Efficacy of ilaprazole in the treatment of duodenal ulcers:A meta-analysis

AIM: To compare the efficacy and tolerance of ilaprazole compared with other proton pump inhibitors (PPIs) in the treatment of duodenal ulcer.

Patients with Helicobacter pylori positive and negative duodenal ulcers have distinct clinical characteristics

AIM: To assess the clinical characteristics of Helicobacterpylori(H pylori) negative duodenal ulcer.METHODS: Patients with an endoscopic diagnosis of duodenal ulcer between 1996 and 2002 were included in the present study. Patients were considered to be negative for Hpylori, if both histological examination and rapid urease test of biopsy specimens were negative. A comparison was made between patients with H pyloripositive and negative duodenal ulcers.RESULTS: A total of 1 343 patients were studied. Their mean age was 54.7±0.5 years. There was a male preponderance (M:F = 2.5:1). Three hundred and ninetyeight patients (29.6%) did not have H pylori infection. The annual proportion of patients with H pylori negative duodenal ulcers increased progressively from 1996 to2002. On multivariate analysis, patients with H pylorinegative duodenal ulcer were more likely to be older, have concomitant medical problem, pre-existing malignancy, recent surgery, underlying sepsis, or taken non-steroidal anti-inflammatory drugs. In terms of clinical presentations, patients with H pylori negative duodenal ulcer were more likely to present with bleeding, multiple ulcers and larger ulcers.CONCLUSION: The proportion of patients with H pylori negative duodenal ulcers is on the rise because of a continued drop in incidence of H pylori positive duodenalulcers in recent years. Such patients have distinct clinical characteristics and it is important to ascertain the H pylori status before starting eradication therapy.

Bromophenacyl bromide,a phospholipase A_2 inhibitor attenuates chemically induced gastroduodenal ulcers in rats

AIM: To study the effect of bromophenacyl bromide (BPB), a phospholipase A2 inhibitor on gastric secretion and to protect chemically induced gastric and duodenal ulcers in rats. METHODS: Acid secretion studies were undertaken in pylorus-ligated rats with BPB treatment (0, 5, 15 and 45 mg/kg). Gastric and duodenal lesions in the rats were induced by ethanol and cysteamine respectively. The levels of gastric wall mucus, nonprotein sulfhydryls (NP- SH) and myeloperoxidase (MPO) were also measured in the glandular stomach of rats following ethanol induced gastric lesions. RESULTS: BPB produced a dose-dependent inhibition of gastric acid secretion and acidity in rats. Pretreatment with BPB significantly attenuated the formation of etha- nol induced gastric lesion. BPB also protected intestinal mucosa against cysteamine-induced duodenal ulcers. The antiulcer activity of BPB was associated with signifi- cant inhibition of ethanol-induced depletion of gastric wall mucus, NP-SH and MPO. These findings pointed towards the mediation of sulfhydryls in BPB induced gas- trointestinal cytoprotection. CONCLUSION: BPB possesses significant antiulcer and cytoprotective activity against experimentally induced gastroduodenal lesions.

Giant duodenal ulcers

Giant duodenal ulcers （GDUs） are a subset of duodenal ulcers that have historically resulted in greater morbidity than usual duodenal ulcers. Until recently, few cases had been successfully treated with medical therapy. However, the widespread use of endoscopy, the introduction of H-2 receptor blockers and proton p^Jmp inhibitors, and the improvement in surgical techniques all have revolutionized the diagnosis, treatment and outcome of this condition. Nevertheless, GDUs are still associated with high rates of morbidity, mortality and complications. Thus, surgical evaluation of a patient with a GDU should remain an integral part of patient care. These giant variants, while usually benign, can frequently harbor malignancy. A careful review of the literature highlights the important differences when comparing GDUs to classical peptic ulcers and why they must be thought of differently than their more common counterpart.

Helicobacter pylori infection alters gastric microbiota structure and biological functions in patients with gastric ulcer or duodenal ulcer

