Ulcer recurrence among Filipino patients: Clinical profile and risk factors

Abstract Patients with endoscopic diagnosis of gastric and/or duodenal ulcers who eventually had endoscopic confirmation of ulcer healing after any anti-ulcer medication were entered in a 3 year study to determine ulcer recurrence rate, onset of ulcer recurrence and factors associated with ulcer recurrence. Patients from two participating centres who are not on any maintenance treatment had endoscopic examinations at 3, 6 and 12 months after ulcer healing or at any time of symptom recurrence. There were 144 patients entered into the study. The 1 year recurrence rate observed among 125 Filipino patients who completed the study was 73% wherein 71% occurred within the first six months. This was comparable with those reported in the world literature. Thirty-three per cent of those with recurrent ulcers were asymptomatic. The difference in the recurrence rate between gastric and duodenal ulcers was not statistically significant. The only risk factors found to be associated with ulcer relapse were history of smoking and alcohol intake. CLO test for Helicobacter pylori done in 45 patients with recurrent ulcers were all positive, suggesting a strong association between H. pylori and ulcer recurrence.     

Effect of treatment of Helicobacter pylori infection on the long-term recurrence of gastric or duodenal ulcer. A randomized, controlled study.

OBJECTIVE: To determine the effect of treating Helicobacter pylori infection on the recurrence of gastric and duodenal ulcer disease. DESIGN: Follow-up of up to 2 years in patients with healed ulcers who had participated in randomized, controlled trials. SETTING: A Veterans Affairs hospital. PARTICIPANTS: A total of 109 patients infected with H. pylori who had a recently healed duodenal (83 patients) or gastric ulcer (26 patients) as confirmed by endoscopy. INTERVENTION: Patients received ranitidine, 300 mg, or ranitidine plus triple therapy. Triple therapy consisted of tetracycline, 2 g; metronidazole, 750 mg; and bismuth subsalicylate, 5 or 8 tablets (151 mg bismuth per tablet) and was administered for the first 2 weeks of treatment; ranitidine therapy was continued until the ulcer had healed or 16 weeks had elapsed. After ulcer healing, no maintenance antiulcer therapy was given. MEASUREMENTS: Endoscopy to assess ulcer recurrence was done at 3-month intervals or when a patient developed symptoms, for a maximum of 2 years. RESULTS: The probability of recurrence for patients who received triple therapy plus ranitidine was significantly lower than that for patients who received ranitidine alone: for patients with duodenal ulcer, 12% (95% CI, 1% to 24%) compared with 95% (CI, 84% to 100%); for patients with gastric ulcer, 13% (CI, 4% to 31%) compared with 74% (44% to 100%). Fifty percent of patients who received ranitidine alone for healing of duodenal or gastric ulcer had a relapse within 12 weeks of healing. Ulcer recurrence in the triple therapy group was related to the failure to eradicate H. pylori and to the use of nonsteroidal anti-inflammatory drugs. CONCLUSIONS: Eradication of H. pylori infection markedly changes the natural history of peptic ulcer in patients with duodenal or gastric ulcer. Most peptic ulcers associated with H. pylori infection are curable.     

Role of Helicobacter pylori in ulcer healing and recurrence of gastric and duodenal ulcers in longterm NSAID users. Response to omeprazole dual therapy.

