Helicobacter pylori eradication improves gastric histology and decreases serum gastrin, pepsinogen I and pepsinogen II levels in patients with duodenal ulcer

Background and Aim: The aim of this study was to assess the gastric histopathology and serum gastrin‐17 and pepsinogens profiles in patients with duodenal ulcer before and after Helicobacter pylori eradication in a population with a very high prevalence of H. pylori. At the same time we assessed the role of H. pylori density on these variables. Methods: Eighty Caucasian patients with H. pylori–associated duodenal ulcer before treatment and 1 year after randomized eradication were studied. Among patients with unsuccessful eradication two groups were distinguished according to the data obtained after treatment: the group with negative rapid urease test and decreased bacterial density according to morphological score (partial elimination group); the group with positive rapid urease test and high bacterial density (failed eradication group). Results: One year after successful eradication, serum levels of gastrin‐17, pepsinogen I and pepsinogen II decreased. Similar changes of serum pepsinogen I and pepsinogen II levels were observed in patients with partial elimination of H. pylori infection. In the group with successful eradication, inflammation, activity, atrophy and number of lymphoid follicles in the antral mucosa fell. In the group with partial elimination, antral mucosa activity and H. pylori score reduced. Other morphological changes were statistically non‐significant. Conclusion: Patients with duodenal ulcer after successful eradication have improvement of morphological and functional characteristics of gastric mucosa.     

Relapsed duodenal ulcer after cure of Helicobacter pylori infection

We report a patient—a 42-year-old man—who had suffered from recurrent duodenal ulcer for about 20 years. Successful curative therapy for Helicobacter pylori infection was performed for 2 weeks with new triple omeprazole, anoxicillin, clarithromycin (OAC) treatment in October 1995, and cure of the infection was repeatedly confirmed by histology, culture, and the ¹³C urea breath test. One month after the curative therapy, recurrence of a small duodenal ulcer was observed and in February another duodenal ulcer and reflux esophagitis occurred, with severe symptoms, despite the continuous administration of ranitidine. None of the examinations to reconfirm cure of the infection revealed the presence of H. pylori. As the patient experienced continual psychological stress and smoked more frequently during the recurrent episode and had not used nonsteroidal anti-inflammatory drugs, stress and smoking appeared to play important roles in the relapse of duodenal ulcer in this patient after cure of H. pylori infection. (Received Aug. 18, 1997; accepted Jan. 23, 1998)     

Effect of Helicobacter pylori eradicated therapy on water gastric emptying in patients with active duodenal ulcer

BACKGROUND AND AIMS: It remains debatable if duodenal ulcer (DU) or Helicobacter pylori infection has a definite impact on human gastric emptying (GE). We explored the nature of water GE in active DU patients before and after ulcer healing and the influence of H. pylori eradication on GE. METHODS: A home made applied potential tomography (APT) was used to measure liquid GE. Twelve electrodes were placed in a circular array around the upper abdomen of studied subjects. After drinking 500 mL of ion-free water, paired electrodes injected electrical current and the remaining 10 electrodes recorded signals, one-by-one in a rotating order. Based on tomographical calculation, the serial changes of averaged signals from altered resistivities were constructed to display GE. Initially, 64 H. pylori infected active DU patients were enrolled. After APT measurement, one-week triple therapy (omeprazole, amoxicillin and clarithromycin) was dispensed. Patients were asked back to determine ulcer/H. pylori status and GE on a scheduled date 3 months later. Finally, 58 patients finished the trial with valid and readable GE data obtained. RESULTS: The ulcer healing and H. pylori eradicated rates were 91.4% and 82.8%, respectively. In general, liquid GE was prolonged in all DU patients at follow up. Of 48 eradicated patients, 35.4% manifested either enhanced or delayed GE before treatment, whereas only five (10.4%) had abnormal GE after treatment (P < 0.0001). In contrast, this characteristically normalized GE was not found in non-eradicated patients. CONCLUSIONS: Water GE of active DU patients ranges from enhanced to delayed, while an effective H. pylori triple therapy is useful not only for healing ulcers, but also for restoring abnormal GE.     

