Recurrent Peptic Ulcer Research Articles

Mo1202 - Once Versus Twice Daily Oral Proton Pump Inhibitor Therapy for Prevention of Recurrent Peptic Ulcer Bleeding: A Propensity Score Matched Analysis

Mo1202 - Once Versus Twice Daily Oral Proton Pump Inhibitor Therapy for Prevention of Recurrent Peptic Ulcer Bleeding: A Propensity Score Matched Analysis

Non-invasive diagnostic tests for Helicobacter pylori infection.

Non-invasive diagnostic tests for Helicobacter pylori infection.

Післяопераційний рефлюкс-гастрит у хворих, оперованих з приводу пер-форативної виразки

Постановка проблеми і аналіз останніх досліджень та публікацій. До теперішнього часу рефлюкс-гастрит - найменш вивчене ускладнення післяопераційного періоду хворих, оперованих з приводу перфоративної пілородуоденальної виразки.Мета роботи – покращення результатів хірургічного лікування хворих, оперованих з приводу перфоративної виразки.Матеріали та методи. Нами прооперовано 204 хворих із приводу перфоративної виразки в період з 2005 по 2015 роки. Пацієнтам виконувались органозберігаючі операції у поєднанні з одним із видів ваготомії, а також висічення виразкового субстрату з одним з видів пілоропластики без ваготомії та ушивання перфоративного отвору, як із традиційного доступу, так і лапароскопічно.Результати досліджень та їх обговорення. При закиданні дуоденального вмісту в шлунок відбувається його взаємодія з вмістом шлунку з утворенням вільних іонів водню Н+, що в свою чергу призводить до різкого підвищення кислотності в цій зоні. Надалі відбувається зворотна перфузія іонів Н + в слизову оболонку. У хворих з рефлюксом II ступеня виявлено площинні ерозії і ерозії змішаного типу, у решти хворих зазначалося наявність дрібнокрапкових ерозій. У хворих з рецидивом виразкової хвороби був рефлюкс II-III ступеня. Аналіз причин рецидиву виразкової хвороби і розвитку езофагогастродуоденіту показав, що ці захворювання розвиваються не тільки на тлі підвищеної кислотопродукції внаслідок неповної ваготомії у 2 (1,9%) хворих, а й при нормальній кислотопродукції у 3 (2,9%) хворих.Висновки: Рефлюкс дуоденального вмісту в порожнину шлунка є пусковим моментом як у розвитку рецидиву виразкової хвороби, так і ерозивного гастродуоденіту. Найбільш дієвим заходом спрямованим на його профілактику є збереження замикальних функції пілоричного жому під час операції. Всім хворим, які перенесли пілорусруйнуючу операцію, слід з першої доби призначати препарати, які нормалізують моторику шлунку і дванадцятипалої кишки. При наявності протипоказань з урахуванням інтраопераційного pH вище 2,0 та експресії антигену Кі-67 більше 20% можна рекомендувати ушивання перфоративної виразки з лапароскопічного або лапаротомного доступів без ваготомії з подальшою терапією блокаторами протонної помпи.

Fast track rehabilitation in perforated duodenal ulcer

To analyze the outcomes of fast track rehabilitation program in patients with perforated duodenal ulcer (PDU). For the period 2013-2016 at the Department of Surgery and Endoscopy 206 PDU patients have been treated. Inclusion criterion for the main group (n=77) was duodenal ulcers, their dimension up to 1 cm, laparoscopic suture of perforated ulcer, fast track rehabilitation program implementation. The control group consisted of 129 patients who underwent open suturing of perforated ulcer followed by conventional treatment in postoperative period. In the main group (n=77) laparoscopic suturing of ulcerative defect with the use of Fast Track program was performed. Postoperative complication i.e. sutures failure was observed in 1 (1.3%) case. There were no lethal outcomes in the main group. Mean length of hospital-stay was 4.8 days. In 129 patients of the control group open suturing of the perforated ulcer and conventional postoperative therapy were applied. Postoperative surgical complications were absent in the control group; mortality rate was 2.3%. Mean length of postoperative hospital-stay was 8.1 days. Laparoscopic treatment of perforated ulcers facilitates application of fast track rehabilitation program in emergency patients. Fast track rehabilitation protocol after laparoscopic suturing of the perforated ulcer creates conditions for early discharge and is followed by good clinical and economic effects. Recurrent peptic ulcers are noted if antiulcer therapy is absent.

