联合应用奥美拉唑、甲硝唑和阿莫西林治疗消化道溃疡的效果探析

目的 :探讨联合应用奥美拉唑、甲硝唑和阿莫西林治疗消化道溃疡的临床效果。方法 :对2013年5月~2014年7月期间我院收治的80例肠道或胃部溃疡患者的临床资料进行回顾性研究。将这80例患者随机分为实验组和对照组,每组各有40例患者。我院为对照组患者使用奥美拉唑进行治疗,为实验组患者联合应用奥美拉唑、甲硝唑和阿莫西林进行治疗。治疗结束后,比较两组患者的治疗效果。结果 :实验组患者治疗的康复率及治疗的总有效率均明显高于对照组患者,二者相比差异具有显著性(P<0.05)。结论:联合应用奥美拉唑、甲硝唑和阿莫西林治疗消化道溃疡可有效地提高治疗的总有效率,促使患者早日康复。此治疗方法值得在临床上推广应用。

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.

Effects of Aloe vera and sucralfate on gastric microcirculatory changes,cytokine levels and gastric ulcer healing in rats

AIM： To compare the effects of Aloe vera and sucralfate on gastric microcirculatory changes, cytokine levels and gastric ulcer healing. METHODS： Male Spraque-Dawley rats （n=48） were divided into four groups. Group 1 served as control group, group 2 as gastric ulcer group without treatment, groups 3 and 4 as gastric ulcer treatment groups with sucralfate and Aloe vera. The rats from each group were divided into 2 subgroups for study of leukocyte adherence, TNF-α and IL-10 levels and gastric ulcer healing on days 1 and 8 after induction of gastric ulcer by 20% acetic acid. RESULTS： On day 1 after induction of gastric ulcer, the leukocyte adherence in postcapillary venule was significantly （P〈 0.05） increased in the ulcer groups when compared to the control group. The level of TNF-α was elevated and the level of IL-10 was reduced. In the ulcer groups treated with sucralfate and Aloe vera, leukocyte adherence was reduced in postcapillary venule. The level of IL-10 was elevated, but the level of TNF-a had no significant difference. On day 8, the leukocyte adherence in postcapillary venule and the level of TNF-α were still increased and the level of IL-10 was reduced in the ulcer group without treatment. The ulcer treated with sucralfate and Aloe vera had lower leukocyte adherence in postcapillary venule and TNF-α level. The level of IL-10 was still elevated compared to the ulcer group without treatment. Furthermore, histopathological examination of stomach on days 1 and 8 after induction of gastric ulcer showed that gastric tissue was damaged with inflammation. In the ulcer groups treated with sucralfate and Aloe vera on days 1 and 8, gastric inflammation was reduced, epithelial cell proliferation was enhanced and gastric glands became elongated. The ulcer sizes were also reduced compared to the ulcer group without treatment. CONCLUSION： Administration of 20% acetic acid can induce gastric inflammation, increase leukocyte adherence in postcapillary venule and TNF-α level and reduce IL-10 level. Aloe vera treatment can reduce leukocyte adherence and TNF-αlevel, elevate IL-10 level and promote gastric ulcer healing.

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.

“Rescue” regimens after Helicobacter pylori treatment failure

Helicobacter pylori (H pylori) infection is the main cause of gastritis, gastroduodenal ulcer disease, and gastric cancer. After more than 20 years of experience in H pylori treatment, in my opinion, the ideal regimen to treat this infection is still to be found. Currently, apart from having to know first-line eradication regimens well, we must also be prepared to face treatment failures. Therefore, in designing a treatment strategy we should not focus on the results of primary therapy alone, but also on the final (overall) eradication rate. The choice of a "rescue" treatment depends on which treatment is used initially. If a clarithromycin- based regimen was used initially, a subsequent metronidazole-based treatment (quadruple therapy) may be used afterwards, and then a levofloxacin- based combination would be a third "rescue" option. Alternatively, it has recently been suggested that levofloxacin-based rescue therapy constitutes an encouraging second-line strategy, representing an alternative to quadruple therapy in patients with previous PPI-clarithromycin-amoxicillin failure, with the advantage of efficacy, simplicity and safety. In this case, a quadruple regimen may be reserved as a third-line rescue option. Finally, rifabutin-based rescue therapy constitutes an encouraging empirical fourth- line strategy after multiple previous eradication failures with key antibiotics such as amoxicillin, clarithromycin, metronidazole, tetracycline, and levofloxacin. Even after two consecutive failures, several studies have demonstrated that H pylori eradication can finally be achieved in almost all patients if several rescue therapies are consecutively given. Therefore, the attitude in H pylori eradication therapy failure, evenafter two or more unsuccessful attempts, should be to fight and not to surrender.

