幽门螺杆菌与胃食管反流病

幽门螺杆菌（Helicobacter pylori，H．pylori）与胃食管反流病（gastroesophageal reflux disease，GERD）的关系各研究结果不尽一致，流行病学研究表明，在GERD中不仅Mpylori感染率较低，而且cagA的检出率也低，二者都与食管疾病严重程度呈负相关。亦有文献报告H．pylori感染与GERD发生无明显关系。H．pylori对食管保护作用机制可能与其能提高LES压力、降低胃内酸度和影响食管对酸的敏感性有关。有研究表明，H．pylori可以提高质子泵抑制剂的抑酸效果，亦有人认为H．pylori并不影响GERD疗效。因此H．pylori与GERD的关系仍需进一步的临床和基础研究来评价。     

胃食管反流病与幽门螺杆菌感染的关系探讨

目的探讨胃食管反流病与幽门螺杆菌感染之间的相关性。方法将经过电子胃镜确诊的GERD患者120例及对照组轻度慢性浅表性胃炎患者120例予血清幽门螺杆菌抗体检测和14C呼气试验法进行H.pylori检测,对比两组H.pylori感染情况;将90例反流性食管炎患者分为LA-A、B组及LA-C、D组,对比两组H.pylori感染情况;将120例GERD患者分为轻度症状组、中度症状组、重度症状组及极重度症状组,比较组间H.pylori感染情况。结果 GERD组H.pylori感染的阳性率(39.17%)低于对照组H.pylori感染的阳性率(62.50%),差异有统计学意义(P<0.05)。LA-A、B组H.pylori感染的阳性率(60.87%)高于LA-C、D组H.pylori感染的阳性率(29.55%),差异有统计学意义(P<0.05)。轻度症状组、中度症状组、重度症状组及极重度症状组H.pylori感染的阳性率分别是40.00%、41.67%、40.63%、31.82%。结论幽门螺杆菌感染是反流性食管炎的保护因素,幽门螺杆菌感染与GERD症状的发生无相关性。     

Potential mechanism of corpus-predominant gastritis after PPI therapy in Helicobacter pylori-positive patients with GERD

The long-term use of proton pump inhibitors (PPIs) exacerbates corpus atrophic gastritis in patients with Helicobacter pylori (H. pylori) infection. To identify a potential mechanism for this change, we discuss interactions between pH, bile acids, and H. pylori. Duodenogastric reflux, which includes bile, occurs in healthy individuals, and bile reflux is increased in patients with gastroesophageal reflux disease (GERD). Diluted human plasma and bile acids have been found to be significant chemoattractants and chemorepellents, respectively, for the bacillus H. pylori. Although only taurine conjugates, with a pKa of 1.8-1.9, are soluble in an acidic environment, glycine conjugates, with a pKa of 4.3-5.2, as well as taurine-conjugated bile acids are soluble in the presence of PPI therapy. Thus, the soluble bile acid concentrations in the gastric contents of patients with GERD after continuous PPI therapy are considerably higher than that in those with intact acid production. In the distal stomach, the high concentration of soluble bile acids is likely to act as a bactericide or chemorepellent for H. pylori. In contrast, the mucous layer in the proximal stomach has an optimal bile concentration that forms chemotactic gradients with plasma components required to direct H. pylori to the epithelial surface. H. pylori may then colonize in the stomach body rather than in the pyloric antrum, which may explain the occurrence of corpus-predominant gastritis after PPI therapy in H. pylori-positive patients with GERD.     

Trends in the eradication rates of Helicobacter pylori infection for eleven years