Patients with Helicobacter pylori positive and negative duodenal ulcers have distinct clinical characteristics

AIM: To assess the clinical characteristics of Helicobacter pylori (H pylori) negative duodenal ulcer. METHODS:Patients with an endoscopic diagnosis of duodenal ulcer between 1996 and 2002 were included in the present study. Patients were considered to be negative for H pylori, if both histological examination and rapid urease test of biopsy specimens were negative. A comparison was made between patients with H pylori positive and negative duodenal ulcers. RESULTS: A total of 1 343 patients were studied. Their mean age was 54.7±0.5 years. There was a male preponderance (M:F=2.5:1). Three hundred and ninety-eight patients (29.6%) did not have H pylori infection. The annual proportion of patients with H pylori negative duodenal ulcers increased progressively from 1996 to 2002. On multivariate analysis, patients with H pylori negative duodenal ulcer were more likely to be older, have concomitant medical problem, pre-existing malignancy, recent surgery, underlying sepsis, or taken non-steroidal anti-inflammatory drugs. In terms of clinical presentations, patients with H pylori negative duodenal ulcer were more likely to present with bleeding, multiple ulcers and larger ulcers. CONCLUSION:The proportion of patients with H pylori negative duodenal ulcers is on the rise because of a continued drop in incidence of H pyloripositive duodenal ulcers in recent years. Such patients have distinct clinical characteristics and it is important to ascertain the H pylori status before starting eradication therapy.     

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.     

Prevalence of Helicobacter pylori infection in duodenal ulcer and gastro‐duodenal ulcer diseases in Taiwan

Background and Aim: The prevalence of Helicobacter pylori‐negative duodenal ulcer (DU) is increasing in Western countries but is rare in Japan. We aimed to examine the prevalence of H. pylori infection and the characteristics in DU and gastro‐duodenal ulcer (GDU) diseases in Taiwan. Study: All patients with an endoscopic diagnosis of DU or GDU from September 2003 to May 2004 at Taipei Veterans General Hospital were included. Rapid urease test was done for all patients, while urea breath test was carried out on those with negative rapid urease tests. A patient was considered infected if either test was positive. Results: The prevalence of H. pylori was 88.7% (555/626) in DU and 90.5% (95/105) in GDU patients. There was no difference in sex and prevalence of H. pylori between the two groups but age was higher in the GDU patients (60.1 ± 15.5 vs. 55.4 ± 15.5, P = 0.005). Of H. pylori‐negative DU patients, 28.2% (20/71) reported using non‐steroidal anti‐inflammatory drugs (NSAIDs)/aspirin, which were used by all 10 H. pylori‐negative GDU patients (100%) (P < 0.001). There was no difference in sex and age between H. pylori‐positive and negative DU patients. The prevalence rate of H. pylori in DU was not statistically different among outpatients, inpatients, and physical check‐up subjects (86.8% vs. 93.3% vs. 90.7%, P = 0.163). Conclusion: The prevalence of H. pylori infection in DU appears to be decreasing in Taiwan. Thus, eradication therapy without confirming the presence of H. pylori in DU patients cannot be recommended. NSAIDs/aspirin is the major risk factor for H. pylori‐negative DU patients, especially those with co‐morbid gastric ulcer.     

Helicobacter pylori in duodenal ulcer patients with idiopathic gastric acid hypersecretion

Thirty-three consecutive patients with idiopathic gastric acid hypersecretion (defined as a basal acid output >10.0 meq/hr with a normal fasting serum gastrin level and negative secretin stimulation test) who were being treated for duodenal ulcer disease and other acid-peptic disorders were evaluated for the presence ofHelicobacter pylori by means of a rapid urease test. Fourteen patients had duodenal ulcer and 19 had other acid-peptic disorders (gastroesophageal reflux in 14, including six with Barrett's esophagus; four with nonulcer dyspepsia; and one with erosive gastritis).Helicobacter pylori was present in 12 of the 14 ulcer patients (86%) compared to only two of the 19 nonulcer patients (11%) (P<0.0001). The distribution of basal acid output for patients with duodenal ulcer was similar to that for nonulcer patients, and no significant difference in the mean basal acid output was found amongHelicobacter pylori-positive compared toHelicobacter pylori-negative patients. Seven of the duodenal ulcer patients with a basal acid output greater than 15.0 meq/hr wereHelicobacter pylori-positive, suggesting that the organism can withstand even extreme levels of gastric acidity. In conclusion, this study demonstrates that the prevalence ofHelicobacter pylori infection in patients with duodenal ulcer disease associated with idiopathic gastric acid hypersecretion is not different from a majority of ulcer patients with normal acid secretory profiles and offers additional evidence that extreme levels of gastric acid are not bactericidal for the organism.     