Application of endoscopic hemoclips for nonvariceal bleeding in the upper gastrointestinal tract

AIM： To investigate acute nonvariceal bleeding in the upper gastrointestinal （GI） tract and evaluate the effects of endoscopic hemoclipping. METHODS： Sixty-eight cases of acute nonvariceal bleeding in the upper GI tract were given endoscopic treatment with hemoclip application. Clinical data, endoscopic findings, and the effects of the therapy were evaluated. RESULTS： The 68 cases （male：female = 42：26, age from 9 to 70 years, average 54.4） presented with hernatemesis in 26 cases （38.2%）, melena in nine cases （13.3%）, and both in 33 cases （48.5%）. The causes of the bleeding included gastric ulcer （29 cases）, duodenal ulcer （11 cases）, Dieulafoy＇s lesion （11 cases）, Mallory-Weiss syndrome （six cases）, post-operative （three cases）, post-polypectomy bleeding （five cases）, and post-sphincterotomy bleeding （three cases）; 42 cases had active bleeding. The mean number of hemoclips applied was four. Permanent hemostasis was obtained by hemoclip application in 59 cases; 6 cases required emergent surgery （three cases had peptic ulcers, one had Dieulafoy＇s lesion, and two were caused by sphincterotomy）; three patients died （two had Dieulafoy＇s lesion and one was caused by sphincterotomy）; and one had recurrent bleeding with Dieulafoy＇s lesion 10 mo later, but in a different location. CONCLUSION： Endoscopic hemoclip application was an effective and safe method for acute nonvariceal bleeding in the upper GI tract with satisfactory outcomes.

Role of transcatheter arterial embolization for massive bleeding from gastroduodenal ulcers

Intractable bleeding from gastric and duodenal ulcers is associated with significant morbidity and mortality. Aggressive treatment with early endoscopic hemostasis is essential for a favourable outcome. In as many as 12%-17% of patients,endoscopy is either not available or unsuccessful. Endovascular therapy with selective catheterization of the culprit vessel and injection of embolic material has emerged as an alternative to emergent operative intervention in high-risk patients. There has not been a systematic literature review to assess the role for embolotherapy in the treatment of acute upper gastrointestinal bleeding from gastroduo-denal ulcers after failed endoscopic hemostasis. Here,we present an overview of indications,techniques,and clinical outcomes after endovascular embolization of acute peptic-ulcer bleeding. Topics of particular relevance to technical and clinical success are also discussed. Our review shows that transcatheter arterial embolization is a safe alternative to surgery for massive gastroduodenal bleeding that is refractory to endoscopic treatment,can be performed with high technical and clinical success rates,and should be considered the salvage treatment of choice in patients at high surgical risk.

Endoscopic findings in patients with upper gastrointestinal bleeding clinically classified into three risk groups prior to endoscopy

AIM: To investigate in a prospective study whether a simplifi ed clinical score prior to endoscopy in upper gastrointestinal bleeding (UGIB) patients was able to predict endoscopic findings at urgent endoscopy. METHODS: All consecutive UGIB patients referred to a single endoscopic center during a 16 mo period were enrolled. Before endoscopy patients were strati- fied according to a simple clinical score (T-score), including T1 (high-risk), T2 (intermediate-risk) and T3 (low-risk). Endoscopy was performed in all cases within 2 h, and high-risk stigmata were considered for further analysis. RESULTS: Out of the 436 patients included into the study, 126 (29%) resulted to be T1, 135 (31%) T2, and 175 (40%) T3. Overall, stigmata of recent haem-orrhage (SRH) were detected in 118 cases (27%). SRH occurred more frequently in T1 patients than in T2/T3 cases (85% vs 3.2%; χ2 = 304.5309, P < 0.001). Older age (t=3.311; P < 0.01) and presence of comor-bidities (χ2 = 14.7458; P < 0.01) were more frequently detected in T1 than in T2/T3 patients. CONCLUSION: Our simplifi ed clinical score appeared to be associated with the detection of endoscopic findings which may deserve urgent endoscopy. A further,randomised study is needed to assess its accuracy in safely scheduling endoscopy in UGIB patients.