AIM: To evaluate the trends in the eradication rate of Helicobacter pylori (H. pylori) over the past 11 years in a single center.METHODS: This retrospective study covered the period from January 2000 to December 2010. We evaluated 5746 patients diagnosed with gastric ulcers (GU), duodenal ulcers (DU), GU + DU, or nonpeptic ulcers associated with an H. pylori infection. We treated them annually with the 2 wk standard first-line triple regimen, proton pump inhibitor (PPI) + amoxicilin + clarithromycin (PAC; PPI, clarithromycin 500 mg, and amoxicillin 1 g, all twice a day). The follow-up test was performed at least 4 wk after the completion of the 2 wk standard H. pylori eradication using the PAC regimen. We also assessed the eradication rates of 1 wk second-line therapy with a quadruple standard regimen (PPI b.i.d., tripotassium dicitrate bismuthate 300 mg q.i.d., metronidazole 500 mg t.i.d., and tetracycline 500 mg q.i.d.) after the failure of the first-line therapy. Statistical analysis was performed with 95%CI for the differences in the annual eradication rates.RESULTS: A total of 5746 patients [2333 males (58.8%), 1636 females (41.2%); mean age of males vs females 51.31 ± 13.1 years vs 52.76 ± 13.6 years, P < 0.05, total mean age 51.9 ± 13.3 years (mean ± SD)] were investigated. Among these patients, 1674 patients were excluded: 35 patients refused treatment; 18 patients ceased H. pylori eradication due to side effects; 1211 patients had inappropriate indications for H. pylori eradication, having undergone stomach cancer operation or chemotherapy; and 410 patients did not undergo the follow-up. We also excluded 103 patients who wanted to stop eradication treatment after only 1 wk due to poor compliance or the side effects mentioned above. Finally, we evaluated the annual eradication success rates in a total of 3969 patients who received 2 wk first-line PAC therapy. The endoscopic and clinical findings in patients who received the 2 wk PAC were as follows: gastric ulcer in 855 (21.5%); duodenal ulcer in 878 (22.1%); gastric and duodenal ulcer in 124 (3.1%), erosive, atrophic gastritis and functional dyspepsia in 2055 (51.8%); and other findings (e.g., MALToma, patients who wanted to receive the therapy even though they had no abnormal endoscopic finding) in 57 (0.5%). The overall eradication rate of the 2 wk standard first-line triple regimen was 86.5%. The annual eradication rates from 2000 to 2010 were 86.7%, 85.4%, 86.5%, 83.3%, 89.9%, 90.5%, 88.4%, 84.5%, 89.1%, 85.8%, and 88.3%, sequentially (P = 0.06). No definite evidence of a significant change in the eradication rate was seen during the past eleven years. The eradication rates of second-line therapy were 88.9%, 82.4%, 85%, 83.9%, 77.3%, 85.7%, 84.4%, 87.3%, 83.3%, 88.9%, and 84% (P = 0.77). The overall eradication rate of 1 wk quadruple second-line therapy was 84.7%. There was no significant difference in the eradication rate according to the H. pylori associated diseases.CONCLUSION: This study showed that there was no trend change in the H. pylori eradication rate over the most recent 11 years in our institution.     

Treatment of Helicobacter pylori infection:Current status and future concepts

Helicobacter pylori(H.pylori)infection is highly associated with the occurrence of gastrointestinal diseases,including gastric inflammation,peptic ulcer,gastric cancer,and gastric mucosa-associated lymphoid-tissue lymphoma.Although alternative therapies,including phytomedicines and probiotics,have been used to improve eradication,current treatment still relies on a combination of antimicrobial agents,such as amoxicillin,clarithromycin,metronidazole,and levofloxacin,and antisecretory agents,such as proton pump inhibitors(PPIs).A standard triple therapy consisting of a PPI and two antibiotics(clarithromycin and amoxicillin/metronidazole)is widely used as the first-line regimen for treatment of infection,but the increased resistance of H.pylori to clarithromycin and metronidazole has significantly reduced the eradication rate using this therapy and bismuth-containing therapy or 10-d sequential therapy has therefore been proposed to replace standard triple therapy.Alternatively,levofloxacin-based triple therapy can be used as rescue therapy for H.pylori infection after failure of first-line therapy.The increase in resistance to antibiotics,including levofloxacin,may limit the applicability of such regimens.However,since resistance of H.pylori to amoxicillin is generally low,an optimized high dose dual therapy consisting of a PPI and amoxicillin can be an effective first-line or rescue therapy.In addition,the concomitant use of alternative medicine has the potential to provide additive or synergistic effects against H.pylori infection,though its efficacy needs to be verified in clinical studies.     