BACKGROUND Helicobacter pylori(H.pylori)infection is closely associated with gastrointestinal diseases.Our preliminary studies have indicated that H.pylori infection had a significant impact on the mucosal microbiome structure in patients with gastric ulcer(GU)or duodenal ulcer(DU).AIM To investigate the contributions of H.pylori infection and the mucosal microbiome to the pathogenesis and progression of ulcerative diseases.METHODS Patients with H.pylori infection and either GU or DU,and healthy individuals without H.pylori infection were included.Gastric or duodenal mucosal samples was obtained and subjected to metagenomic sequencing.The compositions of the microbial communities and their metabolic functions in the mucosal tissues were analyzed.RESULTS Compared with that in the healthy individuals,the gastric mucosal microbiota in the H.pylori-positive patients with GU was dominated by H.pylori,with signi-ficantly reduced biodiversity.The intergroup differential functions,which were enriched in the H.pylori-positive GU patients,were all derived from H.pylori,particularly those concerning transfer RNA queuosine-modification and the synthesis of demethylmenaquinones or menaquinones.A significant enrichment of the uibE gene was detected in the synthesis pathway.There was no significant difference in microbial diversity between the H.pylori-positive DU patients and healthy controls.CONCLUSION H.pylori infection significantly alters the gastric microbiota structure,diversity,and biological functions,which may be important contributing factors for GU.

Reduced secretion of epidermal growth factor in duodenal ulcer patients with Helicobacter pylori infection

AIM To investigate the concentration changes of epidermal growth factor (EGF) in duodenal ulcer patients with H. pylori infection.

Mediastinal emphysema in the context of perforated gastric ulcer

In the context of mediastinal emphysema/pneumomediastinum,the main aetiologies are associated with oesophageal perforation,lung pathology or post head and neck surgery related.The main way to differentiate the pathologies would be through Computed Tomographic Imaging of the Thorax and abdomen with oral and intravenous contrast in the context of triple phase imaging.The causes of pneumomediastinum should be differentiated between traumatic and non-traumatic.Oesophageal perforation(Boerhaave syndrome)is associated with Mackler’s triad in upto 50%of patients(severe retrosternal chest pain,pneumomediastinum,mediastinitis).Whereas in cases of lung pathology this can be associated with pneumothorax and pleural effusion.

Perforated gastrointestinal ulcers presenting as acute respiratory distress

BACKGROUND:Dyspnea is one of the most common complaints facing the emergency medicine physician.Some of the gastrointestinal causes of dyspnea are self-limited and not lifethreatening,yet others are,and early diagnosis and treatment are crucial.METHODS:In this article we presented one of these life-threatening conditions through a clinical description of a patient presenting with acute respiratory distress that was finally diagnosed to be the result of a perforated gastric ulcer.RESULTS:An emergent thoracotomy revealed a small ulcer with perforation in the fundus of the stomach.The patient was transferred after the operation to the intensive care unit and after a prolonged hospitalization discharged home.Biopsies taken from the ulcer showed diffuse inflammation,with no evidence of microorganisms or malignancy.CONCLUSION:Perforation of gastric and duodenal ulcers is a rare yet existing cause of dyspnea and respiratory failure and should be kept in mind by the emergency physician,especially when other more common causes are ruled out.

History of Helicobacter pylori,duodenal ulcer,gastric ulcer and gastric cancer

Helicobacter pylori (H. pylori) infection underlies gastric ulcer disease, gastric cancer and duodenal ulcer disease. The disease expression reflects the pattern and extent of gastritis/gastric atrophy (i.e., duodenal ulcer with non-atrophic and gastric ulcer and gastric cancer with atrophic gastritis). Gastric and duodenal ulcers and gastric cancer have been known for thousands of years. Ulcers are generally non-fatal and until the 20th century were difficult to diagnose. However, the presence and pattern of gastritis in past civilizations can be deduced based on the diseases present. It has been suggested that gastric ulcer and duodenal ulcer both arose or became more frequent in Europe in the 19th century. Here, we show that gastric cancer and gastric ulcer were present throughout the 17th to 19th centuries consistent with atrophic gastritis being the predominant pattern, as it proved to be when it could be examined directly in the late 19th century. The environment before the 20th century favored acquisition of H. pylori infection and atrophic gastritis (e.g., poor sanitation and standards of living, seasonal diets poor in fresh fruits and vegetables, especially in winter, vitamin deficiencies, and frequent febrile infections in childhood). The latter part of the 19th century saw improvements in standards of living, sanitation, and diets with a corresponding decrease in rate of development of atrophic gastritis allowing duodenal ulcers to become more prominent. In the early 20th century physician’s believed they could diagnose ulcers clinically and that the diagnosis required hospitalization for “surgical disease” or for “Sippy” diets. We show that while H. pylori remained common and virulent in Europe and the United States, environmental changes resulted in changes of the pattern of gastritis producing a change in the manifestations of H. pylori infections and subsequently to a rapid decline in transmission and a rapid decline in all H. pylori-related diseases.