Peptic ulcer bleeding patients with Rockall scores ≥6 are at risk of long-term ulcer rebleeding: A 3.5-year prospective longitudinal study.

Patients with high Rockall scores have increased risk of rebleeding and mortality within 30days after peptic ulcer bleeding, but long-term outcomes deserve follow-up after cessation of proton pump inhibitors. The paper aimed to validate whether patients with high Rockall scores have more recurrent ulcer bleeding in a 3.5-year longitudinal cohort. Between August 2011 and July 2014, 368 patients with peptic ulcer bleeding were prospectively enrolled after endoscopic hemostasis to receive proton pump inhibitors for at least 8 to 16weeks. These subjects were categorized into either a Rockall scores ≥6 group (n=257) or a Rockall scores <6 group (n=111) and followed up until July of 2015 to assess recurrent ulcer bleeding. The proportion of patients with rebleeding during the 3.5-year follow-up was higher in patients with Rockall scores ≥6 than in those with scores <6 (10.51 vs. 3.63 per 100person-year, P=0.004, log-rank test). Among patients with Rockall scores ≥6, activated partial thromboplastin time prolonged ≥1.5-fold (P=0.045), American Society of Anesthesiologists physical status class ≥III (P=0.02), and gastric ulcer (P=0.04) were three additional independent factors found to increase rebleeding risk. The cumulative rebleeding rate was higher in patients with Rockall scores ≥6 with more than or equal to any two additional factors than in those with fewer than two additional factors (15.69 vs. 7.63 per 100person-year, P=0.012, log-rank test). Patients with Rockall scores ≥6 are at risk of long-term recurrent peptic ulcer bleeding. The risk can be independently increased by the presence of activated partial thromboplastin time prolonged ≥1.5-fold, American Society of Anesthesiologists class ≥III, and gastric ulcer in patients with Rockall scores ≥6.

Time latencies of Helicobacter pylori eradication after peptic ulcer and risk of recurrent ulcer, ulcer adverse events, and gastric cancer: a population-based cohort study

Helicobacter pylori is associated with peptic ulcer disease and gastric cancer. Therefore we wanted to test how various lengths of delays in H pylori eradication therapy influence the risk of recurrent peptic ulcer, ulcer adverse events, and gastric cancer. This population-based nationwide Swedish cohort study included 29,032 patients receiving H pylori eradication therapy after peptic ulcer disease in 2005 to 2013. Predefined time intervals between date of peptic ulcer diagnosis and date of eradication therapy were analyzed in relation to study outcomes. Cox regression provided hazard ratios (HRs) and 95% confidence intervals (95% CIs), adjusted for age, sex, comorbidity, history of ulcer disease, use of ulcerogenic drugs, and use of proton pump inhibitors (PPIs). Compared with eradication therapy within 7 days of peptic ulcer diagnosis, eradication therapy within 8 to 30, 31 to 60, 61 to 365, and >365 days corresponded with HRs of recurrent ulcer of 1.17 (95% CI, 1.08-1.25), 2.37 (95% CI, 2.16-2.59), 2.96 (95% CI, 2.76-3.16), and 3.55 (95% CI, 3.33-3.79), respectively. The corresponding HRs for complicated ulcer were 1.55 (95% CI, 1.35-1.78), 3.19 (95% CI, 2.69-3.78), 4.00 (95% CI, 3.51-4.55), and 6.14, (95% CI, 5.47-6.89), respectively. For gastric cancer the corresponding HRs were .85 (95% CI, .32-2.23), 1.31 (95% CI, .31-5.54), 3.64 (95% CI, 1.55-8.56), and 4.71 (95% CI, 2.36-9.38), respectively. Delays in H pylori eradication therapy after peptic ulcer diagnosis time-dependently increase the risk of recurrent ulcer, even more so for complicated ulcer, starting from delays of 8 to 30 days.