Long-term pretreatment with proton pump inhibitor and Helicobacter pylori eradication rates

AIM:To investigate whether proton pump inhibitor(PPI)pretreatment influences Helicobacter pylori eradication rate.METHODS:We retrospectively reviewed H.pylori-infected patients who were treated with a standard triple regimen(PPI,amoxicillin 1 g,and clarithromycin 500mg,all twice daily for 7 d).The diagnosis of H.pylori infection and its eradication was assessed with the rapid urease test,histological examination by silver staining,or the13C-urea breath test.We divided the patients into two groups:one received the standard eradication regimen without PPI pretreatment(Group A),and the other received PPI pretreatment(Group B).The patients in Group B were reclassified into three groups based on the duration of PPI pretreatment:Group B-Ⅰ(3-14 d),Group B-Ⅱ(15-55 d),and Group B-Ⅲ(≥56 d).RESULTS:A total of 1090 patients were analyzed and the overall eradication rate was 80.9%.The cure rate in Group B(81.2%,420/517)was not significantly different from that in Group A(79.2%,454/573).The eradication rates in Group B-Ⅰ,B-Ⅱand B-Ⅲwere80.1%(117/146),81.8%(224/274)and 81.4%(79/97),respectively.CONCLUSION:PPI pretreatment did not affect H.pylori eradication rate,regardless of the medication period.     

Esophageal Helicobacter pylori colonization aggravates esophageal injury caused by reflux

AIM: To investigate esophageal Helicobacter pylori (H. pylori) colonization on esophageal injury caused by reflux and the related mechanisms.METHODS: An esophagitis model, with acid and bile reflux, was surgically produced in male rats. The rats were randomly divided into either: (1) an esophagogastroduodenal anastomosis (EGDA) group; (2) an EGDA with H. pylori infection group; (3) a pseudo-operation with H. pylori infection group; or (4) a pseudo-operation group. All rats were kept for 36 wk. Based on the location of H. pylori colonization, the EGDA rats with H. pylori infection were subdivided into those with concomitant esophageal H. pylori colonization or those with only gastric H. pylori colonization. The esophageal injuries were evaluated grossly and microscopically. The expressions of CDX2 and MUC2 were determined by real-time polymerase chain reaction (RT-PCR) and immunohistochemistry. Ki-67 antigen expression was determined by immunohistochemistry. The mRNA levels of cyclin D1, c-Myc, Bax and Bcl-2 were determined by RT-PCR. Cell apoptosis was evaluated using the TdT-mediated dUTP nick-end labeling method.RESULTS: Esophagitis, Barrett’s esophagus (BE), and esophageal adenocarcinoma (EAC) developed in rats that underwent EGDA. When comparing rats with EGDA and concomitant esophageal H. pylori colonization to EGDA-only rats, the severity of injury (87.9 ± 5.2 vs 77.2 ± 8.6, macroscopically, 92.5 ± 8.0 vs 83.8 ± 5.5, microscopically, both P < 0.05) and the incidences of BE (80.0% vs 33.3%, P = 0.055) and EAC (60.0% vs 11.1%, P < 0.05) were increased. These increases were associated with upregulation of CDX2 and MUC2 mRNA (10.1 ± 5.4 vs 3.0 ± 2.9, 8.4 ± 4.6 vs 2.0 ± 3.2, respectively, Ps < 0.01) and protein (8.1 ± 2.3 vs 3.3 ± 3.1, 7.3 ± 4.0 vs 1.8 ± 2.7, respectively, all P < 0.05). The expression of Ki-67 (8.9 ± 0.7 vs 6.0 ± 1.7, P < 0.01) and the presence of apoptotic cells (8.3 ± 1.1 vs 5.3 ± 1.7, P < 0.01) were also increased significantly in rats with EGDA and concomitant esophageal H. pylori colonization compared with rats with EGDA only. The mRNA levels of cyclin D1 (5.8 ± 1.9 vs 3.4 ± 1.3, P < 0.01), c-Myc (6.4 ± 1.7 vs 3.7 ± 1.2, P < 0.01), and Bax (8.6 ± 1.6 vs 5.1 ± 1.3, P < 0.01) were significantly increased, whereas the mRNA level of Bcl-2 (0.6 ± 0.3 vs 0.8 ± 0.3, P < 0.01) was significantly reduced in rats with EGDA and concomitant esophageal H. pylori colonization compared with rats with EGDA only.CONCLUSION: Esophageal H. pylori colonization increases esophagitis severity, and facilitates the development of BE and EAC with the augmentation of cell proliferation and apoptosis in esophageal mucosa.     