Protective Effect of Holothurian Intestine Against Indomethacin Induced Gastric Mucosal Damage in Rats

Our study aimed to investigate the protective effects of Holothurian intestines(HI) on NSAIDs-induced gastric mucosal damage and the possible mechanism. At first, 60 male Wistar rats were induced of gastric lesions with indomethacin(IDM, 30 mg kg^(-1)). The rats were pretreated for 15 consecutive days with saline, sucralfate, or HI(0.4g kg^(-1) d-1, 0.8 g kg^(-1) d^(-1) and 1.6 g kg^(-1) d^(-1)) prior to IDM treatment, followed by evaluations of macroscopic damage and microscopic features; and investigation of the levels of inflammatory cytokines, oxidative stress parameters, gastric mucosal prostaglandin E2(PGE2) and total hexosamine in tissues. The expression of COX-1 and COX-2 m RNA in the gastric tissue were determined by quantitative polymerase chain reaction(q PCR). Pathological gastric ulcer indexes, levels of pro-inflammatory cytokines(IL-1β, IL-17, TNF-α) and lipid peroxidation were significantly decreased in HI-treated groups, whereas the levels of protective factors(TGF-β, GSH, SOD activity and PGE2) were significantly elevated especially in the group with HI 1.61 g kg^(-1) d^(-1)(P < 0.05). Furthermore, the expression of COX-2 mRNA decreased significantly in HI groups(P < 0.05). The study investigates that holothurian intestines may act as a kind of marine medicine which have protective effect on IDM-induced gastric ulcer, which could be a dietary preventive agent for the prevention of gastric damage.

Evidence for the role of gastric mucosa at the secretion of soluble triggering receptor expressed on myeloid cells(strem-1) in peptic ulcer disease

AIM： To investigate the role of gastric mucosa at the secretion of sTREM-1 in peptic ulcer.METHODS： Seventy two patients were enrolled; 35 with duodenal, 22 with gastric ulcer and 26 with chronic gastritis. Patients were endoscoped and gastric juice was aspirated. Patients with duodenal and gastric ulcer underwent a second endoscopy post-treatment. Biopsies were incubated in the absence/presence of endotoxins or gastric juice. Supernatants were collected and sTREM-2 and TNF~ were measured by enzyme immunoabsorbent assays. Scoring of gastritis was performed before and after treatment according to updated Sydney score.RESULTS： Patients with duodenal and gastric ulcer and those with chronic gastritis had similar scores of gastritis, sTREM-1 was higher in supernatants of tissue samples of H pylori-positive than of H pylori-negative patients with gastric ulcer. Median （± SE） sTREM-1 was found increased in supernatants of patients with gastric ulcer before treatment （203.21 ± 88.91 pg/1000 cells） compared to supernatants either from the same patients post-treatment （8.23 ± 5.79 pg/1000 cells） or from patients with chronic gastritis （6.21 ± 0.71 pg/1000 cells） （P 〈 0.001 and 〈 0.001, respectively）. Similar differences for sTREM-1 were recorded among LPS-stimulated tissue samples of patients （P = 0.001）. Similar differences were not found for TNFα. Positive correlations were found between sTREM-1 of supernatants from patients with both duodenal and gastric ulcer before treatment and the degree of infiltration of neutrophils and monocytes.CONCLUSION： sTREM-1 secreted by the gastric mucosa is an independent mechanism connected to the pathogenesis of peptic ulcer, sTREM-1 was released at the presence of H pylori from the inflamed gastric mucosa in the field of gastric ulcer.

Lower gastrointestinal bleeding: Association with Sevelamer use

Stercoral ulceration results from impaction of hard fecal mass on the colonic wall and is a relatively unknown cause of lower gastrointestinal bleeding. In this report, we describe a case of lower gastrointestinal bleeding due to stercoral ulceration resulting from Sevelamer, a drug which is commonly associated with constipation.