Vonoprazan prevents low-dose aspirin-associated ulcer recurrence: randomised phase 3 study

ObjectiveCompare efficacy and safety of vonoprazan and lansoprazole for secondary prevention of low-dose aspirin (LDA)-associated peptic ulcers in a 24-week study and long-term extension therapy in separate study.DesignDouble-blind, randomised, non-inferiority...

Vonoprazan prevents ulcer recurrence during long-term NSAID therapy: randomised, lansoprazole-controlled non-inferiority and single-blind extension study

ObjectiveTo assess the non-inferiority of vonoprazan to lansoprazole for secondary prevention of non-steroidal anti-inflammatory drug (NSAID)-induced peptic ulcer (PU) and the safety of vonoprazan during extended use.DesignA phase 3, 24-week,...

Pathogenetic bases and efficacy of slow calcium channel blockers in the therapy of recurrent peptic ulcer disease associated with hypertension

To clarify blood calcium concentrations (BCCs) as an indicator of the functional state of the calcium-regulating system in the concomitant course of recurrent peptic ulcer disease (PUD) and hypertension, by comparing with the severity of a ulcerous process, with changes in regional microcirculation, and with the functions of the stomach. To elucidate the pathogenetic justification for and clinical efficacy of slow calcium channel blockers (SCCBs) in the treatment of this comorbidity. In the case-control study, each patient with recurrent PUD and grade 1, Stage I hypertension (Group 1; n=23) corresponded to a recurrent PUD patient matched for sex, age, and ulcer site (Group 2, n=23). The complex of treatment for these patients included the SCCB nifedipine. A control group consisted of 56 recurrent PUD patients who received combination therapy without nifedipine. All the patients over time underwent clinical and endoscopic examinations and determinations of BCCs, indicators of gastric secretory and motor functions, and regional microcirculation in the gastroduodenal mucosal biopsy specimens. Recurrent PUD was present with a reliable BCC increase that was more substantial when it was associated with hypertension. Calcium imbalance was accompanied by changes in regional microcirculation and gastric secretory and motor functional indicators forming an acid peptic factor, as well as by hypermotor dyskinesia, which were more pronounced in patients with comorbidity. Incorporation of a SCCB into a complex of therapy for recurrent PUD to eliminate the pathogenic effect of blood calcium contributed to more rapid arrest of the clinical symptoms of a recurrence, to elimination of acute-phase microcirculatory disorders in the gastroduodenal zone, and to the recovery of gastric functional indicators. Elevated blood pressure was ruled out during the therapy of concomitant diseases. Incorporation of a SCCB into the combination therapy of recurrent PUD associated with hypertension is pathogenetically sound and clinically effective.

Efficacy and Safety of Esomeprazole in the Prevention of Recurrent Peptic Ulcer in Patients Receiving Low-Dose Acetyl Salicylic Acid for Cardiovascular Protection: A Meta-analysis of Multicenter Double-Blind Randomised Controlled Trial

Efficacy and Safety of Esomeprazole in the Prevention of Recurrent Peptic Ulcer in Patients Receiving Low-Dose Acetyl Salicylic Acid for Cardiovascular Protection: A Meta-analysis of Multicenter Double-Blind Randomised Controlled Trial

Histamine-2 Receptor Antagonist Cannot Prevent Recurrent Peptic Ulcers in Patients With Atherosclerotic Diseases Who Receive Platelet ADP Receptor Antagonist Monotherapy: A Randomized-Controlled, Double-Blind, and Double-Dummy Trial.

