with respect to their duration of symptoms. Retrospective case note review. Patients were categorized as having a history greater or less than 6 months, and as H. pylori-positive or -negative, using biopsy rapid urease, culture and PCR tests. Thirty-two duodenal ulcer patients with a history >6 months were all H. pylori-positive according to the PCR test; the five with a shorter history were H. pylori-negative. No patient H. pylori-negative by PCR was positive by the other tests. H. pylori was (at least) less commonly present before 6 months. It is possible that H. pylori, although nearly always present after 6 months, is not present at the onset of the disease. Confirmation of this finding would imply that infection with the organism is not the cause of duodenal ulceration, but a factor producing recurrence and chronicity.

Is Helicobacter pylori the primary cause of duodenal ulceration?

Helicobacter pylori infection may not be the primary cause of duodenal ulceration in cases not associated with non-steroidal anti-inflammatory drugs, but may be a secondary complication. In developing countries with a uniformly high prevalence of H. pylori infection there are marked regional differences in the prevalence of duodenal ulcer (DU). In some countries, especially those with a low prevalence of H. pylori, 30-40% or more patients with DU may be H. pylori negative. The absence of H. pylori infection in early cases of DU is also reported. In DU patients with antral H. pylori infection, duodenal colonization by H. pylori may often be absent. After complete H. pylori eradication, recurrence of DU within 6 months in some reports is as high as 20%. The evidence suggests that high acidity and reduced duodenal mucosal resistance remain the primary causes of DU and that H. pylori infection, when present, results in chronicity. Reduced mucosal resistance results in duodenal gastric metaplasia which permits colonization of the duodenum with H. pylori from the antrum. Therefore, whatever causes reduced mucosal resistance may be the primary factor and evidence suggests that this cause may be diet related. This would explain the enigma of regional variations in DU prevalence unrelated to H. pylori prevalence.

Healing of duodenal ulcer after eradication of Helicobacter heilmannii

Helicobacter pylori is the main cause of duodenal ulcer, and eradication of this organism leads to ulcer healing and prevents relapse. We describe successful healing of duodenal ulcer after eradication of another Helicobacter spp, H heilmannii.

Helicobacter pylori Infection in Patients with Chronic Pancreatitis and Duodenal Ulcer

Background: The prevalence of duodenal ulcer is high in patients with chronic pancreatitis. Patients with simple duodenal ulcer without chronic pancreatitis are mostly Helicobacter pylori-infected, and the prevalence of IgG seropositivity is >95%. The prevalence of H. pylori infection in patients with chronic pancreatitis is not known. Methods: IgG antibodies against H. pylori were measured in a cross-sectional survey of consecutive patients who had their exocrine pancreas function examined with a Lundh meal test in the period 1988–95 and in a control group of patients with simple duodenal ulcer. Results: Twenty-seven per cent of the patients with chronic pancreatitis had duodenal ulcer during the observation period. The prevalence of IgG antibodies against H. pylori was 22% in patients with chronic pancreatitis without duodenal ulcer as compared with 27% with non-organic abdominal pain. The prevalence of IgG antibodies against H. pylori was 60% in patients with chronic pancreatitis complicated by duodenal ulcer as compared with 86% in controls with simple duodenal ulcer. Conclusions: H. pylori infection contributes but may not be the only cause of duodenal ulcer in patients with chronic pancreatitis.

The economics of eradicating Helicobacter pylori infection in duodenal ulcer disease.

Approximately 5 million people in the United States suffer from peptic ulcer disease, making this an important clinical problem. In addition to the huge costs associated with treatment, peptic ulcer disease also results in losses to industry as a result of loss of productivity. Infection with Helicobacter pylori is now accepted as the cause of duodenal ulcer in the majority of patients. Eradication of this infection leads to healing of the ulcer and prevents disease recurrence. A number of treatment regimens have been described for the eradication of H. pylori, but there is uncertainty regarding the optimum regimen to be used. Economic analyses allow an assessment of the probable costs associated with existing and new treatment strategies. In an era of increasing cost awareness, the results of such analyses are becoming increasingly important determinants of management strategies for the treatment of H. pylori infection.