内镜对十二指肠溃疡幽门螺杆菌感染的预测

目的 分析内镜下十二指肠溃疡对H.pylori感染的预测价值。并评价对十二指肠溃疡病人予经验性根除H.pylori治疗的合理性。方法 以盲法比较311例病人胃粘膜病变与H.pylori感染的关系,H.pylori感染以胃粘膜Giemsa染色和^14C-尿素呼吸试验确定,选择十二指肠溃疡作为H.pylori感染的预测指标并计算敏感性、特异性、预测值和似然比。结果 311例病人H.pyloi感染162例,H.pylori感染者十二批肠溃疡发生率显著高于H.pylori阴性之者（21.6%vs4.7%)。以十二指肠溃疡预测H.pylori感染其行异性、阳性预测值和阳性似然比分别为95.3%(C191.9-98.7%)、83.3%(C172.0-94.6%)和4.59。结论 内镜下十二指肠小疡对H.pylori感染具有较高的阳性预测价值;建议临床对十二指肠溃疡病人应于内镜诊断后即直接予经验性根除H.pylori治疗。     

幽门螺杆菌根除后再感染与溃疡复发

目的明确广州地区十二指肠溃疡患者幽门螺杆菌（Ｈｐ）根除后再感染和溃疡复发情况。方法以１４Ｃ－尿素呼气试验和胃镜检查（尿素酶、组织学及细菌培养），对十二指肠溃疡患者Ｈｐ根除后共１８４例进行２年定期随访，并配合随机引物扩增的ＤＮＡ多态指模技术鉴定Ｈｐ菌株复发与再感染。结果Ｈｐ根除后第１、２年再感染率分别为１．１０％和０．５６％；溃疡复发率分别为２．７２％和０．５６％；全部病例未发生溃疡出血，而同期Ｈｐ未根除的对照组２年溃疡累积再出血率为２６．９％（Ｐ＜０．００５）。结论成人患者Ｈｐ根除后对Ｈｐ再感染不易感，而且发展中国家Ｈｐ根除后再感染率也相当低，以预防溃疡复发为目的的Ｈｐ根除疗法同样适用于高Ｈｐ感染率地区。     

幽门螺杆菌阳性十二指肠溃疡患者表皮生长因子分泌减少的意义(英文)

目的检测胃液和唾液表皮生长因子、胃泌素和生长抑素浓度的变化并评价表皮生长因子分泌减少在幽门螺杆菌（Ｈｐ）阳性十二指肠溃疡发病中的意义．方法１４例健康人、２７例慢性胃炎和１２例十二指肠溃疡．用尿素酶试验、组织学检查和细菌培养判断Ｈｐ感染状态．胃液和唾液表皮生长因子、胃泌素和生长抑素的检测用放免法．结果Ｈｐ阳性的慢性胃炎和十二指肠溃疡患者胃液中胃泌素的浓度高于健康人（Ｐ＞００５），但生长抑素的浓度却显著低于对照组．另外，Ｈｐ感染的十二指肠溃疡患者胃液和唾液中ＥＧＦ的浓度（ｎ＝１０，２７２０ｎｇ／Ｌ±９６３ｎｇ／Ｌ和８３ｎｇ／Ｌ±２４ｎｇ／Ｌ）显著低于健康人（ｎ＝１２，４０５６ｎｇ／Ｌ±３５６ｎｇ／Ｌ和２２０ｎｇ／Ｌ±１７０ｎｇ／Ｌ）和Ｈｐ阳性的慢性胃炎患者（ｎ＝２５，４２３０ｎｇ／Ｌ±１０４０ｎｇ／Ｌ和２２０ｎｇ／Ｌ±１１１ｎｇ／Ｌ）（Ｐ＜００５）．结论ＥＧＦ的分泌减少可能在Ｈｐ阳性十二指肠溃疡发病中起着重要作用．     