Influence of proton pump inhibitor treatment on Helicobacter pylori stool antigen test

AIM: To investigate the effects of proton pump inhibitor (PPI) treatment on stool antigen test using the TestMate pylori enzyme immunoassay.METHODS: This study assessed 28 patients [16 men and 12 women; mean age (63.1 ± 5.9) years; range, 25-84 years] who underwent stool antigen test and urea breath test (UBT) before and after PPI administration.RESULTS: Using the UBT as the standard, the sensitivity, specificity and agreement of the stool antigen test in all 28 patients were 95.2%, 71.4%, and 89.3%, respectively, before PPI administration, and 88.9%, 90.9%, and 89.3%, respectively, after PPI treatment. Mean UBT values were 23.98% ± 5.33% before and 16.19% ± 4.75% after PPI treatment and, in 15 patients treated for ≥ 4 wk, were significantly lower after than before 4 wk of PPI treatment (12.58% ± 4.49% vs 24.53% ± 8.53%, P = 0.048). The mean optical density (A_450/630) ratios on the stool antigen test were 1.16 ± 0.20 before and 1.17 ± 0.24 after PPI treatment (P = 0.989), and were 1.02 ± 0.26 and 0.69 ± 0.28, respectively, in the group treated for > 4 wk (P = 0.099).CONCLUSION: The stool antigen test was equally sensitive to the UBT, making it a useful and reliable diagnostic method, even during PPI administration.     

The significance of cagA(+) Helicobacter pylori in reflux oesophagitis

BACKGROUND: Helicobacter pylori is a gastroduodenal pathogen associated with ulceration, dyspepsia, and adenocarcinoma. Recent preliminary studies have suggested that H pylori may be protective for oesophageal adenocarcinoma. In addition, strains of H pylori identified by the presence of the cytotoxin associated gene A (cagA) are shown to have a significant inverse association with oesophageal adenocarcinoma. Given that cagA(+) H pylori may protect against oesophageal carcinoma, these strains may be protective for oesophagitis, a precursor of oesophageal carcinoma. AIMS: The aim of this study was to investigate the association between cagA(+) H pylori and endoscopically proved oesophagitis. PATIENTS: The study group included 1486 patients attending for routine upper gastrointestinal tract endoscopy. METHODS: At endoscopy the oesophagus was assessed for evidence of reflux disease and graded according to standard protocols. Culture and histology of gastric biopsy specimens determined H pylori status. The prevalence of cagA was identified by an antibody specific ELISA (Viva Diagnostika, Germany). RESULTS: H pylori was present in 663/1485 (45%) patients and in 120/312 (38%) patients with oesophagitis. Anti-CagA antibody was found in 499/640 (78%) H pylori positive patients. Similarly, anti-CagA antibody was found in 422/521 (81%) patients with a normal oesophagus and in 42/60 (70%) with mild, 24/35 (69%) with moderate, and 11/24 (46%) with severe oesophagitis. The risk of severe oesophagitis was significantly decreased for patients infected with cagA(+) H pylori after correction for confounding variables (odds ratio 0.57, 95% confidence interval 0.41-0.80; p=0.001). CONCLUSIONS: These results suggest that infection by cagA(+) H pylori may be protective for oesophageal disease.     

胃食管反流病与幽门螺杆菌感染的关系探讨

为了探讨胃食管反流病(GERD)与幽门螺杆菌(Helicobacter pylori, H.pylori)感染的关系,我们将经过电子胃镜确诊的GERD患者115例及对照组轻度慢性浅表性胃炎患者90例予活检胃窦组织快速尿素酶法及14C呼气试验法进行H.pylori检测,对比两组H.pylori感染情况.结果 显示:115例GERD组H.pylori感染率为37.39%,90例对照组H.pylori感染率为62.22%,GERD组H.pylori感染率明显低于对照组,有显著性差异(P＜0.01).     

胃食管反流病与幽门螺杆菌及胃排空关系的研究

目的探讨幽门螺杆菌(H.pylori)与胃食管反流病(GERD)的关系,以及H.pylori对GERD患者胃动力的影响。方法按中华医学会的GERD诊断标准,确诊GERD患者200例,进行胃镜、胃排空时间及H.pylori检查,依据洛杉矶分级将反流性食管炎(RE)分为A、B、C、D四级,200例无消化道症状的健康体检者作为对照组,进行H.pylori检查。结果 GERD组的感染率明显低于对照组(P<0.05),反流性食管炎(RE)的炎症程度与H.pylori的感染率呈负相关,GERD患者中H.pylori阳性组和H.pylori阴性组间胃排空情况无统计学差异(P>0.05)。结论 H.pylori可能对GERD有潜在的保护作用;RE炎症程度越重,H.pylori感染率越低;H.pylori不影响GERD患者的胃动力。     