H pylori infection and other risk factors associated with peptic ulcers in Turkish patients: A retrospective study

AIM: To identify and evaluate the relative impact of H pylori infection and other risk factors on the occurrence of gastric ulcer (GU), duodenal ulcer (DU) and gastritis in Turkish patients. METHODS: A total of 4471 patients (48.3% female) out of 4863 attended the Samatya hospital in Istanbul (June 1999 - October 2003) were included. The records of H pylori status (CLO-test), endoscopic f indings of GU, DU and gastritis, personal habits (smoking, alcohol intake) and medication [non-steroidal anti-inflammatory drugs (NSAIDs), aspirin intake] were analyzed using multi-way frequency analysis. RESULTS: We have found that GU in the presence of H pylori had significant association with aspirin (P = 0.0001), alcohol (P = 0.0090) and NSAIDs (P = 0.0372). DU on the other hand had significant association with aspirin/ smoking/NSAIDs (P = 0.0259), aspirin/alcohol (P = 0.0002) and aspirin/smoking (P = 0.0233), also in the presence of H pylori. In the absence of H pylori GU had significant association with alcohol/NSAIDs (P = 0.0431), and NSAIDs (P = 0.0436). While DU in the absence of H pylori had significant association with smoking/alcohol/ NSAIDs (P = 0.0013), aspirin/NSAIDs (P = 0.0334), aspirin/alcohol (P = 0.0360). CONCLUSION: In the presence of H pylori, aspirin, alcohol and NSAIDs intake act as an independent risk factors that had an augmenting impact on the occurrence of GU and only together on the occurrence of DU in Turkish patients.

Helicobacter pylori: the primary cause of duodenal ulceration or a secondary infection?

INTRODUCTIONIt is generally accepted that Helicobacter pylori ( H.pylori) infection has a role in duodenal ulceration .Eradicaton of H .pylori accelerates healing compared with placebo in the absence of control of gastric secretion and reduces ulcer recurrence .There is increasing evidence ,however ,that is may not be the primary cause of duodenal ulceration ,but that is may be a secondary factor in a nnmber of cases .This possibility is supported by four sets of observations : 1 Geographical distribution:

Effect of Xiaokuiling Prescription on the Expression of HSP_(72) , HSP B in Gastric Mucosa of Patients with Helicobacter Pylori associated Duodenal Ulcer

In order to investigate the mechanism of Xiaokuiling prescription (XKL) in the treatment of Helicobacter pylori (HP) associated duodenal ulcer (DU) and the pathophysiologic role of heat shock proteins (HSPs) in the healing of ulcer, the expression of HSP 72 and HSP B in gastric mucosa was detected by using SABC immunohistochemistry method and processed by micro image analysis system. The method of Western blotting was used to measure the contents of HSP 72 and HSP B in the tissue emulsion of gastric mucosa. The results were as follows: (1) HSP 72 expression of the gastric mucosa in the treated group was obviously increased as compared with that in the control group ( P <0.05); (2) HSP B expression of the gastric mucosa in the treated group was significantly decreased as compared with that in the control group ( P <0.01). It was suggested that the increased expression of HSP 72 and the elimination of HP might be related to the mechanism of action of XKL. HSPs might play an pathological and physiological role in the process of healing of gastric ulcer.

Emergency transcatheter arterial embolization for patients with acute massive duodenal ulcer hemorrhage

AIM：To evaluate the efficacy and safety of emergency transcatheter arterial embolization （ETAE） for patients with acute massive duodenal ulcer hemorrhage. METHODS：Twenty-nine consecutive patients with acute massive bleeding of duodenal ulcer were admitted to our hospital from 2006 to 2011. Superselective angiography of the celiac and gastroduodenal arteries was performed to find out the bleeding sites before ETAE, then, embolotherapy was done with gelatin sponge particles or microstrips via a 5 French angio-graphic catheter or 3 French microcatheter. After ETAE, further superior mesenteric arteriography was under-taken in case collateral circulation supplied areas of the duodenal ulcer. Technical and clinical success rates were analyzed. Changes in the mucous membrane were observed using endoscopy following ETAE. RESULTS：Angiography showed active bleeding with extravasation of contrast medium in seven cases with a 24% positive rate of celiac artery bleeding, and in 19 cases with a 65.5% rate of gastroduodenal artery bleeding. There were no angiographic signs of bleeding in three patients who underwent endoscopy prior to ETAE. Twenty-six patients achieved immediate hemostasis and technical success rate reached 90%. No hemostasis was observed in 27 patients within 30 d after ETAE and clinical success rate was 93%. Recurrent hemorrhage occurred in two patients who drank a lot of wine who were treated by a second embolotherapy in the same way. Five patients underwent transient ischem with light abdominal pain under xiphoid, spontaneous restoration without special treatment. No mucous necrosis happened to 29 cases for ischem of gastroduodenal arteries embolized. CONCLUSION：ETAE is an effective and safe measure to control acute massive bleeding of duodenal ulcer.