Dyspepsia and Helicobacter pylori in Japanese employees with and without ulcer history

In a Dutch working population, the apparent association between dyspeptic symptoms and Helicobacter pylori infection was found to be entirely due to subjects with an ulcer history. In general populations with a much higher prevalence of H. pylori infection and peptic ulcer disease, such as in Japan, the relationship between dyspepsia and H. pylori has yet to be clarified. A questionnaire on ulcer history and dyspeptic symptoms during the preceding 3 month period was obtained from apparently healthy Japanese employees who underwent a periodic medical examination. In addition, serum samples were analysed for anti-H. pylori IgG antibodies. A total of 196 men and 35 women, aged 23–71 years, participated in the study. Seven women (20%) and 49 men (25%) had a diagnosis of peptic ulcer disease. Among 41 subjects with verified duodenal (26) and/or gastric (17) ulcer, 95% were H. pylori positive while 32% had had frequent dyspeptic symptoms in the 3 months prior to the study (29% of the 35 men and 50% of the 6 women). Among the 147 men and 28 women without an ulcer history, the 3 month period prevalence of frequent dyspepsia was 14 and 32%, respectively. The rate of H. pylori positivity was 80% in non-ulcer dyspeptics and 68% in all other non-ulcer subjects (95% confidence intervals: 61–92 and 61–76%, respectively). Significant differences in symptoms between H. pylori positive and negative subjects could not be detected, neither in the whole population nor in the non-ulcer group. In conclusion, in this Japanese working population, no association was found between dyspeptic symptoms and H. pylori infection, irrespective of the inclusion of subjects with a peptic ulcer history.     

广州胃病患者幽门螺杆菌多株感染的研究

目的了解我国Ｈｐ感染人群中的多株感染状况．方法取因上腹不适行内镜检查的２０例Ｈｐ阳性患者（胃溃疡６例,十二指肠溃疡８例,慢性胃炎６例）的胃窦和胃体粘膜组织,进行Ｈｐ培养．初代培养后,分别取胃窦和胃体各１０个菌落进行传代,抽提各菌落ＤＮＡ,应用聚合酶链反应随机引物扩增的ＤＮＡ多态指模技术［ＲＡＰＤＰＣＲ］进行菌株鉴定．结果ＰＣＲ扩增产物电泳分析显示有１８例患者胃窦和胃体的ＨｐＤＮＡ指模一致,提示这１８例患者均是单株感染;另有２例胃体菌株表现为两种指模形态,提示为２株Ｈｐ感染．结论广州地区存在Ｈｐ多株感染,但不普遍．     

How does Helicobacter pylori cause duodenal ulcer disease: The bug, the host, or both?

Abstract Helicobacter pylori infection is the most common cause of duodenal ulcer disease, yet duodenal ulcer is an uncommon outcome of H. pylori infection. We reviewed the possible explanations such as differences in the host or in the strain of H. pylori. Host factors reviewed included genetic susceptibility to H. pylori infection and excess gastric acid secretion. The role of potential H. pylori virulence factors not present in all strains such as the cagA gene and the results of other molecular methods to identify disease-specific differences among isolates was also reviewed. Although cure of H. pylori infection resolves gastrin releasing peptide stimulated acid secretion there was no change in parietal cell mass. Twin studies have shown genetic differences in H. pylori susceptibility. There was no difference in the prevalence of the cagA gene between H. pylori infected asymptomatic volunteers and duodenal ulcer patients ( P = 1.0). DNA-DNA hybridization of whole genomic DNA in solution and cluster analysis of rep-PCR genomic DNA fingerprints suggest that isolates from patients with duodenal ulcer disease are different from those obtained from individuals with asymptomatic gastritis. Cluster analysis of the rep-PCR DNA fingerprints revealed two major groups of the strains; one set consisted of strains from patients with duodenal ulcer disease and the second cluster consisted largely of strains from individuals with asymptomatic gastritis. Recent molecular studies suggest that disease-specific cell lineages or strains may exist among H. pylori isolates leading to the various outcomes observed in patients with H. pylori infection.     

