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.

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.

The relation between HLA-DQA1 genes and genetic susceptibility to duodenal ulcer in Wuhan Hans

AIM To study the genetic susceptibility of HLA-DQA1 alleles to duodenal ulcer in Wuhan Hans.METHODS Seventy patients with duodenalulcer and fifty healthy controls were examinedfor HLA-DQA1 genotypes.HLA-DQA1 typing wascarried out by digesting the locus specificpolymerase chain reaction amplified productswith alleles specific restriction enzymes(PCR-RFLP),i.e.,Apal Ⅰ,Bsaj Ⅰ,Hph Ⅰ,Fok Ⅰ,Mbo Ⅱ and Mnl Ⅰ.RESULTS The allele frequencies of DQA1 * 0301and DQA1 * 0102 in patients with duodenal ulcerwere significantly higher and lower respectivelythan those in healthy controls(0.40 vs 0.20,P = 0.003,mcorret = 0.024)and(0.05 vs 0.14,P = 0.012,but Pcorret】0.05),respectively.CONCLUSION DQA1 * 0301 is a susceptiblegene for duodenal ulcer in Wuhan Hans,andthere are immunogenetic differences in HLA-DQA1 locus between duodenal ulcer patients andhealthy controls.

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.

Management of duodenal ulcer bleeding resistant to endoscopy:Surgery is dead!

Acute massive duodenal bleeding is one of the most frequent complications of peptic ulcer disease.Endoscopy is the first-line method for diagnosing and treating actively bleeding peptic ulcers because its success rate is high.Of the small group of patients whose bleeding fails to respond to endoscopic therapy,increasingly the majority is referred for embolotherapy.Indeed,advances in catheter-based techniques and newer embolic agents,as well as recognition of the effectiveness of minimally invasive treatment options,have expanded the role of interventional radiology in the management of hemorrhage from peptic ulcers over the past decade.Embolization may be effective for even the most gravely ill patients for whom surgery is not a viable option,even when extravasation is not visualized by angiography.However,it seems that careful selection of the embolic agents according to the bleeding vessel may play a role in a successful outcome.The role of the surgeon in this clinical sphere is dramatically diminishing and will certainly continue to diminish in ensuing years,surgery being typically reserved for patients whose bleeding failed to respond all previous treatments.Such a setting has become extremely rare.

Mechanisms involved in Helicobacter pylori induced duodenal ulcer disease:an overview

Duodenal ulcer (DU) can be developed viaseveral different mechanisms.Hypersecretion ofgastric acid is,however,a common denominator.Amassive hypersecretion of acid can by itself evoke aDU,e.g.in the Zollinger-Ellison syndrome.Irrespective of the mechanism behind thedevelopment of a DU,powerful antisecretorytreatment will heal the ulcer and preventrecurrence.

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.

Gastroduodenal ulcer treated by pylorus and pyloric vagus-preserving gastrectomy

AIM To evaluate the curative effect of pylorus and pyloric vagus-preserving gastrectomy (PPVPG) on peptic ulcer.METHODS Treating 132 cases of GU and DU with PPVPG, and comparative studies made with 24 cases treated with Billroth Ⅰ (BⅠ) and 20 cases with Billroth Ⅱ (BⅡ); advantages and shortcomings evaluated.RESULTS Not a single death after PPVPG. No recurrence of the disorder in the subsequent follow-up for an average of 6.5 years. Curative effect (visik Ⅰ & Ⅱ) 97.7%. Acidity reduction similar to that found in BⅠ and BⅡ, but 97.7% of the BⅠ and all BⅡ cases having more than second degree intestinal fluid reflux, in contrast to 7.1% in PPVPG cases. Dumping syndrome occurred in the BⅠ and BⅡ cases, none in PPVPG cases. With regard to gastric emptying, food digestion, absorption, body weight and life quality, PPVPG proved to be superior to Billroth procedure.CONCLUSION PPVPG has the advantages of conventional Billroth gastrectomy in reducing acid, removing ulcer focus, and at the same time preserves the pylorus and pyloric vagus for maintaining the normal gastric physiological function. Dumping syndrome, intestinal fluid reflux and other complications of conventional gastrectomy may be avoided.

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:

Successful treatment of life-threatening bleeding from a duodenal posterior bulb peptic ulcer by an over-the-scope-clip

Bleeding of peptic ulcer at the posterior duodenal bulb still is a particular endoscopic challenge with increased risk of treatment failure and worse outcome.In this article,we report successful treatment of an actively bleeding peptic ulcer located at the posterior duodenal wall,using an over-the-scope-clip in the case of a 54-year-old male patient with hemorrhagic shock.Incident primary hemostasis was achieved and no adverse events occurred during a follow-up of 60 d.