Proton pump inhibitor can effectively prevent recurrent peptic ulcers among atherosclerotic patients receiving clopidogrel monotherapy. However, the interaction between proton pump inhibitors and clopidogrel has raised concerns over the safety of combined use of the two medicines in clinical practice. The aims of this randomized-controlled, double-blind and double-dummy trial were to investigate the efficacy of histamine-2 receptor antagonist (H2RA) in the prevention of recurrent peptic ulcer in patients undergoing thienopyridine monotherapy. From January 2012 to 2016, long-termed thienopyridine users with a peptic ulcer history who did not have peptic ulcers at initial endoscopy were randomly assigned to receive either famotidine (40 mg, before bedtime) or placebo (before bedtime) for 6 months. Follow-up endoscopy was performed at the end of the 6th month and whenever dyspepsia, hematemesis, or melena occurred. The cumulative incidence of recurrent peptic ulcer during the 6-month period was 7.0% in famotidine group (n=114) and 11.4% in the placebo group (n=114). The two patient groups had comparable cumulative incidence of peptic ulcer (difference, 4.4%; 95% confidence interval (CI), -11.7 to 2.9%; P=0.239). Additionally, there was no difference in the cumulative incidence of ulcer bleeding (2.6% vs. 1.8%; difference, 0.8%; 95% CI, -0.6 to 2.4%, P=1.000) between famotidine and placebo groups. However, the former had a lower incidence of gastroduodenal erosion than the latter (21.1% vs. 36.8%; difference, 15.7%; 95% CI, -27.3 to -4.1%; P=0.013). Famotidine cannot decrease the incidence of peptic ulcer or ulcer bleeding in thienopyridine users with atherosclerotic disease and a history of peptic ulcer.

Chronic obstructive pulmonary disease is associated with increased recurrent peptic ulcer bleeding risk

BackgroundThe association between chronic obstructive pulmonary disease (COPD) and the risk of recurrent peptic ulcer bleeding (PUB) remains unclear. In this study, we compared the risk of recurrent PUB between patients with and those without COPD. MethodsUsing the Taiwan National Health Insurance Research Database, we first selected patients newly diagnosed with PUB in 2002–2009. Two groups comprising 13,732 COPD cases and 13,732 non-COPD matched controls were created using propensity score matching, thereby making the differences in basic demographics, medication use, and disease conditions between the two groups negligible. Cox proportional hazard regression was used to evaluate the risk of recurrent PUB during the follow-up period. ResultsThe cumulative recurrence rate of PUB was significantly higher in the patients with COPD than in the non-COPD matched controls (2years: 10.8% vs 9.3%; 6years: 18.3% vs 15.7%, P all <0.05), with an adjusted hazard ratio (HR) of 1.17 (95% confidence interval [CI], 1.08–1.26, P<0.001) and 1.19 (95% CI, 1.12–1.26, P<0.001) within 2-year and 6-year follow-ups, respectively. Patients with COPD using steroids were at a marginally higher risk of recurrent PUB than those who did not use steroids. Multivariate stratified analysis revealed similar results in many subgroups. ConclusionsThe risk of recurrent PUB is higher in patients with COPD than in patients without COPD.

Helicobacter pylori and non-malignant upper gastrointestinal diseases.

Peptic ulcer disease (PUD) has been further decreased over the last decades along with decreasing prevalence of Helicobacter pylori-associated PUD. A delayed H.pylori eradication has been associated with an increased risk of rehospitalization for complicated recurrent peptic ulcer and reemphasized the importance of eradication especially in patients with peptic ulcer bleeding (PUB). PUB associated with NSAID/aspirin intake and H.pylori revealed an additive interaction in gastric pathophysiology which favors the "test-and-treat" strategy for H.pylori in patients with specific risk factors. The H.pylori-negative and NSAID-negative "idiopathic PUD" have been increasingly observed and associated with slower healing tendency, higher risk of recurrence, and greater mortality. Helicobacter pylori-associated dyspepsia has been further investigated and finally defined by the Kyoto consensus. Helicobacter pylori eradication therapy is advised as first option in this group of patients. Only in the case of symptom persistence or recurrence after eradication therapy, dyspeptic patients should be classified as functional dyspepsia (FD). There were few new data in 2015 on the role of H.pylori infection in gastroesophageal reflux disease (GERD), and in particular Barrett's esophagus. A lower prevalence of gastric atrophy with less acid output in patients with erosive esophagitis confirmed previous findings. In patients with erosive esophagitis, no difference was observed in healing rates neither between H.pylori-positive and H.pylori-negative patients nor between patients that underwent eradication therapy compared to patients without eradication. These findings are in line with the current consensus guidelines concluding that H.pylori eradication has no effects on symptoms and does not aggravate preexisting GERD.