Omeprazole maintenance therapy prevents recurrent ulcer bleeding after surgery for duodenal ulcer

AIM： To evaluate the omeprazole maintenance therapy in patients with recurrent ulcer bleeding after surgery for duodenal ulcer. METHODS： We studied 15 consecutive patients with recurrent ulcer bleeding after surgery for duodenal ulcer. Omeprazole （20 mg/d） maintenance therapy was given after ulcer healing. In addition to clinical follow-up, ambulatory 24-h gastric pH assay was performed before and during omeprazole therapy in those patients and controls with previous duodenal ulcer surgery but no ulcer recurrence. RESULTS： All the 15 ulcers were healed after being treated with omeprazole （40 mg/d） for 2 too. Eleven patients with two （1-9） episodes of recurrent ulcer bleeding completed the follow-up （43, 12-72 too）. None of them had a bleeding episode while on omeprazole. One patient discontinued the therapy and had recurrent bleeding. The median 24-h fraction time of gastric pH 〈4 in patients was 80, 46-95%, and was reduced to 32, 13-70% by omeprazole （P= 0.002）. CONCLUSION： Long-term maintenance therapy with omeprazole （20 rag/day） is effective in preventing recurrent ulcer bleeding.

Azithromycin in a triple therapy for H.pylori eradication in active duodenal ulcer

AIM:To assess and compare the efficacy and safety of two triple regimes:A)metronidazole,amoxicillin and omeprazole, which is still widely used in Russia,and B)azithromycin, amoxicillin and omeprazole in healing active duodenal ulcer and H.pylori eradication. METHODS:100 patients with active duodenal ulcer were included in the open,multicentre,randomized study with comparative groups.Patients were randomly assigned to one of the following one-week triple regimes:A) metronidazole 500 mg bid,amoxicillin I g bid and omeprazole 20 mg bid(OAM,n=50)and B)azithromycin 1 god for the first 3 days(total dose 3 g),amoxicillin 1 g bid and omeprazole 20 mg bid(OAA,n=50).Omeprazole 20 mg od was given after the eradication course as a monotherapy for three weeks.The control endoscopy was performed 8 weeks after the entry.H.pyloriinfection was determined in the entry of the study and four weeks after the cessation of treatment by means of histology and CLO-test. RESULTS:97 patients completed the study according to the protocol(1 patient of the OAM group did not come to the control endoscopy,2 patients of the OAA group stopped the treatment because of mild allergic urticaria).Duodenal ulcers were healed in 48 patients of the OAM group(96 %, C190.5-100 %)and in 46 patients of the OAA group(92 %, CI 89.5-94.5 %)(p=ns).H.pyloHinfection was eradicated in 15 out of 50 patients with OAM(30 %,CI 17-43 %)and in 36 out of 50 patients treated with OAA(72 %;CI 59-85 %) (P<0.001)-ITT analysis.CONCLUSION: The triple therapy with omeprazole, amoxicillin and metronidazole failed to eradicate H.pylori'vc\ the majority of patients, which is an essential argument to withdraw this regimen out of the national recommendations. Macrolide with amoxicillin are preferable to achieve higher eradication rates. Azithromycin (1 g od for the first 3 days) can be considered as a successful component of the triple PPI-based regimen.

Helicobacterpylori virulence 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 Hpylori infection and virulence factors. Although virulent strains of Hpylori 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, nonulcer dyspepsia or normal subjects in many countries, where the prevalence of both Hpylori 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.

