Duodenal ulcer in South Africa: home-pounded versus milled maize

BACKGROUND: In South Africa there is suggestive evidence that home-pounded maize protects against duodenal ulceration. Therefore the purpose of the present paper was to test, in an animal model, whether oil from home-pounded maize gives protection against ulceration and whether this effect is present in commercially prepared maize oil. METHODS: Gastric ulceration was induced in rats with topical ethanol 1 h after giving oil prepared either from fresh-pounded or from commercially treated maize. The lengths of the linear ulcers produced were measured with a planimeter and summed in each rat. Control observations were made using arachis oil (which is known not to be ulceroprotective) and horse gram lipid (which is known to be strongly ulceroprotective). Statistical comparisons were performed mainly with the Mann-Whitney U-test, but also with reference to the normal distribution. Thin-layer chromatography (TLC) was performed on the oil from fresh maize, and the fractions similarly investigated for ulceroprotective activity. RESULTS: Fresh maize oil was strongly ulceroprotective (P = 0.0039), commercial maize oil was not (P = 0.2864). The active ingredient in the fresh maize oil was located in the fraction near the solvent front. CONCLUSION: These findings support the hypothesis that home-pounded maize protects against duodenal ulceration.     

Catecholamine concentrations in biopsied gastroduodenal tissue specimens of patients with duodenal ulcer

We measured dopamine and norepinephrine concentrations in the biopsied gastroduodenal mucosa obtained from 12 ulcer-free dyspeptic patients, nine patients with active duodenal ulcer, and eight patients with inactive (or healed) duodenal ulcer using a high-performance liquid chromatography with electrochemical detection method. Biopsy specimens were taken from endoscopically normal-appearing mucosa in the gastric body and antrum as well as in the duodenal bulb. Additional specimens were obtained from the outer edge of the ulcer margin in patients with active duodenal ulcer. The mean (±SD) mucosal dopamine concentrations in the gastric body and duodenum (7.6±2.8 and 6.8±2.6 pg/mg tissue) obtained from patients with inactive duodenal ulcer were significantly (P<0.05) lower than those from dyspeptic patients (13.6±6.9 and 10.9±3.5 pg/mg tissue, respectively). In contrast, no significant differences were observed in the mean norepinephrine concentrations in these gastroduodenal tissues among the three study groups. However, the mean mucosal norepinephrine concentration in the outer edge of duodenal ulcer (86.2±125.6 pg/mg tissue) was significantly (P<0.05 and 0.01) reduced as compared with that in the ulcer-free area of duodenum obtained from patients with inactive duodenal ulcer (257.1±188.2 pg/mg tissue) and from dyspeptic patients (276.8±138.3 pg/mg tissue). The results suggest that an alteration in the catecholaminergic system may be associated with one of the pathogenic factors of duodenal ulcer.This study was supported by a grant-in-aid from the Ministry of Human Health and Welfare, Tokyo.     

Doxepin in the Treatment of Duodenal Ulcer

In the double-blind study of 51 patients with duodenal ulcer the effect of doxepin and placebo was evaluated. Complete healing of the ulcer was found in 19 of 23 patients after 4 weeks of treatment with 50 mg doxepin (83%) and in 14 of 27 patients given placebo (52%) (p < 0.05). Two patients in the placebo group developed complications necessitating surgical intervention. No serious side effects were registered in the doxepin group.     

Duodenal mucosal histology and histochemistry in active, treated and healed duodenal ulcer: Correlation with duodenal prostaglandin E2 production