Evidence-based assessment of proton-pump inhibitors in Helicobacter pylori eradication: A systematic review

Peptic ulcer disease continues to be issue especially due to its high prevalence in the developing world. Helicobacter pylori (H. pylori) infection associated duodenal ulcers should undergo eradication therapy. There are many regimens offered for H. pylori eradication which include triple, quadruple, or sequential therapy regimens. The central aim of this systematic review is to evaluate the evidence for H. pylori therapy from a meta-analytical outlook. The consequence of the dose, type of proton-pump inhibitor, and the length of the treatment will be debated. The most important risk factor for eradication failure is resistance to clarithromycin and metronidazole.     

非糜烂性胃食管反流病与幽门螺杆菌感染的相关性研究

目的探讨非糜烂性胃食管反流病(non-erosive gastroesophageal reflux disease,NERD)与幽门螺杆菌(Helicobacter pylori,H.pylori)感染的关系。方法将确诊为军人NERD患者156例(A组)、军人慢性浅表性胃炎患者120例(B组)和军人十二指肠球部溃疡患者60例(C组),予活检胃窦组织快速尿素酶法及14C呼气试验法进行H.pylori检测;比较A组与B组、C组H.pylori感染情况。结果 A组H.pylori感染率12.82%,B组H.pylori感染率68.33%,C组H.pylori感染率85.00%,A组感染率明显低于B组、C组,差异均有显著统计学意义(P0.01)。结论 NERD发生时,H.pylori感染几率明显减小。     

Helicobacter pylori and skin autoimmune diseases

Autoimmune skin diseases are characterized by dysregulation of the immune system resulting in a loss of tolerance to skin self-antigen(s). The prolonged interaction between the bacterium and host immune mechanisms makes Helicobacter pylori(H. pylori) a plausible infectious agent for triggering autoimmunity. Epidemiological and experimental data now point to a strong relation of H. pylori infection on the development of many extragastric diseases, including several allergic and autoimmune diseases. H. pylori antigens activate cross-reactive T cells and induce autoantibodies production. Microbial heat shock proteins(HSP) play an important role of in the pathogenesis of autoimmune diseases because of the high level of sequence homology with human HSP. Eradication of H. pylori infection has been shown to be effective in some patients with chronic autoimmune urticaria, psoriasis, alopecia areata and Schoenlein-Henoch purpura. There is conflicting and controversial data regarding the association of H. pylori infection with Beh et’s disease, scleroderma and autoimmune bullous diseases. No data are available evaluating the association of H. pylori infection with other skin autoimmune diseases, such as vitiligo, cutaneous lupus erythematosus and dermatomyositis. The epidemiological and experimental evidence for a possible role of H. pylori infection in skin autoimmune diseases are the subject of this review.     

Inverse background of Helicobacter pylori antibody and pepsinogen in reflux oesophagitis compared with gastric cancer: analysis of 5732 Japanese subjects

BACKGROUND: The relationship between Helicobacter pylori and reflux oesophagitis remains controversial. AIMS: To evaluate the relationship between H pylori and reflux oesophagitis in a large number of Japanese subjects. SUBJECTS: A total of 5732 consecutive Japanese subjects during a health screening were enrolled. METHODS: Gastrointestinal endoscopy was performed on all subjects. We simultaneously measured serum anti-H pylori antibody and pepsinogen as markers of H pylori infection together with gastric atrophy. The risk of reflux oesophagitis was evaluated in relation to these markers, and the results were compared with those of gastric cancer. RESULTS: Reflux oesophagitis was found in 108 subjects. Both positivity for H pylori antibody (adjusted odds ratio (OR) 0.67 (95% confidence interval 0.45-1.0)) and "low" pepsinogen indicating gastric atrophy (OR 0.35 (0.18-0.68)) were negatively associated with reflux oesophagitis. After subjects were classified into four groups based on positivity or negativity for H pylori antibody and "low" pepsinogen, the prevalence of reflux oesophagitis showed a decreasing trend as H pylori induced gastric atrophy became more severe. The risk of gastric cancer showed an increasing trend, exactly the opposite to that of reflux oesophagitis. CONCLUSIONS: Analysis of a large series of Japanese subjects revealed a decreasing prevalence of reflux oesophagitis in conjunction with progress of gastric atrophy induced by H pylori infection. This pattern was completely opposite to that of gastric cancer cases. A protective role of H pylori for reflux oesophagitis through the development of gastric atrophy has been suggested.     