BACKGROUND: The relation between Helicobacter pylori infection and non-steroidal anti-inflammatory drug (NSAID)-associated peptic ulcers remains unclear; in particular, it is not known whether H pylori plays a part in the healing and recurrence of these ulcers. AIMS: To evaluate prospectively in a consecutive series of arthritis patients receiving longterm NSAID treatment the prevalence of peptic ulcer as well as the effect of H pylori eradication on the healing and recurrence of gastric and duodenal ulcer found. PATIENTS: Some 278 consecutive patients underwent gastroscopy with multiple biopsies of the gastric antrum and corpus for histological examination and rapid urease test. One hundred peptic ulcers (59 gastric ulcers, 39 duodenal ulcers, and two gastric ulcers concomitant with a duodenal ulcer) were found. Seventy per cent of these ulcers were H pylori positive. METHODS: According to their H pylori status, ulcer patients were randomised to one of the following treatments: H pylori negative ulcers received omeprazole 20 mg twice daily for four to eight weeks, whereas H pylori positive lesions were treated with omeprazole 20 mg twice daily plus amoxycillin 1 g twice daily (the second of these for the first two weeks) or omeprazole alone for four to eight weeks while continuing NSAID therapy. Patients with healed ulcers were endoscopically followed up for six months after stopping antiulcer therapy while continuing NSAIDs. RESULTS: Endoscopic healing rates for gastric and duodenal ulcers in the three different groups were similar both at four and eight weeks. H pylori eradication did not influence healing, which occurred in 14 of 20 (70%) of patients in whom H pylori was eradicated, compared with 14 of 17 (82%) of patients with persistent infection. Cumulative recurrence rates at six months did not statistically differ among the three different groups (27% in H pylori negative, 46% in H pylori positive, and 31% in those where H pylori was eradicated during the healing phase), although a numerical trend in favour of a higher recurrence rate in infected patients was evident. CONCLUSIONS: H pylori eradication does not confer any significant advantage on the healing of gastric and duodenal ulcers associated with longterm NSAID use. It remains to be established with certainty whether eradication may be helpful in the reduction of recurrence in a specific subset of NSAID associated ulcer.     

Influence of Helicobacter pylori Infection on Healing and Relapse of Acetic Acid Ulcers in Mongolian Gerbils

Both Helicobacter pylori and NSAIDs play important roles in the healing and relapse of peptic ulcers in man. We examined how H. pylori infection, indomethacin, and their combination affects the healing of gastric ulcers and whether or not such factors provoke a relapse of healed gastric ulcers in Mongolian gerbils. Gastric ulcers were induced by serosal application of an acetic acid solution. H. pylori (ATCC43504) was orally administered once into animals with active and healed ulcers. Ulcers healed within eight weeks and remained healed for the following six months. H. pylori infection significantly delayed ulcer healing four weeks following infection. Indomethacin treatment showed a tendency to delay ulcer healing. Ulcer healing in H. pylori-infected Mongolian gerbils was significantly delayed by indomethacin. H. pylori infection resulted in a relapse of healed ulcers from one to six months after infection, with a gradual increase in size. By the fourth month following a relapse, the serum gastrin level had significantly increased. H. pylori-induced ulcers in the posterior wall coexisted with relapsed ulcers in the anterior wall five and six months later. Omeprazole markedly prevented the ulcer relapse caused by H. pylori infection. It is concluded that, in Mongolian gerbils, H. pylori infection delayed the healing of preexisting gastric ulcers and resulted in the relapse of healed ulcers, yet indomethacin had little or no effect on ulcer healing or relapse.     

Evidence for the essential role of Helicobacter pylori in gastric ulcer disease.

