Helicobacter pylori and Bleeding Duodenal Ulcer: Prevalence of the Infection and Role of Non-steroidal Anti-inflammatory Drugs

Background: Several authors have reported low prevalence of Helicobacter pylori infection in patients with upper gastrointestinal bleeding (UGIB). Our aim was to study the prevalence of H. pylori in bleeding duodenal ulcer (DU), with both invasive and non-invasive methods, and to assess the role of non-steroidal anti-inflammatory drugs (NSAIDs). Methods: Ninety-two patients with bleeding DU were prospectively studied. The use of NSAIDs was evaluated by specific questionnaire. As a control group, 428 patients undergoing outpatient evaluation for the investigation of dyspepsia and found to have a DU at endoscopy were included. At endoscopy, two antral biopsies were obtained (H&E stain). A 13C-urea breath test was carried out in all patients. Breath test was repeated in patients treated with omeprazole during the hospitalization if H. pylori was not detected with the first test. Results: Gastric biopsies could be obtained in 39 patients with UGIB. Three patients with UGIB treated with omeprazole and being H. pylori negative with the first breath test were finally considered infected with the second test. Overall, 92.4% (95% CI, 85%-96%) of the patients with UGIB were infected (89.7% with histology and 92.4% with breath test (P = 0.15)). Concordance kappa value for both diagnostic tests was 0.64. NSAID intake was more frequent in patients with UGIB (34%) than in those without UGIB (5.6%) (P < 0.001), while H. pylori infection was less frequent in patients with UGIB (92.4% (85%-96%)) than in those without UGIB (99.1% (98%-100%); P < 0.001). Even in patients with UGIB, NSAID intake was the only risk factor in 5% of cases. The proportion of cases without H. pylori infection and without NSAID intake was very low in both bleeding and non-bleeding ulcers (2% and 0.5%, respectively; P = 0.146). H. pylori prevalence in bleeding ulcers was of 84% (67%-93%) in patients with NSAID intake, and 96.7% (89%-99%) when patients taking NSAIDs were excluded. In the multivariate analysis, NSAID intake (odds ratio, 9.8 (5.2-18.4)) correlated with UGIB; however, neither H. pylori status nor the interaction between H. pylori infection and NSAID intake correlated with UGIB. In the multivariate analysis in the subgroup of patients with UGIB, NSAID use was the only variable which correlated with H. pylori prevalence (odds ratio, 0.18 (0.03-0.97)). Conclusions: The most important factor associated with H. pylori-negative bleeding DU is NSAID use, and if this factor is excluded prevalence of infection is almost 100% (97%), similar to that found in patients with non-bleeding DU (and without NSAID intake). Bleeding DU patients with neither H. pylori infection nor NSAID use are extremely rare (only 2%), which suggests that the pathogenesis of bleeding DU is similar to that of non-complicated DU disease.     

Helicobacter pylori Genotypes and Expression of Gastritis in Erosive Gastro-oesophageal Reflux Disease

Background: Epidemiological studies suggest a negative association between Helicobacter pylori and gastro-oesophageal reflux disease (GORD). Moreover, cagA-positive strains are reported to protect from complications of GORD. The aim of this study was to determine virulence factors (cagA, vacA and iceA) of H. pylori strains and the pattern of gastritis in patients with GORD in comparison with patients with duodenal ulcer (DU) or functional dyspepsia (FD). Methods:H. pylori strains isolated from gastric biopsies of 105 consecutive patients with mild to moderate erosive GORD (n?=?35, LA grade A-B), and from sex- and age-matched patients with DU (n?=?35) or FD (n?=?35 without reflux symptoms) were investigated. CagA, vacA, and iceA genotypes were determined by PCR analysis of the isolates. Gastritis was classified in accordance with the updated Sydney classification. Results: The prevalence of all three H. pylori virulence factors was higher in patients with GORD (cagA[Formula: See Text] 80%, vacA s1 77%, iceA1 71%) and DU (cagA[Formula: See Text] 83%, vacA s1 80%, iceA1 74%) than in patients with FD (cagA[Formula: See Text] 40%, vacA s1 49%, iceA1 46%). Gastritis activity in the antrum and corpus did not differ between the three groups. However, lymphocytic infiltration of the gastric antral mucosa was more pronounced in DU patients than in those with GORD or FD. Conclusions:H. pylori strains obtained from patients with mild to moderate erosive GORD show a virulence pattern similar to that found in DU patients. The presence of these virulence factors does not appear to protect against erosive lesions in the oesophagus.     