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.

Perforated duodenal ulcer:An unusual manifestation of allergic eosinophilic gastroenteritis

Spontaneous perforation of a duodenal ulcer secondary to allergic eosinophilic gastroenteritis(EGE) has not been previously reported. We present such a case in a teenager who presented with peritonitis. After exploration and operative repair of his ulcer, he continued to experience intermittent abdominal pain, and further evaluation revealed eosinophilic gastroenteritis in the setting of multiple food allergies. His EGE resolved after adhering to a restrictive diet. Both duodenal ulcers and EGE are very rarely seen in pediatric patients. EGE has a variable presentation depending on the layer(s) of bowel wall affected and the segment of the gastrointestinal tract that is involved. Once diagnosed, it may respond to dietary changes in patients with recognized food allergies, or to steroids in patients in whom an underlying cause is not identified. Our case highlights the need to keep EGE in the differential diagnosis when treating pediatric patients with duodenal ulcers. The epidemiology, pathophysiology, and treatment of EGE are also discussed, along with a review of the current literature.

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.

Successful endovascular treatment of endoscopically unmanageable hemorrhage from a duodenal ulcer fed by a renal artery: A case report

A 52-year-old woman was admitted with hypovolemic shock. Emergency endoscopy revealed three hemorrhagic duodenal ulcers(all stage A1) with exposed vessels. Two ulcers were successfully treated by endoscopic clipping; however, the remaining ulcer on the posterior wall of the horizontal portion of the duodenum could not be clipped. Because her vital signs were rapidly worsening, we performed transcatheter arterial embolization(TAE) as it is less invasive than surgery. Computed tomography aortography showed that the duodenal hemorrhage was sourced from the lower branch of the right renal artery. In general, the duodenum is fed by branches from the gastroduodenal artery or superior mesenteric artery. However, this patient had three right renal arteries. The lower branch of the right renal artery at the L3 vertebral level was at the same level as the horizontal portion of the duodenum. Complete hemostasis was achieved by TAE using metallic coils and n-butyl-2-cyanoacrylate. After TAE, she recovered from the hypovolemic shock and was discharged from hospital. She has had no recurrence of the hemorrhagic duodenal ulcer for over 1 yr, and followup endoscopy showed no necrosis or stricture of the duodenum. Although she developed a small infarct of her right kidney, her renal function was satisfactory. In summary, the present case is the first reported case of hemorrhagic duodenal ulcer in which the culprit vessel was a renal artery that was successfully treated by TAE. Computed tomography aortography before TAE provides valuable information regarding the source of a duodenal hemorrhage.

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.

Life threatening bleeding from duodenal ulcer after Roux-en-Y gastric bypass: Case report and review of the literature

Acute upper gastrointestinal bleeding is a rare, but serious complication of gastric bypass surgery. The inaccessibility of the excluded stomach restrains postoperative examination and treatment of the gastric remnant and duodenum, and represents a major challenge, especially in the emergency setting. A 59-year-old patient with previous history of peptic ulcer disease had an upper gastrointestinal bleeding from a duodenal ulcer two years after having a gastric bypass procedure for morbid obesity. After negative upper endoscopy finding, he was urgently evaluated for gastrointestinal bleeding. At emergency laparotomy, the bleeding duodenal ulcer was identified by intraoperative endoscopy through gastrotomy. The patient recovered well after surgical hemostasis, excision of the duodenal ulcer and completion of the remnant gastrectomy. Every general practitioner, gastroenterologist and general surgeon should be aware of growing incidenceof bariatric operations and coherently possible complications after such procedures, which modify patient's anatomy and physiology.

Pathogenetic factors affecting gastroesophageal refluxin patients with esophagitis and concomitant duodenal ulcer:a multivariate analysis

AIM To assess the relationship between gastric acid output (GAO) and both pattern of gastroesophageal reflux (GER) and esophageal lesions, and to evaluate the role of GAO and other potential pathogenetic factors in the development of esophagitis. METHODS Gastric acid secretory testing and 24 h intraesophageal pH monitoring were performed in 31 patients with esophagitis and concomitant duodenal ulcer (E+DU) and compared with those of 72 patients with esophagitis (E) alone. RESULTS The GAO in patients with E+DU was significantly higher than in patients with E ( P <0 05). There was no significant difference between the two groups of patients as to endoscopicl findings and parameters of GER ( P >0 05). A multiple regression analysis with stepwise deletion showed that the pre sence of hiatal hernia (HH), GER in upright position and age appeared to correlate significantly with the presence of esophagitis. CONCLUSIONS No parallel relationship between GAO and severity of GER or esophageal lesions exists in patients with E+DU, and that GAO is not a major pathogenetic factor in GER disease.

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.