The uncovering and characterization of a CCKoma syndrome in enteropancreatic neuroendocrine tumor patients

Objective: Neuroendocrine tumors in the pancreas and the gastrointestinal tract may secrete hormones which cause specific syndromes. Well-known examples are gastrinomas, glucagonomas, and insulinomas. Cholecystokinin-producing tumors (CCKomas) have been induced experimentally in rats, but a CCKoma syndrome in man has remained unknown until now.Material and methods: Using a panel of immunoassays for CCK peptides and proCCK as well as for chromogranin A, we have examined plasma samples from 284 fasting patients with gastroenteropancreatic neuroendocrine tumors. In hyperCCKemic samples, plasma CCK was further characterized by chromatography.Results: One of the patients displayed gross hyperCCKemia. She was a 58-year old woman with a pancreatic endocrine tumor, liver metastases, 500–1000-fold elevated basal CCK concentration in plasma, diarrhea, severe weight loss, recurrent peptic ulcer and bilestone attacks from a contracted gallbladder. The CCK concentrations in plasma were not affected by resection of the pancreatic tumor, but decreased to normal after hemihepatectomy with removal of the metastases.Conclusion: A CCKoma syndrome with severe hypersecretion of CCK exists in man. The duodenal ulcer disease and diarrhea with permanently low gastrin in plasma suggest that CCKomas may mimic gastrinoma-like symptoms, because CCK peptides are full agonists of the gastrin/CCK-B receptor.

Eradication therapy for peptic ulcer disease in Helicobacter pylori-positive people.