Refinement of the 14C-urea Breath Test for Detection of Helicobacter pylori

Background: Helicobacter pylori is recognized as the main etiological factor for chronic gastritis, peptic ulcer and possibly also gastric malignancies. A ¹⁴C-urea breath test was successively refined to correctly diagnose the presence of H. pylori. Methods: After intake of a ¹⁴C-urea cocktail, ¹⁴CO₂ in breath was trapped in benzethoniumhydroxide/ethanol. Serology by ELISA, followed by Western blot, was used as reference method for confirmation of presence or absence of H. pylori. Results: Breath measurements at 10 and 20 min were determined to be optimal for diagnostic purposes. With 2.5 µCi of ¹⁴C-urea, a sensitivity of 86% and specificity of 100% was obtained for the 10-min values. Corresponding data for the 20-min values were 86% and 99%, respectively. When 50 mmol L^-1 citric acid was added to the 2.5 µCi ¹⁴C-urea cocktail, separation between positive and negative results became more distinct along with improved sensitivity of 91% and specificity of 100%. As the isotope amount was reduced to 1.0 µCi in the citric acid-containing cocktail, a sensitivity of 93% and specificity of 100% were obtained at both 10 and 20 min. Conclusion: Diagnostic urea breath test has a high concordance with H. pylori serology, combining ELISA and Western blot. Stepwise refinements proved the optimal urea breath test cocktail to include 1.0 µCi ¹⁴C-urea in citric acid solution with breath measurement at 10 min.     

十二指肠溃疡患者根除幽门螺杆菌后抑酸维持治疗的疗效研究

背景：对感染幽门螺杆菌（H.pylori）的消化性溃疡患者成功根除且H.ylori后,是否应继续行抑酸治疗,目前尚存在争议。目的：探讨合并H.pylori感染的十二指肠溃疡（DU）患者根除H.pylori后抑酸维持治疗的疗效。方法：112例合并H.pylori感染的DU患者随机分为A组和B组,A组给予10d四联疗法：兰索拉唑30mg＋阿莫西林1g＋克拉霉素0．5gbid＋枸橼酸铋钾110mg qid,疗程10d。B组：在A组方案的基础上,疗程结束后再予兰索拉唑30mg,1次／d,维持4周。治疗结束4周后复查胃镜,评估H.pylori根除疗效、溃疡愈合率和腹痛缓解率。结果：109例患者完成方案。A、B两组按意向治疗（ITT）和按方案（PP）分析的H.pylori根除率（ITT：85．7％对87．5％;PP：88．9％对89．1％）和溃疡愈合率（ITT：87．5％对94．6％;PP：90．7％对96．4％）以及腹痛缓解率（95．6％对95．7％）相比差异均无统计学意义（P〉0．05）。结论：以10d四联疗法根除H.pylori后,可使多数DU患者的溃疡愈合,无需进一步行维持抑酸治疗。     

消化性溃疡患者血管活性肠肽与十二指肠胃反流和幽门螺杆菌感染关系的研究

背景：消化性溃疡（PU）和十二指肠胃反流（DGR）患者的血浆血管活性肠肽（VIP）含量常高于正常水平，而幽门螺杆菌（H.pylori)感染可能参与PU的发病。目的：探讨PU患者的VIP和DGR和H.pylori感染的关系。方法：采用放射免疫测定（RIA）检测34例胃溃疡（GU）患者、42例十二指肠球部溃疡（DU）患者和30例健康人的血浆VIP含量；放射性核素^99mTc-EHIDA显像法测定DGR；双抗体夹心酶联免疫吸附测定（ELISA）检测血清H.pylori IgG抗体，Giemsa染色检测胃黏膜H.pylori。结果：GU组的血浆VIP含量显著高于DU组和正常对照组（P＜0．01）；DGR阳性率亦显著高于DU组（P＜0．05）。DGR阳性组的血浆VIP含量显著高于DGR阴性组（P＜0．01）。H.pyori阳性组的血浆VIP含量显著低于H.pylori阴性组（P＜0．05）。结论：PU患者血浆VIP含量升高可能是DGR发生的重要因素之一。     

幽门螺杆菌感染与慢性肝病及肝源性溃疡的相关性研究

目的：探讨慢性肝病患者的幽门螺杆菌（HP）感染情况及HP感染与肝源性溃疡的关系。方法：268例胃镜检查患者同时采用血清学、尿素酶试验、组织学染色行HP检查。结果：慢性肝病患者HP感染率为58．70％,非慢性肝病患者为54．62％（P＞0．05）;肝源性溃疡患者为56．52％,消化性溃疡患者为92．06％（P＜0．05）。轻、中、重三组食管静脉曲张患者溃疡发生率分别为11．11％、43．48％、73．91％。结论：慢性肝病患者HP感染率与非慢性肝病患者无显著性差异;肝源性溃疡患者HP感染率明显少于消化性溃疡患者;食管静脉曲张程度越高,溃疡发生率越高,HP感染不是其主要病因。     

Helicobacter pylori Infection and Development of Gastric or Duodenal Ulcer in Arthritic Patients Receiving Chronic NSAID Therapy