Quadruple therapy with furazolidone for retreatment in patients with peptic ulcer disease

AIM: To establish the efficacy and safety of a 7-d therapeutic regimen using omeprazole,bismuth subcitrate,furazolidone and amoxicillin in patients with peptic ulcer disease who had been previously treated with other therapeutic regimens without success.METHODS: Open cohort study which included patients with peptic ulcer who had previously been treated unsuccessfully with one or more eradication regimens.The therapeutic regimen consisted of 20 mg omeprazole,240 mg colloidal bismuth subcitrate,1000 mg amoxicillin,and 200 mg furazolidone,taken twice a day for 7 d.Patients were considered as eradicated when samples taken from the gastric antrum and corpus 12 wk after the end of treatment were negative for Helicobacter pylori (H pylori) (rapid urease test and histology).Safety was determined by the presence of adverse effects.RESULTS: Fifty-one patients were enrolled.The eradication rate was 68.8% (31/45).Adverse effects were reported by 31.4% of the patients,and these were usually considered to be slight or moderate in the majority of the cases.Three patients had to withdraw from the treatment due to the presence of severe adverse effects.CONCLUSION: The association of bismuth,furazolidone,amoxicillin and a proton-pump inhibitor is a valuable alternative for patients who failed to respond to other eradication regimens.It is an effective,cheap and safe option for salvage therapy of positive patients.

Clinical characteristics of peptic ulcer perforation in Korea

AIM To elucidate the epidemiological characteristics and associated risk factors of perforated peptic ulcer(PPU).METHODS We retrospectively reviewed medical records of patients who were diagnosed with benign PPU from 2010 through 2015 at 6 Hallym university-affiliated hospitals.RESULTS A total of 396 patients were identified with postoperative complication rate of 9.1% and mortality rate of 0.8%. Among 174(43.9%) patients who were examined for Helicobacter pylori(H. pylori) infection, 78(44.8%) patients were positive for H. pylori infection, 21(12.1%) were on non-steroidal anti-inflammatory drugs(NSAIDs) therapy, and 80(46%) patients were neither infected of H. pylori nor treated by any kinds of NSAIDs. Multivariate analysis indicated that older age(OR = 1.09, 95%CI: 1.04-1.16) and comorbidity(OR = 4.11, 95%CI: 1.03-16.48) were risk factors for NSAID-associated PPU compared with non-H. pylori, non-NSAID associated PPU and older age(OR = 1.04, 95%CI: 1.02-1.07) and alcohol consumption(OR = 2.08, 95%CI: 1.05-4.13) were risk factors for non-H. pylori, non-NSAID associated PPU compared with solely H. pylori positive PPU.CONCLUSION Elderly patients with comorbidities are associated with NSAIDs-associated PPU. Non-H. pylori, non-NSAID peptic ulcer is important etiology of PPU and alcohol consumption is associated risk factor.

Diffuse gastroduodenitis and pouchitis associated with ulcerative colitis

We experienced a very rare case of ulcerative colitis (UC) accompanied with analogous lesions in the stomach, duodenum, and ileal J -pouch. Ileal J-pouch anal anastomosis was performed on a 29-year old woman in 1996. Six years later, she was admitted again to our hospital because of epigastralgia, nausea, watery diarrhea and low fever. Based on the results of endoscopic examination, we diagnosed it as pouchitis. Moreover, on hypotonic duodenography, expansion of the duodenal bulb and the descending portion were poor. Kerckring folds disappeared with typical lead-pipe appearance. The pathogenesis of the gastric and duodenal lesion in this patient was similar to that of the colonic lesions of UC. For the gastroduodenal lesions in this patient, symptomatic remission was obtained following administration of crushed mesalazine tablets (1500 mg/d) for 14 d with continuous administration of omeprazole. Firstly we used ciprofloxacin to treat pouchitis. On the fifth day, she got a fever because of catheter infection. In the catheter culture, methicillin-resistant Staphylococcus aureus (MRSA) was detected. Therefore we changed ciprofloxacin to vancomycin hydrochloride (Vancomycin?). Vancomycin was very effective, and the stool frequency dramatically improved in three days. Now she continues to take mesalazine, but her condition is stable and there has been no recurrence of pouchitis.

Penetrating ectopic peptic ulcer in the absence of Meckel's diverticulum ultimately presenting as small bowel obstruction

We report here how a heterotopic penetrating peptic ulcer progressed to cause small bowel obstruction in a pa- tient with multiple previous negative investigations. The clinical presentation, radiographic features and patho- logical findings of this case are described, along with the salient lessons learnt. The added value of wireless cap- sule endoscopy （WCE） in such circumstances is debated.