Helicobacter pylori (H pylori) eradication heals chronic active type B gastritis and dramatically changes the natural history of duodenal ulcer disease. There are few data concerning the role of anti-H pylori treatment in gastric ulcer disease. A total of 83 patients presenting with H pylori positive active gastric ulcer disease were treated with omeprazole and antibiotics (amoxicillin, ciprofloxacin, roxithromycin) in seven different clinical protocols, each of which included the attempt to eradicate H pylori infection and to evaluate the post-therapeutic course of ulcer disease. The overall proportion of H pylori eradication was 67.9% (53 of 78 patients available for follow up). Best results were obtained with two week treatment regimens comprising omeprazole 20 mg twice daily and amoxicillin 500 mg four times a day or 1000 mg twice daily (eradication > 80%). Eradication of H pylori speeds up ulcer healing, with a six week healing rate of 84.9% compared with 60% in patients with persistent H pylori infection (p = 0.0148). In a subgroup of 11 patients with refractory ulcers, H pylori eradication (n = 10) was associated with ulcer healing on continued acid suppression in nine cases. One male patient with chronic antral ulcer did not respond to treatment within the next six months (H pylori and ulcer persistence), and in one female patient a resistant body ulcer was identified as gastric lymphoma. Fifty patients with healed ulcers were followed up for one year. Patients with (n = 32) and without (n = 18) bacterial eradication had similar demographic and clinical characteristics. H pylori eradication was associated with a statistically significant reduction of ulcer recurrences (3.1 v 55.6%, p<0.001). This study concludes that H pylori eradication considerably changes the natural history of H pylori associated gastric ulcer disease. In addition, H pylori eradication speeds up ulcers healing and is associated with healing of previously refractory ulcers. Thus, treatment aimed at bacterial eradication should be considered in all patients with gastric ulcers severe enough to contemplate further treatment options.     

根除幽门螺杆菌对出血性十二指肠溃疡自然病程影响的3年随访研究

目的：探讨根除幽门螺杆菌（Ｈｐ）对出血性十二指肠溃疡自然病程的影响。方法：选择胃镜证实的出血性十二指肠溃疡病人１３６例，均有Ｈｐ感染（胃粘膜Ｇｉｅｍｓａ染色和１４Ｃ尿素呼吸试验二项均阳性）。予奥米拉唑２０ｍｇ，每日２次；羟氨苄青霉素７５０ｍｇ，每日２次；甲硝唑４００ｍｇ，每日３次，疗程２周。疗程结束后４周复查胃镜和Ｈｐ，溃疡愈合者分Ａ组（Ｈｐ根除）和Ｂ组（Ｈｐ未根除）进入随访阶段，随访观察３年。结果：溃疡愈合１２４例（９１２％），Ｈｐ根除１１１例（８１６％）；Ｈｐ根除的溃疡愈合率为９９１％（１１０／１１１），显著高于Ｈｐ未根除的５６％（１４／２５，Ｐ＜０００５）；Ｂ组１年内溃疡复发率达１００％，显著高于Ａ组８３％（Ｐ＜００５）；Ｂ组３年累积再出血率１００％，显著高于同期Ａ组的９０％（Ｐ＜００５）。结论：根除Ｈｐ可提高十二指肠溃疡愈合率和减少溃疡复发率，尤可显著减少溃疡再出血率，提示根除Ｈｐ很可能改变出血性十二指肠溃疡的自然病程。     

One week's anti-Helicobacter pylori treatment for duodenal ulcer.

This open study tested whether eradication of Helicobacter pylori (H pylori) heals duodenal ulcers as well as decreasing recurrence. H pylori was detected in patients with endoscopic duodenal ulcers by histology, CLO-test, culture, and 13C-urea breath test (13C-UBT). Tripotassium dicitrato bismuthate (120 mg) and amoxycillin (500 mg) each four times daily, were given for seven days, with 400 mg metronidazole five times a day on days 5-7. The 13C-UBT was repeated immediately after treatment and endoscopy repeated within 21 days. After treatment unhealed ulcers were reinspected one month later and healed ulcers followed up by 13C-UBT alone for 12 months. Of 45 patients, 44 were available for follow up. Mean pretreatment excess delta 13CO2 excretion was 25.6 per mil, which fell to 2.4 per mil immediately after finishing treatment, indicating clearance of H pylori in every patient. At the second endoscopy (median interval 20 days from start of treatment) 33 of 44 (75%) duodenal ulcers had healed. Ten of the remaining 11 duodenal ulcers were smaller and those 10 healed in the next two weeks with no further treatment. Two patients' ulcers that initially healed with clearance of H pylori recurred three weeks later (both had metronidazole resistant H pylori). H pylori was eradicated in 28 of 44 (64%) patients (13C-UBT negative for median follow up 10.2 months). Overall 41 of 43 (93%, 95% confidence intervals 81%-99%) duodenal ulcers were healed at one month. This study suggests that one week of anti-H pylori triple treatment is effective in healing duodenal ulcers.     