Peptic ulcer disease is the cause of dyspepsia in about 10% of people. Ninety-five percent of duodenal and 70% of gastric ulcers are associated with Helicobacter pylori. Eradication of H. pylori reduces the relapse rate of ulcers but the magnitude of this effect is uncertain. This is an update of Ford AC, Delaney B, Forman D, Moayyedi P. Eradication therapy for peptic ulcer disease in Helicobacter pylori-positive patients. Cochrane Database of Systematic Reviews 2006, Issue 2. Art. No.: CD003840. DOI: 10.1002/14651858.CD003840.pub4. To assess the proportion of peptic ulcers healed and the proportion of participants who remained free from relapse with eradication therapy against placebo or other pharmacological therapies in H. pylori-positive people.To assess the proportion of participants that achieved complete relief of symptoms and improvement in quality of life scores.To compare the incidence of adverse effects/drop-outs (total number for each drug) associated with the different treatments.To assess the proportion of participants in whom successful eradication was achieved. In this update, we identified trials by searching the Cochrane Central Register of Controlled Trials (CENTRAL), Ovid MEDLINE (1950 to March 2016) and Ovid EMBASE (1980 to March 2016). To identify further relevant trials, we handsearched reference lists from trials selected by electronic searching, and published abstracts from conference proceedings from the United European Gastroenterology Week (published in Gut) and Digestive Disease Week (published in Gastroenterology). The search was last updated in March 2016. We contacted members of Cochrane Upper GI and Pancreatic Diseases,and experts in the field and asked them to provide details of outstanding clinical trials and any relevant unpublished materials. We analysed randomised controlled trials of short- and long-term treatment of peptic ulcer disease in H. pylori-positive adults. Participants received at least one week of H. pylori eradication compared with ulcer healing drug, placebo or no treatment. Trials were included if they reported assessment from two weeks onwards. We collected data on ulcer healing, recurrence, relief of symptoms and adverse effects. We calculated the risk ratio (RR) with 95% confidence intervals (CI) using both fixed-effect and random-effects models with Review Manager software (RevMan 5.3) based on intention-to-treat analysis as far as possible. A total of 55 trials were included for one or more outcomes for this review.In duodenal ulcer healing, eradication therapy was superior to ulcer healing drug (UHD) (34 trials, 3910 participants, RR of ulcer persisting = 0.66, 95% confidence interval (CI) 0.58 to 0.76; 381/2286 (adjusted proportion: 12.4%) in eradication therapy plus UHD versus 304/1624 (18.7%) in UHD; low quality evidence) and no treatment (two trials, 207 participants, RR 0.37, 95% CI 0.26 to 0.53; 30/125 (adjusted proportion: 21.7%) in eradication therapy versus 48/82 (58.5%) in no treatment; low quality evidence).In gastric ulcer healing, the differences were imprecise between eradication therapy and UHD (15 trials, 1974 participants, RR 1.23, 95% CI 0.90 to 1.68; 220/1192 (adjusted proportion: 16.0%) in eradication therapy plus UHD versus 102/782 (13.0%) in UHD; very low quality evidence). In preventing duodenal ulcer recurrence the differences were imprecise between maintenance therapy with H.pylori eradication therapy and maintenance therapy with UHD (four trials, 319 participants, RR of ulcer recurring 0.73; 95% CI 0.42 to 1.25; 19/159 (adjusted proportion: 11.9%) in eradication therapy versus 26/160 (16.3%) in UHD; very low quality evidence), but eradication therapy was superior to no treatment (27 trials 2509 participants, RR 0.20, 95% CI 0.15 to 0.26; 215/1501 (adjusted proportion: 12.9%) in eradication therapy versus 649/1008 (64.4%) in no treatment; very low quality evidence).In preventing gastric ulcer recurrence, eradication therapy was superior to no treatment (12 trials, 1476 participants, RR 0.31, 95% CI 0.22 to 0.45; 116/697 (adjusted proportion: 16.3%) in eradication therapy versus 356/679 (52.4%) in no treatment; very low quality evidence). None of the trials reported proportion of people with gastric ulcer not healed after initial therapy between H.pylori eradication therapy and no active treatment or the proportion of people with recurrent gastric ulcer or peptic ulcers during maintenance therapy between H.pylori eradication therapy and ulcer healing drug therapy. Adding a one to two-week course of H. pylori eradication therapy is an effective treatment for people with H. pylori-positive duodenal ulcer when compared to ulcer healing drugs alone and no treatment. H. pylori eradication therapy is also effective in preventing recurrence of duodenal and gastric ulcer compared to no treatment. There is currently no evidence that H. pylori eradication therapy is an effective treatment in people with gastric ulcer or that it is effective in preventing recurrence of duodenal ulcer compared to ulcer healing drug. However, confidence intervals were wide and significant benefits or harms of H. pylori eradication therapy in acute ulcer healing of gastric ulcers compared to no treatment, and in preventing recurrence of duodenal ulcers compared to ulcer healing drugs cannot be ruled out.