We investigated whether impaired duodenal mucosal prostaglandin E₂ (PGE₂) production previously observed in duodenal ulcer (DU) was a primary pathophysiological abnormality or secondary to mucosal architectural changes that accompany ulceration. One hundred patients were studied: at endoscopy, paired duodenal biopsies were taken in patients with normal endoscopies and from the ulcer edge or scar and background mucosa in active or healed DU. One of the pair of biopsies was used to estimate PGE₂ synthesis ability, the other was processed for histology and histochemistry. The following features graded: goblet cell numbers and staining with Periodic acid-Schiff reagent (PAS), epithelial staining with PAS, villous atrophy, columnar cell height, inflammatory cell infiltrate and micro-erosions and gastric metaplasia taken as a whole. Patients were found to have normal endoscopy (n= 31), active untreated DU (n= 20), active DU on treatment with either cimetidine or ranitidine (n= 13), healed DU on maintenance treatment (n= 27) and healed DU off treatment (n= 9). Active duodenal ulceration was found to be associated with decreased numbers of goblet cells, loss and blunting of villi, increased columnar cell height, increased epithelial cell PAS staining and with gastric metaplasia. After healing, only villous blunting remained. These changes were present, but less marked, at sites removed from the ulcer and were not apparent in the patient groups with healed ulcers. A strong correlation between overall gastric metaplasia and epithelial cell PAS staining and the reduced ability to synthesize PGE₂ (P < 0.001) was only apparent when biopsies from all patients were grouped together, but not within individual patient subgroups. There was no consistent correlation between PGE₂ generation and individual parameters of pathological change in the duodenum. We conclude that, although inflammatory and mucosal changes may contribute, the evidence suggests that the impaired PGE₂ generation in DU disease is, to a large extent, independent of histological and histochemical features.     

Prevention of Duodenal Ulcer Recurrence with Penicillin: A Double-Blind,Placebo-Controlled Trial

Eradication of Helicobacter pylori is associated with a reduced recurrence of duodenal ulcer (DU). The relationship between H. pylori and DU has been interpreted as causal, but the evidence has been criticized for methodologic reasons. To ascertain whether an antibiotic with no effect on epithelial-cell integrity prevents DU recurrence, we conducted a randomized double-blind trial of phenoxy-methylpenicillin (PEN), 2.4 twice daily, and placebo (PLA). Patients with an active DU and positive H. pylori culture from antral biopsy specimens were treated with 40 mg omeprazole daily for 4 weeks, but at week 2 they were allocated at random to PEN (85 patients) or PLA (85 patients) for up to 14 weeks. Those without recurrence during this treatment were followed up for another 6 months. Endoscopy and H. pylori culture were performed at the end of the treatment period and at the end of follow-up, and in between if ulcer symptoms recurred. During the treatment period the ulcer relapse rate was 5 of 58 (9%) in the PEN group and 34 of 68 (50%) in the PLA group (p < 0.0001, log-rank test), with 53% and 14%, respectively, of the patients in the two groups being H, pylori-negative. The relapse rate in the PEN group did not differ between H. pylori-negative and H. pylori-positive patients. The recurrence rate in the PEN group remained low for another 5 months but then approached the rate in the PLA group. The prevalence of H. pylori-negative patients at the end of follow-up was 20% in the PEN group and 10% in the PLA group. These data provide strong evidence that DU has a bacterial cause, with H. pylori as the likely agent.     

Prevalence of duodenal ulcer in cirrhotic males referred for liver transplantation

The prevalence of symptomatic duodenal ulcer (DU) assessed primarily in alcoholic males with cirrhosis is estimated to be approximately fivefold increased compared to the normal population. Little information is available, however, as to the prevalence of DU in nonbleeding, nonalcoholic subjects with cirrhosis. In order to estimate the prevalence of DU in males with various types of cirrhosis and its relation to the degree of portal hypertension, 216 male cirrhotic patients (165 with parenchymal liver disease and 51 with cholestatic liver disease) being evaluated for liver transplantation at the University of Pittsburgh between January 1985 and June 1987 underwent pan-upper gastrointestinal endoscopy. The prevalence of DU in each group was 7.8%. However, among the various subgroups it was as follows: chronic active hepatitis due to HBV: 9.4%, alcoholic: 12.2%, cryptogenic: 3.5%, autoimmune chronic active hepatitis: 6.6%, primary sclerosing cholangitis (PSC): 9.5%. The reference data for this study consist of data reported in the literature obtained in 355 healthy asymptomatic male volunteers. The prevalence of DU in this group is significantly less than in the study group (2.2% vs 7.8%; P<0.005). While the estimated risk for a DU is increased 3.71-fold (95% CI: 8.74, 1.57; P<0.005) in cirrhotic males in general as compared to normal males, only the subgroups with CAH due to HBV, alcoholism, and PSC were found to have an increased estimated risk of DU (all at least P<0.01). No association between the prevalence of DU and degree of portal hypertension could be demonstrated in either group.This work was supported in part by grants from NIDDK (DK32556) and from NIAAA (A06601).     