Helicobacter pylori and Gastric Atrophy-Cancer Paradoxes

It has long been recognized that chronic gastritis is a precursor of gastric cancer only when atrophy is part of the spectrum of lesions (/). These observations are paradoxical, since atrophy is characterized by the loss of glandular epithelium, whereas cancer represents its excessive and anarchic replication. The phenomena that give rise to atrophy in the chronic gastritis complex are presently a source of considerable interest; they may help us to understand the mechanisms of carcinogenesis, especially those related to biological agents such as bacteria. Environmental factors have been implicated in gastric carcinogenesis: Populations and individuals at high risk of gastric cancer consume excessive amounts of irritants, such as NaCl, as well as inadequate amounts of fresh fruits and vegetables (2). The latter appear to play a protective role in carcinogenesis in several organ systems (3). Helicobacter pylori is the overriding cause of chronic gastritis. Infection with this bacterium is the main cause of duodenal ulcers as well as gastric ulcers. Paradoxically, the former are associated with a decreased risk of gastric cancer, while the latter increase such risk {4$). Many factors have been proposed to explain the divergent pathways of H. pylori infection, possibly involving the genetic makeup of the host, diet, and virulence factors of the bacteria (6). No carcinogens or mutagens have been identified in H. pylori, but several bacterial toxins and products are known. Some strains of bacteria induce vacuolization of epithelial cells. Strains producing the vacuolating cytotoxin, VacA, were found to be overrepresented in isolates from patients with duodenal ulcers (who are not at increased risk of gastric cancer) (7). A new paradoxical observation was made when similar excessive representation of cytotoxin-producing strains was reported for patients with gastric atrophy (which does increase gastric cancer risk) (8). A second cytotoxin-associated protein (CagA, product of the cagA gene) has been identified and linked to tissue injury (9) and to increase in gastric cancer risk {10). Recently, new genes have been identified that also may be involved in the pathogenesis of gastric injury, such as cagll or cagC (11,12). Strains expressing both VacA and CagA were shown to induce gastric pathologic abnormalities in mice similar to those observed in human infections: loss of glands, erosions, ulceration, and inflammatory infiltration. Strains not expressing vacA or cagA induced only mild inflammation (13). This background emphasizes the importance of the report by Kuipers et al. (14) in this issue of the Journal, documenting the role of cagA-positive bacteria in the development of gastric atrophy in humans. The mechanisms by which cagA-positive H. pylori strains induce both atrophy and cancer are not clear. A clue might be provided by the fact that such strains enhance the expression of several proinflammatory cytokines (interleukin la , interleukin ip, and interleukin 8) in the host (15,16). Infection with cagA-positive strains results in a more intense gastritis. Certainly, various inflammatory mediators, including reactive oxygen and nitrogen species, are mutagenic and are released in large amounts during persistent inflammation. Thus, one possibility is that the degree of inflammation determines the degree of DNA damage and point mutations. However, this does not explain why atrophy is part of the precancerous process. One explanation may be provided by new insights on how cells handle DNA damage, specifically the induction of programmed cell death, or apoptosis, in cells that are injured but do not die of necrosis. While, traditionally, apoptosis and necrosis are polarized events, it is becoming evident that, in inflammation, both may be represented in the spectrum of cell responses to the barrage of inflammatory mediators. Following DNA damage, a cell may arrest its reproductive cycle and repair the damaged DNA, or, alternatively, if the damage is more severe, the cell may undergo apoptosis and eliminate the risk of replicating mutated DNA. If the damage is too extensive, then the cell dies by necrosis mechanisms, since it loses control of membrane integrity and organelle function. This spectrum of reactions can be demonstrated in cultured epithelial cells: Nitric oxide at low doses induces apoptosis; however, at higher doses, cell death occurs via necrosis (17). In atrophic gastritis, inducible nitric oxide synthase (the isoform of the enzyme associated with inflammation) is expressed, particularly in infiltrating neutrophils and macrophages in the neck region of the gastric glands where cell replication normally takes place.

Helicobacter pylori and upper gastrointestinal disease: a survey of gastroenterologists in the United Kingdom.