血清胃蛋白酶原和胃泌素检测对幽门螺杆菌相关十二指肠溃疡的意义

目的测定十二指肠溃疡(DU)患者血清胃蛋白酶原PGⅠ、PGⅡ、PGⅠ/PGⅡ、血清胃泌素-17(G-17),分析胃肠肽类激素与幽门螺杆菌(Hp)引起的DU的相关性。方法选取胃镜检查确诊的患者306例,分成Hp阳性、Hp阴性DU组,Hp阳性、Hp阴性浅表性胃炎组,Hp阳性、Hp阴性萎缩性胃炎组,以ELISA检测血清PG和G-17含量。结果 Hp阳性DU组血清PGⅠ较慢性萎缩性胃炎和慢性浅表性胃炎Hp阳性组显著升高,差异有统计学意义(P均<0.05);Hp阴性DU组血清PGⅠ较萎缩性胃炎和慢性浅表性胃炎Hp阴性组明显升高,差异有统计学意义(P均<0.05)。DU各组PGⅠ/PGⅡ比值与慢性浅表性胃炎各组比较,差异有统计学意义(P均<0.05)。结论 Hp阳性DU患者血清PGⅠ和G-17升高;血清PGⅠ和G-17含量对分析胃肠肽类激素与Hp引起的DU以及症状程度和疗效评价有较好的参考价值。     

Duodenal gastric metaplasia and Helicobacter pylori infection in high and low duodenal ulcer-prevalent areas in India

Background: Previous reports, based on surgery, showed duodenal ulcer (DU) to be more common in the rice‐eating areas of southern India than in the northern wheat‐eating areas. Aims: Does this difference persist? Can it be explained by risk factors other than diet? Methods: A total of 20 053 records from patients undergoing endoscopy for dyspepsia, and 590 endoscopy patients from two northern and two southern centers in India were studied prospectively. Records were scrutinized to determine the relative incidence of DU and non‐ulcer dyspepsia in wheat‐ and rice‐eating areas. Age, sex, length of history, smoking and medication were recorded. Three antral biopsies and one from each duodenal quadrant were taken. A rapid urease test was carried out on one of the antral biopsies; the others were examined for Helicobacter pylori, gastritis, duodenitis and duodenal gastric metaplasia. Results: The difference in diet‐associated prevalence persisted. No differences in smoking, Helicobacter pylori infection or duodenal gastric metaplasia were found between the two regions, but all three were more common in DU than in non‐ulcer dyspeptic patients from both dietary areas. Conclusions: The dietary differences between the regions remain the only factor to account for the differences in DU prevalence. A strong interrelationship between duodenal gastric metaplasia and cigarette smoking is demonstrated.     

High acid secretion may protect the gastric mucosa from injury caused by ammonia produced by Helicobacter pylori in duodenal ulcer patients

The aim of the present study was to investigate the mechanism by which gastric atrophy does not tend to occur in patients with duodenal ulcer despite frequent Helicobacter pylori infection. This investigation was performed in 60 patients with duodenal ulcer and 63 age-matched gastritis patients. Endoscopic findings in the antrum and corpus were classified as normal, atrophic and superficial changes. Biopsy specimens were taken from the antrum and corpus. Ninety per cent of patients with duodenal ulcer and 63.5% of patients with gastritis had H. pylori infection (P<0.01). The incidence of normal findings in duodenal patients was 30% in antral regions and 50% in the corpus (P<0.05). Atrophic change was observed in 21.7% of patients in the antrum and 3.3% of patients in the corpus (P<0.01). The grade of inflammation in duodenal ulcer specimens was significantly higher in the antrum than in the corpus (P<0.01). >H. pylori density was significantly higher in the antrum than in the corpus in ulcer patients (P<0.01). No significant difference in endoscopic findings, >H. pylori density or the grade of inflammation was found between the antrum and corpus in patients with gastritis. The mean intragastric ammonia concentration was 10.3 mg/dL in duodenal ulcer patients and 6.2 mg/dL in gastritis patients (P<0.01). The mean pH was 3.5 and 4.6 in ulcer and gastritis specimens, respectively (P<0.01). Our data suggest that gastric mucosa injury is less frequently associated with duodenal ulcers than with gastritis due to the low >H. pylori density in the corpus and to the higher acid output that neutralizes the ammonia produced by H. pylori.     