Serum pepsinogen I and pepsinogen II, and the ratio of pepsinogen I pepsinogen II in peptic ulcer diseases: With special emphasis on the influence of the location of the ulcer crater

To investigate the effect of the location of the ulcer crater on the serum levels of pepsinogen I (PGI), pepsinogen II (PGII) and the ratio of PGI/PGII, these parameters were determined in 161 healthy controls, 29 patients with gastric ulcer in the gastric body (GU-I), 65 with coexistent gastroduodenal ulcer (GU-II), 104 with gastric ulcer in the prepyloric region (GU-III), and 116 with duodenal ulcer (DU). Serum PGI levels were significantly higher (P<0.01) in patients with GU-III (110.6 ± 65.1 ng/mL), GU-II (100.0 ± 46.6 ng/mL), and DU (92.2 ± 35.2 ng/mL) than in the controls (77.4 ± 31.4 ng/mL), while there were no significant differencs between GU-I (82.5 ± 36.3 ng/mL) and the controls. Patients with gastric ulcer in any region had significantly higher (P<0.01) serum PGII levels (GU-I, 20.0 ± 15.7 ng/mL; GU-II, 15.5 ± 10.9 ng/mL; GU-III, 14.3 ± 10.0 ng/mL) than the controls (10.6 ± 6.0 ng/mL) and the patients with DU (10.0 ± 5.5 ng/mL), whereas no significant differences existed between the latter two. The ratio of PGI/PGII in GU-I (5.86 ± 3.90) was significantly lower (P<0.01) than any other group (controls, 8.83 ± 4.70; GU-II, 8.33 ± 4.99; GU-III; 9.64 ± 6.13; DU, 10.45 ± 4.49), while patients with DU it was significantly higher (P<0.01) than any other groups. These findings indicate that peptic ulcer is comprised of a heterogeneous group of diseases. A normal level of serum PGI, an increased level of PGII, and a decreased ratio of PGI/PGII in GU-I patients reflected extensive atrophic gastritis, while an elevated level of PGI, a normal level of PGII, and an increased ratio of PGI/PGII in DU patients implicated hypersecretory status coexistent with superficial fundic gastritis. These findings suggest functional heterogeneity of the gastric mucosa according to the different locations of the ulcer crater.     

腹腔镜修补术治疗老年十二指肠溃疡合并穿孔的疗效分析

目的探讨腹腔镜与开腹修补术对老年十二指肠溃疡合并穿孔(DUP)患者的疗效。方法选取2014年3月至2017年3月秭归县中医医院普外科收治的老年DUP患者100例,依据治疗方法分为腹腔镜组和开腹组,每组50例。开腹组给予开腹修补术治疗,腹腔镜组给予腹腔镜修补术治疗,比较两组疗效、并发症和胃动素水平。采用SPSS 22.0软件进行数据处理。依据数据类型,组间比较分别采用t检验和χ2检验。结果腹腔镜组下床时间[(28.87±3.07)vs(38.02±4.22)h]、住院时间[(3.69±0.82)vs(5.75±1.03)d]、肛门排气时间[(15.08±1.63)vs(27.36±2.86)h]、肠鸣音恢复时间[(64.58±6.62)vs(81.46±8.36)h]、术中出血量[(52.45±5.27)vs(76.74±8.04)ml]、并发症发生率(10.00%vs28.00%)均显著低于开腹组(P0.05)。腹腔镜组术后1 d[(182.43±19.52)vs(233.59±25.47)ng/L]和2 d[(156.37±16.24)vs(180.42±20.18)ng/L]血清胃动素水平显著高于开腹组,差异有统计学意义(P0.05)。随访3个月,腹腔镜组愈合优良率(96.00%vs 80.00%)显著高于开腹组,差异有统计学意义(P0.05)。结论与开腹修补术比较,腹腔镜修补术可有效减少老年DUP患者手术创伤及并发症的发生,有利于患者术后胃肠功能的恢复,值得临床进一步推广。     

Changing trends in peptic ulcer prevalence in a tertiary care setting in the Philippines: a seven-year study