Objectives : Helicobacter pylori infection and nonste-roidal anti-inflammatory drug use are hoth common causes of peptic ulcer. It remains unclear whether H. pylori/NSAlD interactions occur, and if they do, with what result(s). Methods : We prospectively evaluated development of gastric or duodenal ulcers in 181 arthritics followed for up to 3 months while receiving an NSAID chronically and with no active antiulcer medications. H. pylori status was determined with a sensitive, specific ELISA for atiti-H. pylori IgG. Results : H. pylori infection was present in 51%; peptic ulcers de-veloped in 24. H. pylori infection was present in only 36% of those who developed a duodenal ulcer. Stepwise logistic regression analysis indicated none of the vari-able factors of age, gender, alcohol consumption, type of arthritis, or H. pylori status were significantly asso-ciated with development of peptic ulceration. Conclusions : These data suggest that H. pylori does not confer increased risk of ulceration in arthritics receiving NSAIDs chronically.     

Comparison of Gastric Histology Among Swedish and Japanese Patients with Peptic Ulcer and Helicobacter pylori Infection

Background: The natural course of Helicobacter pylori gastritis may vary between different ethnic groups. Gastric histopathology and the occurrence of H. pylori organisms in the stomach were investigated in healed duodenal (DU) and gastric (GU) ulcer patients recruited in Sweden (S) and Japan (J) in an identical trial. Methods: In 203 patients (JGU?=?39, JDU?=?55, SDU?=?109), various morphological gastritis variables and H. pylori were assessed from biopsy specimens obtained using a specific sampling protocol and interpreted according to guidelines of the updated Sydney grading system. Results: The ratio of GU:DU was observed to be very different between the recruited Japanese (39:55) and Swedish (0:109) patients. A comparison of data from SDU and JDU showed that the prevalence of H. pylori infection and the antral predominant gastritis demonstrated by both SDU and JDU were essentially identical. A comparison of data from JDU and JGU demonstrated a greater prevalence of H. pylori infection in the antrum, but not corpus, of JDU compared to JGU patients. The prevalence of atrophy and intestinal metaplasia was higher in both the antrum and corpus of JGU compared to JDU in all patients. Conclusions: The site specified biopsy methodology and standardized interpretation criteria utilized in this study clearly show that the histotopographic profile of Swedish and Japanese DU patients is essentially the same.     

Comparison of Diagnostic Methods for Helicobacter pylori Infection in Patients with Upper Gastrointestinal Bleeding

Background: Accuracy of the most frequently used tests for diagnosing Helicobacter pylori infection in patients with upper gastrointestinal bleeding of peptic origin is determined. Methods: Seventy-eight patients with endoscopically-proven upper gastrointestinal bleeding of peptic origin were included. The presence of H. pylori was considered when observed from the histology or, if negative, when serology and breath test were both positive. Accuracy of the rapid urease test was estimated in accordance with results obtained with other diagnostic methods. Results: Lesions causing gastrointestinal bleeding were 56 duodenal ulcers, 13 gastric ulcers, 7 pyloric channel ulcers, 13 acute lesions of the gastric mucosa and 16 erosive duodenitis. H. pylori infection was present in 68 patients (87.2%). Forty-four patients had received non-steroidal anti-inflammatory drugs. The sensitivity/specificity (%) of the diagnostic methods was 48.5/100 for the rapid urease test, 91/77.8 for the breath test, 89.5/80 for serology and 86.3/100 for histology. The prior consumption of proton-pump inhibitors and antibiotics induced false-negative results in the rapid urease test and breath test, with no effect on serology and histology. Conclusions: The prevalence of H. pylori infection in patients with upper gastrointestinal bleeding from peptic lesions is high. Sensitivity of the rapid urease test for diagnosing H. pylori is low in this setting. Cases with negative rapid urease test need the combination of two or more additional tests if diagnosis is to be achieved. Cases with positive rapid urease test do not need further investigation for diagnosis.     

Overview: Helicobacter pylori and Extragastric Disease

Isolation of the gastric spiral bacterium Helicobacter pylori totally reversed the false dogma that the stomach was sterile. In addition to its causal role in peptic ulceration, the newly identified bacterium has now been implicated in other gastric and even extragastric diseases, including chronic atrophic gastritis, gastric MALT lymphoma, gastric cancer, functional dyspepsia, idiopathic thrombocytopenic purpura (ITP), iron deficiency anemia, chronic urticaria, ischemic heart disease, and others. The majority of the reports are anecdotal, epidemiologic, or eradication studies, but there are also relevant in vitro studies. ITP represents one disease showing a strong link with H pylori infection. There are also accumulating data on the role of H pylori infection in iron deficiency anemia and ischemic heart disease. In summary, the association between H pylori infection and other extragut diseases is still controversial but worthy of further investigation.     