Triple therapy for the eradication of Helicobacter pylori and reduction of duodenal ulcer relapse: Comparison of 1 week and 2 week regimens and recrudescence rates over 12 months

Abstract The aim of this study is to assess the relationship between Helicobacter pylori and the relapse of duodenal ulcer, and also to evaluate the differences in efficacy and side effects between 1 week and 2 week triple therapy. Sixty-two patients with active duodenal ulcer, which healed within 8 weeks of nizatidine treatment, were randomly allocated to one of two groups. Group 1 ( n = 29) received no drugs, Group II ( n = 33) received triple threapy for 1 week (IIa, n = 16) or 2 weeks (IIb, n = 17). Eleven patients whose ulcer did not heal after an 8 week nizatidine treatment period were randomly assigned into Group IIa ( n = 5) and IIb ( n = 6). Seven patients whose ulcer recurred after discontinuation of nizatidine were allocated to receive 2 weeks of triple therapy. All patients received endoscopy 6 weeks after entry, and again at 3, 6 and 12 months unless both ulcer recurrence and H. pylori infection were found. The frequency of ulcer relapse 6 weeks after the active duodenal ulcer had healed was 83% (24/29) in Group I, 13% in Group IIa and 14% in Group IIb. The cumulative rate of recurrence was significantly higher in Group I than in Group II (90 vs 30% at 12 months, P < 0.01). Ulcer relapse was associated with persistence of H. pylori infection ( P < 0.0001). No statistical difference was found between the 1 week and 2 week regimens in ulcer relapse rate (30 vs 30% in 1 year), H. pylori eradication rate (86 vs 100%), incidence of side effects (48 vs 53%) or recrudescence rate (17 vs 23%). Our study suggests that a 1 week regimen and a 2 week regimen are equally effective in the eradication of H. pylori and reduction of ulcer recurrence in 1 year.     

Medical treatment of duodenal ulcer: Acid inhibition or Helicobacter pylori eradication?

To ascertain whether acid inhibition or Helicobacter pylori (HP) colonization is the decisive factor in the healing of duodenal ulcer, we treated 54 patients with famotidine and carried out long-term follow-up. Helicobacter pylori colonization was found in 70.4% of patients before treatment. There were no differences in the pre-treatment characteristics between patients with HP positive or HP negative ulcers. The 4-week and 8-week healing rates after famotidine treatment were 72.5% and 82.4% respectively. No difference in HP colonization was found between patients with ulcer healed and those with ulcer not healed (78.4% vs 64.3% at 4th week and 77.3% vs 71.4% at 8th week, P greater than 0.05). In patients with ulcer healed at 4th week, the intragastric pH was raised significantly and the antral acute inflammation was less severe than those with ulcer not healed. Ulcer recurrence was found in 76.9% of patients within 1 year, but there was no difference in ulcer recurrence between the patients with positive or negative HP colonization at the time of ulcer healing. Our results suggest that duodenal ulcer healing and recurrence are closely related to acid inhibition rather than to HP colonization.     