BACKGROUND AND AIMS: The declining global prevalence of peptic ulcer disease (PUD) might be because of the decreasing prevalence of Helicobacter pylori (Hp) infection. The aims of the present study were to determine the prevalence of PUD during a 7-year period and to investigate its relationship with the prevalence of Hp infection during the same period. METHODS: All upper gastrointestinal endoscopies carried out at Santo Tomas Hospital in Manila from January 1996 to December 2002 were evaluated. Endoscopies reporting gastric ulcers (GU) and duodenal ulcers (DU) with Hp status were analyzed. RESULTS: A total of 15 341 endoscopies were evaluated. Overall, 2600 (16.95%) GU and 1575 (10.27%) DU were identified. There was a decreasing trend in the prevalence of GU (P < 0.0001) and DU (P < 0.0001) during the study period. Overall PUD prevalence declined from 35.87% in 1996 to 18.80% in 2002. This decline was seen for both GU and DU (20.05 vs 14.34%, and 15.83 vs 7.02%, respectively). The prevalence of Hp infection decreased significantly from 1996 to 2002 for both GU and DU (68.13 vs 33.48%, P < 0.0001; and 76.67 vs 36.50%, P < 0.0001, respectively). The decrease in Hp prevalence was significantly related to the decrease in ulcer prevalence (r = 0.97, P = 0.0004 for GU; r = 0.89, P = 0.0079 for DU; and r = 0.92, P = 0.0035 for all PUD). The prevalence of bleeding secondary to PUD remained stable during the 7-year period (P = 0.87). CONCLUSIONS: During the 7-year period, there was a significant decline in the prevalence of PUD. This decline in PUD prevalence was associated with a corresponding decrease in Hp prevalence.     

Cimetidine, 800 mg at Night,in the Treatment of Duodenal Ulcers

One hundred and eight patients with endoscopically proven duodenal ulcers were randomly allocated to treatment with cimetidine, either 400mg twice daily or 800 mg at night for 4 to 8 weeks in a double-blind study. There was no significant difference between the healing rates of the two groups. Thus, 45 of 52 (87%) healed on cimetidine twice daily and 43 of 51 (84%) healed on 800 mg at night after 4 weeks' treatment. The corresponding healing rates after 8 weeks were 51 of 52 (98%) and 50 of 51 (98%). The intensity of pain decreased more rapidly in the group treated with 800 mg cimetidine at night. These results indicate that 800 mg cimetidine at night is as good as 400 mg given twice daily.     

Cimetidine Reduces the Risk of Rebleeding from Duodenal Ulcers Displaying Signs of Recent Haemorrhage

The presence of endoscopic signs of recent haemorrhage (SRH) greatly increases the risk of rebleeding from peptic ulcers. Fifty-five patients with acute bleeding from chronic duodenal ulcers with SRH completed a randomized double-blind trial to assess the effect of administration of Cimetidine (800 mg daily intravenously for 2 days, then 1000 mg daily orally for 10 days in divided doses) versus placebo on rebleeding and need for emergency surgery. In the Cimetidine group (n = 29), 5 rebled, compared with 11 receiving placebo (n = 26) (p > 0.05; relative risk, 0.28, 95% confidence interval, 0.08-0.97). This reduction in rebleeding rate in the cimetidine-treated patients was observed only in subjects over 60 years of age. Fifteen patients receiving Cimetidine required blood transfusion (mean. 2.3 ± 0.6 (SEM) units per patient) compared with 19 receiving placebo (3.5 ± 0.5) (p > 0.1). Emergency surgery to arrest bleeding was required in three patients receiving Cimetidine and four receiving placebo (p > 0.5). Cimetidine therapy should be considered in patients more than 60 years old who present with haemorrhage from a chronic duodenal ulcer with SRH and who arc at high risk of rebleeding.     

Antacids in the Treatment of Duodenal Ulcer

ABSTRACT Fifty patients with endoscopically proven pyloric-prepyloric ulcers (PU/PPU) and 50 with duodenal ulcers (DU) completed a six-week double-blind clinical trial initially comprising 124 patients. The antacid-treated patients received 10 ml of an antacid suspension seven times a day (buffering 367.5 mmol acid). Healing rate after three weeks of treatment was 74% in the antacid and 42% in the placebo group (p<0.01). After six weeks the corresponding figures were 96 and 68% (p<0.001). Regarding the PU/PPU and DU subgroups we found significant differences compared to placebo in the PU/PPU group only. Antacids caused a significantly faster and more perceptible pain relief than placebo. We found no significant correlation between ulcer healing and smoking habits. Regression analyses showed that, besides antacids, ulcer size and peak acid output influenced the healing rate significantly.     