A cost-effectiveness study on treatment of duodenal ulcer

ＡｃｏｓｔｅｆｅｃｔｉｖｅｎｅｓｓｓｔｕｄｙｏｎｔｒｅａｔｍｅｎｔｏｆｄｕｏｄｅｎａｌｕｌｃｅｒＣＨＥＮＳｈｉＹａｏ，ＷＡＮＧＪｉＹａｏ，ＣＨＥＮＪｉｅ，ＺＨＡＮＧＸｉＤｅａｎｄＺＨＡＮＧＳｈａｎＳｈｅｎＤｅｐａｒｔｍｅｎｔｏｆＧａｓｔｒｏ...     

Response of blood endothelin-1 and nitric oxide activity in duodenal ulcer patients undergoing Helicobacter pylori eradication

AIM: To investigate the effect of Helicobacter pylori eradication on endothelin-1 (ET-1) and nitric oxide (NO) in duodenal ulcer (DU) patients. METHODS: Sixty-six Hpylori-infected active DU patients were consecutively enrolled to receive one-week triple therapy (rabeprazole, amoxicillin and metronidazole) and then one-month rabeprazole therapy. They were asked back to determine ulcer and Hpylori status using endoscopy one month later. Thirty-seven healthy controls (H pylori +/-:17/20) were enrolled for comparison. Blood samples were collected in each visit to measure plasma ET-1 and nitrate/nitrite levels using an enzyme immunoassay kit. RESULTS: Sixty DU patients finished trial per protocol. The ulcer healing and Hpylori-eradication rates were 86.7% and 83.3%, respectively. Plasma ET-1 level in DU patients was higher than that of Hpylori-negative and positive controls (3.59±0.96 vs0.89±0.54 vs0.3±0.2 pg/mL,P<0.01), while nitrate/nitrite levels among them were also significantly different (8.55±0.71 vs5.27±0.68 vs 6.39±0.92 μmol/L, P<0.05). H pylori eradication diminished ET-1 levels (3.64±0.55 vs2.64±0.55 pg/mL, P<0.01) but elevated nitrate/ nitrite level (8.16±0.84 vs11.41±1.42 umol/L,P<0.05). CONCLUSION: Both plasma ET-1 and nitrate/nitrite levels increase in active DU patients. After an effective H pylori eradication, DU healing is associated with diminished blood ET-1 level and elevated nitrate/nitrite level.     

Association of the CagA status of Helicobacter pylori and serum levels of interleukin (IL)‐17 and IL‐23 in duodenal ulcer patients

OBJECTIVE: It has been reported that the cytotoxin‐associated gene A (cagA+) H. pylori strains induce severe gastric mucosal inflammation. The aim of this study was to investigate the association of the virulence factor CagA with IL‐17 and IL‐23 serum levels in duodenal ulcer (DU) patients and H. pylori‐infected asymptomatic (AS) carriers. METHODS: In total, 45 H. pylori‐infected DU patients were enrolled to study: 23 tested positive for the anti‐CagA antibody (anti‐CagA+) and 22 tested negative for the anti‐CagA antibody (anti‐CagA‐), 30 were AS carriers (15 were anti‐CagA+ and 15 were anti‐CagA‐) and 15 were healthy uninfected participants (as a control group). The IL‐17 and IL‐23 serum levels of participants were measured by enzyme‐linked immunosorbent assay method. RESULTS: The mean IL‐17 levels in DU patients were significantly higher than those in AS and control groups (P < 0.001 and P < 0.0001 respectively). In the DU group, the mean IL‐17 levels in participants testing positive for anti‐CagA (10.84 ± 5.79 pg/mL) were significantly higher than those observed in participants testing negative for anti‐CagA (7.65 ± 4.74 pg/mL; P < 0.05). The mean IL‐23 levels in the DU and AS groups were significantly higher than in the control group (P < 0.02 and P < 0.03 respectively) but were not significantly different in participants testing positive and negative for anti‐CagA. CONCLUSION: These results showed higher IL‐17 and IL‐23 serum levels in H. pylori‐infected participants than in the control group. In the DU group the expression of IL‐17 was influenced by the CagA factor.