Attributable Risk of H. pylori in Peptic Ulcer Disease

Recent reports in the United States have found that fewer peptic ulcers are due to Helicobacter pylori than previously believed. The aim of this study is to determine if the declining prevalence of H. pylori infection in the general population can account for the apparent increase in the frequency of non-H. pylori ulcers. A total of 396 patients with peptic ulcer or ulcer scar were enrolled in this study. The pre-1950 population consisted of 149 patients with gastric ulcers and with 44 duodenal ulcers. The post-1950 population consisted of 96 patients with gastric ulcers and 107 with duodenal ulcers. The frequency of H. pylori-negative gastric ulcers was 5.4% in patients born before 1950 and 4.2% in patients born after 1950, and the frequency of H. pylori-negative duodenal ulcers was 0% and 1.9%, respectively. There are no statistical differences between the two populations in gastric and duodenal ulcers. H. pylori seropositivity was 74.9% in asymptomatic volunteers born before 1950 and 20.7% in those born after 1950 (P < 0.01) in the general population. The attributable risk of H. pylori infection in peptic ulcer diseases was not affected by the prevalence of H. pylori infection in the general population in Japan. This suggests that the apparent increase in frequency of non-H. pylori ulcers in the United States is not simply due to the declining prevalence of infection. Other explanations for non-H. pylori ulcers should be sought.     

Prospective,randomized, investigator-blind trial ofHelicobacter pylori infection treatment in patients with refractory duodenal ulcers

In this study, 26 patients with duodenal ulcers refractory to treatment with H₂-receptor antagonists for 8–12 weeks were randomly assigned to eight weeks of treatment with colloidal bismuth subcitrate (120 mg four times a day) alone (N=12) or in combination with tetracycline hydrochloride (500 mg four times a day, days 0–14) and metronidazole (500 mg three times a day, days 15–28). Symptoms were scored and endoscopy, histology, and CLO tests were performed before, on completion of treatment, and 3, 6, 12, and 18 months after treatment. Treatment was considered successful whenHelicobacter pylori was not detected by CLO tests and Warthin-Starry stains on gastric biopsies taken from antrum, body, and fundus. On triple therapy, ulcers healed in 12/14 patients (85.71%) and 10/14 (71.42%) patients becameHelicobacter pylori-negative. On bismuth, only one patient becameHelicobacter pylori-negative (8.33%,P<0.0001), but ulcers healed in 8/12 patients (67%,P=NS). Six patients on bismuth, whose ulcers remained unhealed or relapsed early after healing, were offered triple therapy, which resulted in ulcer healing in three and Helicobacter pylori clearance in two patients. At 18 months, none of theHelicobacter pylori-negative patients had ulcer relapse. On the contrary, ulcers relapsed in all but one patient, who remainedHelicobacter pylori-positive. Smoking and drinking did not influence the therapeutic outcome. The data confirm previous reports that many duodenal ulcers are infectious and therefore curable.     

根除幽门螺杆菌对胃溃疡愈合质量及复发的影响研究

目的探讨幽门螺杆菌（Helicobacter pylori，Up）对胃溃疡愈合质量及复发的影响。方法120例坳阳性活动期胃溃疡患者，口服泮托拉唑、阿莫西林、甲硝唑一周后，继续口服泮托美拉唑5周。治疗结束后复查胃镜取病理组织学检查并检测Hp根除情况，对比却根除组与却根除失败组内镜下溃疡愈合形态差异和愈合质量（包括内镜下再生黏膜成熟度和再生黏膜组织学成熟度）。所有患者随诊1年以上了解溃疡复发情况。结果治疗后92例胃溃疡患者月p检测阴性，坳根除率为80．43％；却根除组与跏根除失败组在内镜下愈合率方面的差异无显著性意义（P〉0．05），但两组在再生黏膜成熟度和再生黏膜组织学成熟度方面的差异有显著性意义（P〈0．01）。坳根除组1年溃疡复发率为4．35％，却根除失败组为21．43％，两组差异有显著性意义（P〈0．05）。结论根除Hp可提高胃溃疡的愈合质量，减少溃疡病复发。     

Mucosal expression and luminal release of epidermal and transforming growth factors in patients with duodenal ulcer before and after eradication of Helicobacter pylori.