Comparison of esomeprazole enteric-coated capsules vs esomeprazole magnesium in the treatment of active duodenal ulcer: A randomized, double-blind, controlled study

AIM： To evaluate the efficacy and tolerability of two different preparations of esomeprazole in healing duodenal ulcers. METHODS： A total of 60 patients with active duodenal ulcers were enrolled and randomized to receive esomeprazole enteric-coated capsules （40 mg） or esomeprazole magnesium （40 mg）, once daily, for 4 consecutive wk, with ulcer healing being monitored by endoscopy. Safety and tolerability were also assessed. RESULTS： Fifty seven patients completed the whole trial. The ulcer healing rates at the end of wk 2 were 86.7% and 85.2% in the esomeprazole enteric-coated capsules and esomeprazole magnesium groups, respectively （P = 0.8410）, and reached 100% at the end of wk 4 in beth groups. Symptom relief at the end of wk 2 was 90.8% in the esomeprazole enteric-coated capsules group and 86.7% in the esomeprazole magnesium group （P = 0.5406）; at the end of wk 4 symptom relief was 95.2% and 93.2%, respectively （P = 0.5786）. Adverse events occurred in 16.7% of the esomeprazole entericcoated capsules group and 14.8% of the esomeprazole magnesium group （P = 1.0000）. CONCLUSION： The efficacies of esomeprazole entericcoated capsules and esomeprazole magnesium in healing duodenal ulcer lesions and relieving gastrointestinal symptoms are equivalent. The tolerability and safety of beth drugs were comparable.

Perforated duodenal ulcer presenting with massive hematochezia in a 30-month-old child

Peptic ulcer disease is uncommon in children and rarely suspected as a cause of abdominal complaints in this age group; the diagnosis is therefore made almost exclusively when complications develop. Peptic ulcer disease is usually not considered in the differential diagnosis of pediatric patients. We present the case of a 30-month-old boy with duodenal perforation due to a peptic ulcer without a known etiology. The patient was admitted through the emergency department due to severe hematochezia and ongoing anemia; he presented with neither abdominal pain nor abdominal distension. There were no medical problems, and no drugs, such as corticosteroids or nonsteroidal anti-inflammatory drugs, had been prescribed or administered recently. We tried to control the active bleeding by medical treatment including arterial embolization, but the active bleeding was not controlled. Finally, an exploratory laparotomy was performed. A discrete anterior perforation with active bleeding of the duodenal wall was found. After the operation, there were no complications and the patient recovered fully.

Precise role of H pylori in duodenal ulceration

The facts that H pylori infection is commoner in duodenal ulcer (DU) patients than in the normal population, and that eradication results in most cases being cured, have led to the belief that it causes DU. However, early cases of DU are less likely than established ones to be infected. H pylori-negative cases are usually ascribed to specific associated factors such as non-steroidal anti-inflammatory drugs (NSAIDs), Crohn’s disease, and hypergastrinaemia, but even after excluding these, several H pylori-negative cases remain and are particularly common in areas of low prevalence of H pylori infection. Moreover, this incidence of H pylori negative DU is not associated with a fall in overall DU prevalence when compared with countries with a higher H pylori prevalence. In countries with a high H pylori prevalence there are regional differences in DU prevalence, but no evidence of an overall higher prevalence of DU than in countries with a low H pylori prevalence. There is no evidence that virulence factors are predictive of clinical outcome. After healing following eradication of H pylori infection DU can still recur. Medical or surgical measures to reduce acid output can lead to long-term healing despite persistence of H pylori infection. Up to half of cases of acute DU perforation are H pylori negative. These findings lead to the conclusion that H pylori infection does not itself cause DU, but leads to resistance to healing, i.e., chronicity. This conclusion is shown not to be incompatible with the universally high prevalence of DU compared with controls.

Association of the myeloperoxidase ^(468)G→K polymorphism with gastric inflammation and duodenal ulcer risk

AIM: To elucidate the relations between the myeloperoxidase ^(-468)G→a polymorphism and the development of duodenal ulcer (DU), and to investigate the impacts of this host genetic polymorphism on the histopathological features of Helicobacter pylori (H py/ori)-related gastritis. METHODS: In a case-control study of 115 consecutive DU patients and 182 controls, the myeloperoxidase ^(-468)G→A polymorphism was genotyped. Additionally, gastric mucosal changes were examined according to the updated Sydney System. RESULTS: The two study groups differed in the distributions of myeloperoxidase genotypes (P=0.008). All six individuals carrying myeloperoxidase A/A genotypes were in the DU group. The carriage of myeloperoxidase allele A and H pylori infection were associated with an increased risk of DU with odds ratios (OR) of 2.3 and 5.8, respectively. The combined risk of the carriage of myeloperoxidase allele A and H pylori infection for DU was 8.7 (95% CI, 3.5-21.8). In the H pylori-infected individuals, allele A carriers displayed higher bacterial density scores (P=0.04) in the antrum than did non-carriers. CONCLUSION: This work verifies for the first time the association of myeloperoxidase ^(-468)G→A polymorphism with antral H pylori density and DU disease. The mechanisms underlying this genetic polymorphism in developing DU disease merit further investigations.