The objective of this study was to conduct a survey of the opinions and practices of gastroenterologists in the United Kingdom concerning the impact of Helicobacter pylori infection on the management of upper gastrointestinal diseases. A postal questionnaire was sent to all medically qualified members of the British Society of Gastroenterology working in the UK. Replies were received from 670 of 1037 eligible BSG members (65%). Of these, 73% thought that H pylori was a cause of duodenal ulcer and 84% thought that eradication of H pylori decreased ulcer recurrence in comparison with acid suppression. While 80% used anti-H pylori therapy for a chronic relapsing duodenal ulcer, only 25% used such therapy for an ulcer at first presentation and 17% never used anti-H pylori therapy for patients with duodenal ulcer. Although 75% of respondents did not agree that H pylori was a cause of non-ulcer dyspepsia, 69% used anti-H pylori therapy to treat a patient with this condition. At the time of the survey, 69% of those who used anti-H pylori therapy adopted some variant of standard triple therapy. Only 7% routinely tested for bacterial sensitivity to antibiotics and only 22% assessed their patients for eradication after treatment. There was a lack of consensus about whether H pylori was a cause of gastric ulcer or gastric cancer with only 47% and 17% respectively believing in these associations. In conclusion, at the time of the survey, the use of anti-H pylori therapy had been accepted by a majority of specialist UK gastroenterologists in the management of upper gastrointestinal disease. There was, however, a substantial degree of uncertainty and divergence about which patients should be treated.

The somatostatin-gastrin link of Helicobacter pylori infection.

Helicobacter pylori is the new-found cause of duodenal ulcers (DU), but acid secretion remains necessary and is elevated in DU patients. My group and others have asked whether H. pylori itself alters gastric physiology. This infection has been found to decrease local expression of the inhibitory peptide somatostatin, and to increase release of the acid-stimulating hormone gastrin. H. pylori infection can alter acid secretion in both directions. Acid disappears temporarily on first infection, and may dwindle later if H. pylori causes gastric atrophy. DU patients have approximately twice the normal parietal cell mass, which increases their maximal secretory capacity, but it is not clear whether or not this is due to H. pylori. However, the infection certainly does change physiological control of acid secretion, as expected from the endocrine changes. Acid secretion is elevated during fasting, during stimulation with an acidic meal and during infusions of gastrin-releasing peptide. The balance between these opposing effects of H. pylori on acid may be crucial in determining the clinical outcome of H. pylori infection. High-acid secretion leads to DUs whilst low acid secretion is found in patients with gastric ulcers and gastric cancer. Inflammatory cytokines released in H. pylori gastritis may cause some of these changes in gastric physiology.

Helicobacter pylori and duodenal ulcer: a review

EtiologyMarch 1, 1992Helicobacter pylori and duodenal ulcer: a reviewI. David Shocket, MDI. David Shocket, MDDepartment of Veterans Affairs Medical Center Boston, Massachusetts (I.D.S.)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/ACPJC-1992-116-2-061 SectionsAboutFull Text ToolsAdd to favoritesDownload CitationsTrack Citations ShareFacebookTwitterLinkedInRedditEmail Source CitationRabeneck L, Ransohoff DF. Is Helicobacter pylori a cause of duodenal ulcer? A methodologic critique of current evidence. Am J Med. 1991 Dec;91:566-72.References1 Hill AB. The environment and disease: association or causation? Proc R Soc Med. 1965;58:295-300. Google Scholar2 Marshall BJ, Armstrong JA, McGechie DB, Glancy RJ. Attempt to fulfill Koch's postulates for pyloric Campylobacter. Med J Aust. 1985;142:436-9. Google Scholar Author, Article, and Disclosure InformationAffiliations: Department of Veterans Affairs Medical Center Boston, Massachusetts (I.D.S.) PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails March 1, 1992Volume 116, Issue 2Page: 61KeywordsAntimicrobialsBismuthClinical trialsDuodenal ulcersEtiologyGastritisGastroenterology and hepatologyHelicobacter pyloriInformation storage and retrievalLesionsPathogenesisTuberculosisUlcers ePublished: 9 March 2020 Issue Published: March 1, 1992 Copyright & PermissionsCopyright © 1992 by American College of Physicians. All Rights Reserved.Loading ...