A double-blind study of misoprostol (SC-29333) in the healing of duodenal ulcer

In a double-blind randomized placebo controlled trial, 50 patients with endoscopically confirmed duodenal ulcer were treated with either misoprostol 200 micrograms or placebo in q.i.d. doses for 4-8 weeks. Of 25 patients in the placebo group, four defaulted and two were withdrawn due to worsening of symptoms. Of 25 misoprostol-treated cases, 17 cases (68%) and 21 cases (84%) healed at 4 and 8 weeks respectively, compared with three (14%) and five (24%) of the 21 placebo-treated cases (P less than 0.001). Except for diarrhoea in 2 patients in each group and itching in one with misoprostol, no serious side effects were noted.     

胃舒散联合呋喃唑酮和阿莫西林根除幽门螺杆菌阳性十二指肠溃疡及抗复发疗效观察

目的 :观察胃舒散、呋喃唑酮和阿莫西林对幽门螺杆菌 (Hp)阳性十二指肠溃疡 (DU)的疗效及根除Hp对溃疡复发的影响。方法 :73例 Hp阳性 DU患者随机分为两组 :三联组 4 1例 ,服用胃舒散 2 .0 g,呋喃唑酮 0 .1g,阿莫西林 0 .5 g,各 3次 /d ,2周后再继服胃舒散 4周。雷尼替丁组 32例 ,服用雷尼替丁 0 .15 g,3次 /d,共 6周。治疗前后均记录胃痛症状 ,内镜观察溃疡情况 ,并进行 2年随访。Hp检测采用 Warthin- Starry银染色法 ,1 4C-尿素呼气试验或快速尿素酶试验 ,2项阳性为 Hp感染 ,阴性为 Hp根除。结果 :6周治疗结束后 ,两组溃疡愈合率均为10 0 %。三联组临床症状缓解率、副反应发生率为 97.6 %和 18.8% ,雷尼替丁组为 93.8%和 9.4 % (均 P >0 .0 5 )。三联组 Hp根除率 (92 .7% )显著高于雷尼替丁组 (0 % ,P <0 .0 1)。 Hp根除的 38例中 ,1年及 2年溃疡复发率为(5 .3% ,10 .5 % )均显著低于 Hp持续感染者 (2 8.1% ,4 6 .9% ,P <0 .0 1)。结论 :以胃舒散为主的三联疗法具有疗效高、副作用少、溃疡复发率低的优点 ,是一种根除 Hp的较好方案。     

血浆胃动素水平与十二指肠球部溃疡发生与愈合的关系

本文用放免法测定了３３例十二指肠球部溃疡及３５例慢性胃炎患者血浆胃动素水平，同时检测胃粘膜ＨＰ感染情况及胃液ｐＨ值，并对其中１９例十二指肠球部溃疡患者进行抗ＨＰ二联治疗（得乐冲剂＋甲硝唑片）共６周，观察ＨＰ转阴后胃动素变化，结果表明十二指肠球部溃疡患者血浆胃动素显著高于慢性胃炎患者，分别为４４７．２３±９８．４ｎｇ／Ｌ及３５３．５±１００．２ｎｇ／Ｌ（Ｐ＜０．０１），１７例溃疡愈合者血浆胃动素显著下降，与慢性胃炎愈合者无显著性差异（Ｐ＞０．０５），而２例溃疡未愈者血浆胃动素仍持续升高，相关分析显示十二指肠球部溃疡患者血浆胃动素升高与ＨＰ感染及胃液ｐＨ值无关。本文认为十二指肠球部溃疡患者血浆胃动素升高可能是一种继发性改变，其临床意义尚有待进一步阐明。     

Antisecretory effects of three omeprazole regimens for maintenance treatment in duodenal ulcer