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.

Severe ulcerative colitis: At what point should we define resistance to steroids?

Corticoesteroids are still the first-line treatment for active ulcerative colitis more than 50 years after the publication of trials assessing their beneficial effect, with about a 50% remission rate in cases of severe disease. The mortality related to severe attacks of ulcerative colitis has decreased dramatically, to less than 1%, in experienced centers, due to the appropriate use of intensive therapeutic measures (intravenous steroids, fluids and electrolytes, artificial nutritional support, antibiotics, etc), along with timely decision-making about second-line medical therapy and early identification of patients requiring colectomy. One of the most difficult decisions in the management of severe ulcerative colitis is knowing for how long corticosteroids should be administered before deciding that a patient is a non-responder. Studies assessing the outcome of acute attacks after steroid initiation have demonstrated that, in steroid-sensitive patients, the response generally occurs early on, in the first days of treatment. Different indexes to predict treatment failure, when applied on the third day of treatment, have demonstrated a high positive predictive value for colectomy. In contrast to this resolute approach, which is the most widely accepted, other authors have suggested that in some patients a completeand prolonged response to steroids may take longer. Either way, physicians taking care of these patients need to recognize that severe ulcerative colitis may be life-threatening, and they need to be careful with excessively prolonged medical treatment and delayed surgery.

Quality of ulcer healing in gastrointestinal tract:Its pathophysiology and clinical relevance

In this paper, we review the concept of quality of ulcer healing （QOUH） in the gastrointestinal tract and its role in the ulcer recurrence. In the past, peptic ulcer disease （PUD） has been a chronic disease with a cycle of repeated healing/remission and recurrence. The main etiological factor of PUD is Helicobacter pylori （H. pylorl~, which is also the cause of ulcer recur- rence. However, H. pylori-negative ulcers are pres- ent in 12%-20% of patients; they also recur and are on occasion intractable. QOUH focuses on the fact that mucosal and submucosal structures within ulcer scars are incompletely regenerated. Within the scars of healed ulcers, regenerated tissue is immature and with distorted architecture, suggesting poor QOUH. The abnormalities in mucosal regeneration can be the basis for ulcer recurrence. Our studies have shown that persistence of macrophages in the regenerated area plays a key role in ulcer recurrence. Our studies in a rat model of ulcer recurrence have indicated that proinflammatory cytokines trigger activation of macro- phages, which in turn produce increased amounts of cytokines and chemokines, which attract neutrophils to the regenerated area. Neutrophils release proteolytic enzymes that destroy the tissue, resulting in ulcer re- currence. Another important factor in poor QOUH can be deficiency of endogenous prostaglandins and a defi- ciency and/or an imbalance of endogenous growth fac- tors. Topically active mucosal protective and antiulcer drugs promote high QOUH and reduce inflammatory cell infiltration in the ulcer scar. In addition to PUD, the concept of QOUH is likely applicable to inflammatory bowel diseases including Crohn＇s disease and ulcer- ative colitis.

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.

Gastroenterostoma after Billroth antrectomy as a premalignant condition

Gastric stump carcinoma （GSC） following remote gastric surgery is widely recognized as a separate entity within the group of various types of gastric cancer. Gastrecto- my is a well established risk factor for the development of GSC at a long time after the initial surgery. Both exo- as well as endogenous factors appear to be involved in the etiopathogenesis of GSC, such as achlorhydria, hypergastrinemia and biliary reflux, Epstein-Barr virus and Helicobacter pylori infection, atrophic gastritis, and also some polymorphisms in interleukin-l~ and maybe cyclo-oxygenase-2. This review summarizes the litera- ture of GSC, with special reference to reliable early di- agnostics. In particular, dysplasia can be considered as a dependable morphological marker. Therefore, close endoscopic surveillance with multiple biopsies of the gastroenterostomy is recommended. Screening start- ing at 15 years after the initial ulcer surgery can detect tumors at a curable stage. This approach can be ofspecial interest in Eastern European countries, where surgery for benign gastroduodenal ulcers has remained a practice for a much longer time than in Western Eu- rope, and therefore GSC is found with higher frequency.