难治性胃食管反流病诊断方法的研究进展

众多学者把质子泵抑制剂(proton pump inhibitors,PPIs)治疗不应答的胃食管反流病(gastroesophageal reflux disease,GERD)称为难治性胃食管反流病,本病是当前消化系统疾病谱中最为顽固的治疗难题之一.近年来众多研究者运用多种诊察手段来研究本病,希望找到该病的发病机制.本文就最近国内外有关难治性GERD的诊断方案,发病机制及相关研究结果等内容作一综述.     

Clinical significance of Helicobacter pylori cagA and iceA genotype status

AIM:To study the presence of Helicobacter pylori(H.pylori) virulence factors and clinical outcome in H.pylori infected patients.METHODS:A prospective analysis of ninety nine H.pylori-positive patients who underwent endoscopy in our Endoscopy suite were included in this study.DNA was isolated from antral biopsy samples and the presence of cagA,iceA,and iceA2 genotypes were determined by polymerase chain reaction and a reverse hybridization technique.Screening for H.pylori infection was performed in all patie...     

Development of reflux esophagitis following Helicobacter pylori eradication

Background We aimed to determine the incidence and causative factors of reflux esophagitis following Helicobacter pylori eradication in Japanese patients. Methods In patients in whom reflux esophagitis could not be detected endoscopically, we conducted an annual follow-up observation in 326 H. pylori-cured patients, 199 H. pylori-positive patients, and 151 H. pylori-negative patients, to study the incidence and causative factors of reflux esophagitis. Results Development of reflux esophagitis was observed in 74 (22.7%) of the H. pylori-cured patients during a median follow-up period of 6.0 years, in 16 (8.0%) of the H. pylori-positive patients during a median follow-up period of 5.0 years, and in 29 (19.2%) of the H. pylori-negative patients during a median follow-up period of 5.4 years. The results, after correction for sex and age, showed that H. pylori-cured patients had a significantly higher risk of reflux esophagitis than H. pylori-positive patients (risk ratio, 2.43; P < 0.01), but their risk did not differ from that in the H. pylori-negative patients. It was also shown that hiatal hernia (risk ratio, 4.01; P < 0.01) and smoking history (risk ratio, 1.77; P < 0.05) were significant risk factors for the development of reflux esophagitis. Conclusions With regard to the development of reflux esophagitis following H. pylori eradiation therapy, we observed that the frequency was higher in H. pylori-cured patients than in H. pylori-positive patients, but the frequency in H. pylori-cured patients and H. pylori-negative patients was the same. We elucidated that hiatal hernia and smoking history are important risk factors for reflux esophagitis.     

The Influence of CYP2C19 Polymorphism on Eradication of Helicobacter pylori: A Prospective Randomized Study of Lansoprazole and Rabeprazole

Background/Aims

The CYP2C19 polymorphism plays an important role in the metabolism of various proton-pump inhibitors. Several trials have produced conflicting data on eradication rates of Helicobacter pylori (H. pylori) among CYP2C19 genotypes. We investigated whether the CYP2C19 genotype affects the eradication rate of H. pylori by direct comparing the effects of lansoprazole- and rabeprazole-based triple therapies.

Methods

A total of 492 patients infected with H. pylori was randomly treated with either 30 mg of lansoprazole or 20 mg of rabeprazole plus 500 mg of clarithromycin and 1,000 mg of amoxicillin twice daily for 1 week. CYP2C19 genotype status was determined by a PCR-restriction-fragment-length polymorphism method. After 7 to 8 weeks, H. pylori status was evaluated by a C¹³-urea breath test.

Results

Four hundred and sixty-three patients were analyzed, and the eradication rate was 75.2% in a per-protocol analysis. Eradication rates for the lansoprazole regimen (n=234) were 73.8%, 80.7%, and 85.4% in the homozygous extensive (HomEM), heterozygous extensive (HetEM), and poor metabolizers (PM) groups, respectively (p=0.303). In the case of the rabeprazole regimen (n=229), the eradication rates were 68.6%, 73.0%, and 71.9% in the HomEM, HetEM, and PM groups, respectively (p=0.795).

Conclusions

The efficacies of triple therapies that include lansoprazole or rabeprazole are not affected by CYP2C19 genetic polymorphisms.