BACKGROUND: Epidermal growth factor (EGF) and transforming growth factor-alpha (TGF alpha) are potent gastric acid inhibitors and stimuli of mucosal growth and protection but their involvement in Helicobacter pylori associated duodenal ulcer has been little examined. AIM: To assess gastric acid secretion, plasma gastrin concentrations, mucosal content of EGF and TGF alpha, and mucosal expression of these peptides and their receptor (EGFr) as well as salivary and gastric luminal release of EGF under basal conditions and after pentagastrin stimulation in 10 healthy subjects and in 25 H pylori positive patients with duodenal ulcer before and after two weeks of triple anti-H pylori therapy and four weeks after the termination of this therapy. RESULTS: Pentagastrin stimulation caused a significant increase in salivary and gastric release of EGF both in healthy controls and patients with duodenal ulcers but in the patients, the eradication of H pylori resulted in several fold higher gastric luminal (but not salivary) EGF release than before the anti-H pylori therapy. Mucosal contents of immunoreactive EGF and TGF alpha and mucosal expression of EGF, TGF alpha, and EGFr in H pylori positive patients with duodenal ulcer were significantly higher than those in healthy H pylori negative controls and this increase persisted after eradication of H pylori. Basal plasma gastrin was significantly reduced after two weeks of triple therapy and four weeks after the H pylori eradication all ulcers were completely healed. CONCLUSIONS: (1) H pylori infection in patients with duodenal ulcer was accompanied by enhanced plasma gastrin and increased mucosal content and expression of TGF alpha, EGF, and EGFr; (2) H pylori eradication resulted in ulcer healing, reduction in plasma gastrin, and enhancement of gastric (but not salivary) luminal release of EGF, particularly after pentagastrin stimulation; and (3) enhanced mucosal content and expression of TGF alpha, EGF, and EGFr and increased luminal release of EGF may contribute to ulcer healing after eradication of H pylori.     

Factors Influencing the Relapse of Gastric Ulcers During H2-Receptor Antagonist Maintenance Therapy

Abstract: We performed H₂-receptor antagonist maintenance therapy for 2 years on 146 patients with healed gastric ulcers (including those with concurrent duodenal ulcers), and determined the cumulative endoscopic and symptomatic recurrence rates. We also investigated the factors involved in ulcer recurrence in the first 12 months of maintenance therapy. The cumulative endoscopic non-recurrence rate was 70.0% at 12 months and 57.2% at 24 months, while the cumulative symptomatic non-recurrence rate was 84.8% at 12 months and 75.0% at 24 months. The factors contributing to endoscopic recurrence were the presence of a concomitant disease, the presence of duodenal ulcer, the type of ulcer, and the endoscopic stage at healing. The factors related to symptomatic recurrence were smoking and the type of ulcer. Multivariate analysis showed that the type of ulcer, smoking, and the endoscopic stage at healing influenced the risk of recurrence.     

Healing of Helicobacter pylori -Induced Gastric Ulcers in Mongolian Gerbils (Combined Treatment with Omeprazole and Clarithromycin)

Helicobacter pylori can colonize the stomachs ofMongolian gerbils and subsequently induce penetratingulcers five months later. Using this gerbil model, theeffects of both combined treatment with omeprazole and clarithromycin, as well as treatment witheach drug separately, on the healing of H.pylori-induced gastric ulcers, and the effects of thecessation of the drug treatment on healed ulcers wereexamined. Beginning five months after H. pylori(NCTC11637) inoculation, omeprazole (four weeks),clarithromycin (two weeks), their combination, or thevehicle was orally administered once daily. These drugs,in combination or separately, markedly enhancedulcer healing and lowered the increased myeloperoxidase(MPO) activity. While omeprazole had no effect on viableH. pylori, clarithromycin and the drug combination significantly reduced viable H. pylori. Thedegree of bacterial eradication was much higher in thecase of the drug combination compared to clarithromycinalone. Four months after cessation of the treatment, visible ulcers, hypertrophic gastritis andincreased MPO activity were found in the control animals(all H. pylori-positive). Nonetheless, only one of theeight gerbils subjected to the drug combination developed a small ulcer, although nohypertrophic gastritis was exhibited. It is concludedthat: (1) the gerbil model of H. pylori infection isuseful for the study of ulcer healing; (2) combinedtreatment with omeprazole and clarithromycin enhances theulcer healing in infected gerbils; and (3) healed ulcersdo not relapse, despite cessation of the drugtreatment.     