This study was carried out to assess the antisecretory effects and their possible changes over time of three different dose regimens of omeprazole that could be proposed for maintenance treatment in duodenal ulcer. Forty-five patients with endoscopically proven duodenal ulcer were studied by means of 24-hr gastric pH-metry both in basal conditions and on the fifth day of acute treatment with omeprazole 20 mg in the morning. Ulcers healed after four weeks (in three cases after eight weeks) and afterwards, 15 patients were randomized to receive orally at 0800 hr in single-blind fashion omeprazole 10 mg daily (group A), 15 to receive omeprazole 40 mg on Saturday and Sunday followed by a five-day period without medication (group B), and 15 to receive omeprazole 20 mg every other day (group C) for up to three months. On the 20th and 80th days of these maintenance treatments 24-hr gastric pH-metry was repeated to assess the antisecretory effectiveness of each regimen over a two-month period. In patients of group B these tests began at 1700 hr on Friday, the last of five days off treatment, and in those of group C at 1700 hr of the day off medication. All three dose regimens of omeprazole were able to raise pH values significantly (P<0.01–0.001) compared to basal levels. Omeprazole 20 mg every other day was more effective (P<0.01) than omeprazole 40 mg weekend, but did not differ significantly from omeprazole 10 mg daily. The durations of acid inhibition (pH>3.0 units/24 hr) were 12.44, 10.00, and 17.38 hr with groups A, B, and C, respectively. There was no significant difference between the pH profiles of the 20th and 80th days with every dose regimen. It is concluded that all three dose regimens of omeprazole are effective in reducing gastric acidity and their pharmacodynamic action does not change with time. Therefore they are suitable to be assessed in large clinical trials aimed at verifying the prevention of duodenal ulcer recurrence for longer periods.     

Influence of the site of a duodenal ulcer on its subsequent course

The aim of this study was to determine if the site of a duodenal ulcer influences its subsequent course. Three hundred and eighteen duodenal ulcer patients diagnosed by endoscopy in Sydney were studied. The ulcer was situated on the anterior wall of the bulb in 49% and the posterior wall of the bulb in 23%. These patients were followed up until symptoms recurred or for 1–2 years. The risk of symptom recurrence was unaffected by the site of the index ulcer, occurring in 129 of 157 patients with anterior wall ulcer (82%), 56 of 72 patients with posterior wall ulcers (78%), and 27 of 32 patients with anterior and posterior wall ulcers (84%). Sixty-four patients were endoscoped within 1 month of recurrence of ulcer-like symptoms and active ulcer craters were demonstrated in 49 (77%).     

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.     

Do clinicians accept the role of Helicobacter pylori in duodenal ulcer disease: a survey of European gastroenterologists and general practitioners

Abstract. Objectives. To examine to what extent clinicians in Europe accepted the theory of the casual role of Helicobacter pylori (H. pylori) in duodenal ulcer disease in the year 1992, and to what extent the theory had influenced their diagnostic and therapeutic habits in the management of duodenal ulcer patients at that time. Design. Postal questionnaire. Setting. Three European countries: the UK, the Netherlands, and Denmark. Subjects. Three hundred and three gastroenterologists, 250 general practitioners, 83 junior hospital doctors. Main outcome measures. Number of doctors believing H. pylori to be a significant cause of duodenal ulcer disease, use of diagnostic tests for detection of H. pylori and therapeutic regimens for eradicating H. pylori. Results. Four hundred and forty-two doctors replied. Eighty-four per cent of the British doctors, 73% of the Dutch doctors, and 47% of the Danish doctors accepted the role of H. pylori in duodenal ulcer disease. The rates were higher among gastroenterologists than among general practitioners. Eighty-four per cent of the British doctors, 80% of the Dutch doctors, and 48% of the Danish doctors used diagnostic tests for H. pylori, most frequently histological examination (64%). In patients with duodenal ulcer disease, H. pylori eradication was undertaken by 93% of the British doctors, 89% of the Dutch doctors, and 60% of the Danish doctors. A triple therapy (a bismuth salt, metronidazole, and either amoxicillin or tetracycline) was used by 57% (181/315) of the doctors. Conclusions. H. pylori treatment is frequently used in some countries. However, the role of H. pylori in duodenal ulcer disease has not been accepted to the same extent in different European countries.