Medical versus surgical treatment for refractory or recurrent peptic ulcer

Background Refractory peptic ulcers are ulcers in the stomach or duodenum that do not heal after eight to 12 weeks of medical treatment or those that are associated with complications despite medical treatment. Recurrent peptic ulcers are peptic ulcers that recur after healing of the ulcer. Given the number of deaths due to peptic ulcer-related complications and the long-term complications of medical treatment (increased incidence of fracture), it is unclear whether medical or surgical intervention is the better treatment option in people with recurrent or refractory peptic ulcers. Objectives To assess the benefits and harms of medical versus surgical treatment for people with recurrent or refractory peptic ulcer. Search methods We searched the specialised register of the Cochrane Upper GI and Pancreatic Diseases group, the Cochrane Central Register of Controlled Trials (CENTRAL) in the Cochrane Library, MEDLINE, EMBASE, Science Citation Index Expanded, and trials registers until September 2015 to identify randomised trials and non-randomised studies, using search strategies. We also searched the references of included studies to identify further studies. Selection criteria We considered randomised controlled trials and non-randomised studies comparing medical treatment with surgical treatment in people with refractory or recurrent peptic ulcer, irrespective of language, blinding, or publication status for inclusion in the review. Data collection and analysis Two review authors independently identified trials and extracted data. We planned to calculate the risk ratio, mean difference, standardised mean difference, or hazard ratio with 95% confidence intervals using both fixed-effect and random-effects models with Review Manager 5 based on intention-to-treat analysis. Main results We included only one non-randomised study published 30 years ago in the review. This study included 77 participants who had gastric ulcer and in whom medical therapy (histamine H2 receptor blockers, antacids, and diet) had failed after an average duration of treatment of 29 months. The authors do not state whether these were recurrent or refractory ulcers. It appears that the participants did not have previous complications such as bleeding or perforation. Of the 77 included participants, 37 participants continued to have medical therapy while 40 participants received surgical therapy (antrectomy with or without vagotomy; subtotal gastrectomy with or without vagotomy; vagotomy; pyloroplasty and suture of the ulcer; suture or closure of ulcer without vagotomy or excision of the ulcer; proximal gastric or parietal cell vagotomy alone; suture or closure of the ulcer with proximal gastric or parietal cell vagotomy). Whether to use medical or surgical treatment was determined by participant's or treating physician's preference. The study authors reported that two participants in the medical treatment group (2 out of 37; 5.4%) had gastric cancer, which was identified by repeated biopsy. They did not report the proportion of participants who had gastric cancer in the surgical treatment group. They also did not report the implications of the delayed diagnosis of gastric cancer in the medical treatment group. They did not report any other outcomes of interest for this review (that is health-related quality of life (using any validated scale), adverse events and serious adverse events, peptic ulcer bleeding, peptic ulcer perforation, abdominal pain, and long-term mortality). Authors' conclusions We found no studies that provide the relative benefits and harms of medical versus surgical treatment for recurrent or refractory peptic ulcers. Studies that evaluate the natural history of recurrent and refractory peptic ulcers are urgently required to determine whether randomised controlled trials comparing medical versus surgical management in patients with recurrent or refractory peptic ulcers or both are necessary. Such studies will also provide information for the design of such randomised controlled trials. A minimum follow-up of two to three years will allow the calculation of the incidence of complications and gastric cancer (in gastric ulcers only) in recurrent and refractory peptic ulcers. In addition to complications related to treatment and disease, health-related quality of life and loss of productivity should also be measured.

The calcium-regulating system and recurrent peptic ulcer

To elucidate the functional state and value of the calcium-regulating system, calcium and phosphorus metabolism in the pathogenesis and sanogenesis of peptic ulcer (PU); to define the possible ways to correct shifts found in the treatment of disease relapse, by affecting the different levels of their disorders. A total of 220 patients with recurrent PU were examined by determining the blood levels of parathyrin, calcitonin, calcium and phosphorus, as well as gastric secretory and motor functions. Recurrent PU was accompanied by a considerable increase in the blood concentration of parathyroid hormone and calcium, a slight rise in that of calcitonin, and a significant reduction in that of phosphorus. These changes were attended by a substantial increase in gastric acid- and pepsinogen-forming functions, a decrease in the production of gastric mucoproteins, and hypermotor dyskinesia. The use of calcitrin, nifedipine, and etidronic acid, which eliminate dysfunction of the calcium-regulating system at different levels of its impairments, leads to a significant reduction in the time of alleviation of the clinical and endoscopic manifestations of a recurrence. Recurrent PU runs in the presence of calcium-regulating system dysfunction. Incorporation of the thyroid C-cell hormone preparation calcitrin, the slow calcium-channel blocker nifedipine, and etidronic acid bisphosphonate into a complex of treatment for a disease recurrence is pathogenetically sound and clinically effective.

Relation of Smoking in the Development of Mucosal and Ulcerative Lesions in Upper Gastrointestinal Tract

Smoking promotes an increase in both the incidence and recurrence of peptic ulcers. The association of upper gastrointestinal lesions with smoking was studied in 120 patients with or without the symptoms of upper gastrointestinal lesions. Of the total, 50 nonsmoker and 70 smokers (cigarette or bidi). It was observed that, smokers are more prone to develop both mucosal and ulcerative lesions.