Helicobacter pylori eradication in the African setting, with special reference to reinfection and duodenal ulcer recurrence.

The aim of this study was to determine the effect of Helicobacter pylori eradication on the natural history of duodenal ulcer disease, and to determine the incidence of reinfection in adult patients where H pylori had been eradicated in a community with a high prevalence of the infection. An investigator blinded study, with 24 month endoscopic follow up, in subjects where H pylori had been eradicated, and similarly treated subjects where it had not been eradicated was conducted at a tertiary referral hospital. The patients consisted of a volunteer sample of 48 patients with endoscopically proved active duodenal ulcer disease. Duodenal ulcers were healed with omeprazole, 20 mg/day. After endoscopically confirmed healing, patients were treated with either one (17 patients) or two weeks (31 patients) of 'triple therapy'. H pylori status (urease reaction, histological tests, and culture of antral biopsy specimens) was determined at entry, four weeks after the finish of triple therapy and six, 12, and 24 months after this, or whenever an endoscopically proved recurrent duodenal ulcer was found. The main outcome measures were the recurrence of duodenal ulceration, over 24 months in the eradicated and non-eradicated groups and the incidence of reinfection by H pylori in the eradicated group during this follow up period. Five patients in the eradicated group experienced a duodenal ulcer relapse, of which only three were unexplained (1 = reinfected, 1 = gastrinoma). Fifteen of 21 patients in the non-eradicated group relapsed over the same period (p < 0.001). Only two of 27 patients in the eradicated group were reinfected during the 24 month follow up period. It is concluded that H pylori eradication is an effective treatment strategy for the longterm treatment of duodenal ulcer disease, even in the high prevalence, African setting. Reinfection is uncommon.     

Discriminant factors of gastric ulcer healing by colloidal bismuth

One hundred and twelve patients with 49 corpus and 35 prepyloric gastric ulcers and 28 duodenal ulcers associated with gastric ulcers were entered into a stratified, controlled double-blind randomized study comparing the healing efficacy of colloidal bismuth suspension with placebo. Healing of corpus and prepyloric ulcers, but not duodenal-ulcer associated gastric ulcers, was significantly better with the bismuth compound than with placebo. The clinical, personal, ulcer and acid secretory data of these patients were prospectively collected and evaluated by stepwise discriminant analysis in two phases. In the first phase, the collected data of 91 consecutive patients were entered into computer analysis. The derived discriminant function classified patients into healed and unhealed categories with a sensitivity of 82%, specificity of 77%, positive diagnostic value of 73%, negative diagnostic value of 85% and diagnostic efficiency of 79%. In phase two, the discriminant function from phase 1 was applied prospectively to 21 patients to predict the outcome of treatment. Five out of five healed and 11/16 unhealed gastric ulcers were correctly predicted, giving a diagnostic efficiency of 76%. The present study shows that healing or non-healing of gastric ulcer can be predicted with reasonable accuracy by discriminant analysis. In addition, discriminant analysis identified, aside from the efficacious drug, ulcer size, young age, co-existing duodenal ulcer, and concomitant medical condition as adverse factors for gastric ulcer healing.     