Eradication rates for Helicobacter pylori infection a systematic evidence - based review

The aim of this study is to summarize all available published studies regarding pharmacologic management of newly onset and recurrent peptic ulcers, provide a critical insight into indistinguishable features of H. pylori, and construct a useful clinical tool for decision making. A thorough search was performed of electronic databases including MEDLINE, Embase, Pubmed, Scopus and Cochrane Library from 1990 up to 2014. A systematic review and meta-analysis was to be carried out, pooling the effects of outcomes of patients and lesions enrolled in the studies. The primary end-points of this thesis will be the construction of a pharmacological management algorithm of H. Pylori eradication in various disease states. In uncomplicated peptic ulcer, first line eradication therapy of H. pylori should include one of the following: triple [(PPI, clarithromycin, amoxicillin)-(PPI, clarithromycin, metronidazole)]/ quadruple (PPI, clarithromycin, amoxicillin, nitroimidazole)/Bismuth-containing (ranitidine, Bismuth subsalicylate, metronidazole, tetracycline) for 10-14 days or sequential for five days (PPI+amoxicillin) plus five days (PPI, clarithromycin, tinidazole). If the first line H. pylori eradication regimen is unsuccessful, second line H. pylori eradication regimens should comprise one of the following: Bismuth based/triple (levofloxacin substitutes clarithromycin). In cases of clarithromycin resistance, H. pylori eradication regimens should include one of the following: Bismuth-based /quadruple/sequential (levofloxacin substitutes clarithromycin). In cases of metronidazole resistance, H. pylori eradication regimens should incorporate one of the following: triple/ sequential (levofloxacin substitutes clarithromycin). In cases of clarithromycin and metronidazole resistance H. pylori eradication regimens should include the following: sequential (levofloxacin substitutes clarithromycin). Though there is sufficient evidence to safeguard Grade A recommendations for H. pylori eradication regimens in cases of first- and second-line treatments, resistance and peptic ulcer complications, high-quality randomized controlled trials that will include distinct ethnic groups, homogeneous endoscopic diagnosis and treatment, double-blind designs, and evaluation of outcomes operating specific criteria over set follow-up periods are lacking.

Clopidogrel inhibits angiogenesis of gastric ulcer healing via downregulation of vascular endothelial growth factor receptor 2.

Although clopidogrel does not cause gastric mucosal injury, it does not prevent peptic ulcer recurrence in high-risk patients. We explored whether clopidogrel delays gastric ulcer healing via inhibiting angiogenesis and to elucidate the possible mechanisms. Gastric ulcers were induced in Sprague Dawley rats, and ulcer healing and angiogenesis of ulcer margin were compared between clopidogrel-treated rats and controls. The expressions of the proangiogenic growth factors and their receptors including basic fibroblast growth factor (bFGF), bFGF receptor (FGFR), vascular endothelial growth factor (VEGF), VEGFR1, VEGFR2, platelet-derived growth factor (PDGF)A, PDGFB, PDGFR A, PDGFR B, and phosphorylated form of mitogenic activated protein kinase pathways over the ulcer margin were compared via western blot and reverse transcription polymerase chain reaction. Invitro, human umbilical vein endothelial cells (HUVECs) were used to elucidate how clopidogrel inhibited growth factors-stimulated HUVEC proliferation. The ulcer sizes were significantly larger and the angiogenesis of ulcer margin was significantly diminished in the clopidogrel (2 and 10mg/kg/d) treated groups. Ulcer induction markedly increased the expression of phosphorylated form of extracellular signal-regulated kinase (pERK), FGFR2, VEGF, VEGFR2, and PDGFRA when compared with those of normal mucosa. Clopidogrel treatment significantly decreased pERK, FGFR2, VEGF, VEGFR2, and PDGFRA expression at the ulcer margin when compared with those of the respective control group. Invitro, clopidogrel (10(-6)M) inhibited VEGF-stimulated (20ng/mL) HUVEC proliferation, at least, via downregulation of VEGFR2 and pERK. Clopidogrel inhibits the angiogenesis of gastric ulcer healing at least partially by the inhibition of the VEGF-VEGFR2-ERK signal transduction pathway.