THE HEALING PROCESS OF GASTRIC ARTIFICIAL ULCERS AFTER ENDOSCOPIC SUBMUCOSAL DISSECTION

Background: Due to the remarkable progress of endoscopic resection techniques, endoscopic submucosal dissection (ESD) has been widely performed for larger mucosal tumors that would result in large arti?cial ulcers. The healing process of peptic ulcers has been previously studied in detail; however, no precise investigation for arti?cial ulcers after ESD has been reported. To con?rm the validity of the treatment from the aspect of wound healing, we aimed to clarify the healing process of large gastric arti?cial ulcers after ESD. Methods: Seventy patients with gastric mucosal tumors treated by ESD were enrolled. The size, location and time of scar formation of the ulcers were reviewed using endoscopic pictures taken from the same view and angle. Follow‐up endoscopy was performed at 1, 4, 8 and 12 weeks after ESD. For postoperative medication, all patients received normal doses of proton pump inhibitors and sucralfate for 8 weeks. Results: The average size of the resected specimen was 34.7 mm (20–90 mm). Irrespective of ulcer size and location, all of the cases healed up to scarring stages within 8 weeks. Conclusions: Gastric arti?cial ulcers after ESD healed within 8 weeks regardless of size and location using normal doses of medication as peptic ulcers. The fact that even giant ulcers after ESD heal within 8 weeks could be helpful information for candidates for ESD and for postoperative management of patients after ESD.     

Short and long term outcome of Helicobacter pylori positive resistant duodenal ulcers treated with colloidal bismuth subcitrate plus antibiotics or sucralfate alone.

Thirty two patients with Helicobacter pylori positive duodenal ulcers resistant to treatment were randomly assigned to 4 weeks' treatment with sucralphate 4 g/day or colloidal bismuth subcitrate 480 mg/day plus amoxycillin from days 1 to 7 and tinidazole from days 8 to 14. After 4 weeks, patients with unhealed ulcers were crossed over to the other form of treatment for a further 4 week period. Patients with healed ulcers were followed up for 1 year without maintenance therapy with clinical and endoscopic investigations 3, 6, and 12 months after healing. Complete healing rates at 4 weeks were 88% (15 of 17) in the colloidal bismuth subcitrate plus antibiotics group and 40% (six of 15) in the sucralphate group (p < 0.05). After cross over, overall healing rates were 88% (22 of 25) and 47% (eight of 17), respectively (p < 0.05). H pylori eradication occurred in 83% of patients treated with the triple therapy. Cumulative relapse rates at 12 months were 12% (two of 17) in patients in whom H pylori had been eradicated and 100% (10 of 10) in those with persistent infection after short term therapy (p < 0.05). These results show that a colloidal bismuth subcitrate plus antibiotics regimen is highly effective in the short term treatment of resistant duodenal ulcers and that H pylori eradication can change the natural tendency to early recurrence of these ulcers.     

Herpes simplex virus type 1 in peptic ulcer disease： An inverse association with Helicobacterpylori

AIM: To assess the frequency of herpes simplex virus type I in upper gastrointestinal tract ulcers and normal mucosa with the modern and better assays and also with a larger number of well characterized patients and controls and its relationship to Helicobacter pylori(H pylori). METHODS: Biopsy specimens from 90 patients (34 with gastric ulcer of the prepyloric area and 56 with duodenal ulcer) were evaluated. Biopsies from 50 patients with endoscopically healthy mucosa were considered as the control group. The method used to identify herpes simplex virus-1 (HSV-1) was polymerase chain reaction. H pylori was detected by the CLO-test and by histological method. RESULTS: Herpes simplex virus-1 was detected in 28 of 90 patients with peptic ulcer (31%) [11 of 34 patients with gastric ulcer (32.4%) and 17 of 56 with duodenal ulcer (30.4%)] exclusively close to the ulcerous lesion. All control group samples were negative for HSV-1. The likelihood of H pylori negativity among peptic ulcer patients was significantly higher in HSV-1 positive cases than in HSV-1 negative cases (P = 0.009). Gastric ulcer patients with HSV-1 positivity were strongly associated with an increased possibility of Helicobacter pylori negativity compared to duodenal ulcer patients (P = 0.010). CONCLUSION: HSV-1 is frequent in upper gastrointestinal tract ulcers but not in normal gastric and duodenal mucosa. There is an inverse association between HSV-1 and H pylori infection.