根除幽门螺杆菌对消化性溃疡合并胃炎及胃泌素的影响

目的 :评估胃舒散联合呋喃唑酮、阿莫西林对消化性溃疡 (PU)患者Hp根除的效果及其对溃疡合并胃炎、血清胃泌素(Gas)的影响。方法 :77例Hp阳性十二指肠溃疡组 (DU ,52例 )和胃溃疡组 (GU ,2 5例 )患者 ,均服用胃舒散 2 .0g(含铋 0 .1 2g) ,呋喃唑酮0 .1g,阿莫西林 0 .5g ,各 3次 /d ,2周后再继服胃舒散 4周。治疗前及疗程结束 1月后进行内镜检查并对胃窦、胃体胃炎予以内镜下评分。采用放射免疫法于治疗前及结束 1月、6月后检测胃泌素水平。结果 :DU组与GU组溃疡愈合率分别为 1 0 0 %和 92 % ,Hp根除率分别为 90 .3 %和 84.0 % ,二组比较差异均无显著性 (P >0 .0 5)。将根除Hp的 47例DU和 2 1例GU患者分为 2组 ,治疗前 2组胃窦胃炎的评分差异无显著性 (P >0 .0 5) ;GU组胃体胃炎的评分显著高于DU组 (P <0 .0 0 1 ) ;血浆中胃泌素含量 (DU组 39.4± 1 3 .6pg/ml;GU组38.4± 1 2 .3pg/ml)均显著高于正常对照值 (2 8.5± 1 0 .6pg/ml,P <0 .0 5)。Hp根除 1月后 ,2组患者胃窦胃炎与胃体胃炎的评分均显著下降 ,与治疗前自身比较 ,差异有统计学意义 (均P <0 .0 0 1 )。DU组Hp根除治疗 1月后 ,胃泌素水平显著下降到 32 .7± 1 0 .5pg/ml (P <0 .0 5)。GU组Hp根除 1月后 ,胃泌素水平有所下降 ,但与治疗前相比 ,差     

Recrudescence of Helicobacter pylori Infection in Patients with Healed Duodenal Ulcer after Treatment with Different Regimens

Objective: To determine the 12-month posttherapy recurrence (recrudescence) of Helicobacter pylori in patients with healed duodenal ulcer after apparent eradication of the organism with anti- H. pylori treatment. The influence of original anti- H. pylori treatment regimens on the recrudescence was also evaluated. Methods: One hundred and ninety patients who had duodenal ulcer healed and H. pylori eradicated (as assessed by four routine techniques 4 wk after the end of anti- H. pylori therapy) with one of five regimens were studied. The five regimens were: 1) colloidal bismuth suhcitrate (CBS) 120 mg; 2) CBS plus amoxicillin (500 nig); 3) CBS plus mctronidazole (400 mg); 4) CBS plus metronidazole and amoxicillin; and 5) CBS plus metronidazole and tetracycline (500 mg). CBS was taken four times daily for 4 wk, and antihiotics were taken three times daily for the first week. The patients were re-endoscoped. and the status of H. pylori , duodenal ulcer, and gastritis was assessed after a period of follow-up (mean 14 months after commencement of treatment). Results: H. pylori infection recurred in 36 (18.9%) of these patients. Recrudescence rate with monotherapy was 47.1%, with dual therapy 29.2–35% and with tripie therapy 9.2–14.3%. Nineteen (52.7%) of the 36 patients with recrudescent infection had ulcer relapse, and the rate for H, pylori -negative patients was 3.2% (5/154). Conclusion: Recrudeseence of H. pylori infection after apparent eradication can occur, but it could be that the treatment was only suppressing the organism. The definition of eradication of H. pylori infection may need to he revised, and more sensitive techniques to assess eradication of H. pylori are required.     

Neuroimmune Link in the Mucosa of Chronic Gastritis with Helicobacter pylori Infection

It is suggested that different neuropeptides regulate gastric mucosal integrity and participate in the development of chronic gastritis. The aim of this study was to examine the roles and changes of immunoreactive (IR) nerves and immunocompetent cells in human gastritis. Immunohistochemical, immunocytochemical, and confocal laser microscopic methods were used. All investigated nerve fibers were found in different quantities in the mucosa of both control and gastritis samples. The number of SP, NPY, and VIP IR nerve fibers increased significantly (P < 0.05) in gastritis. No IR immunocompetent cells (lymphocytes, plasma cells, mast cells) were found in the control, however, some showed NPY (16.8%) and SP (9.4%) immunoreactivity in chronic gastritis. The distance between nerve fibers and immunocompetent cells was 200 nm to 1 μm. In conclusion, the increased number of SP, NPY, and VIP IR nerves and IR immunocytes suggests that they participate in development of neurogenic inflammation, repairing processes of chronic gastritis.     

Patients with Endoscopic Gastritis and/or Duodenitis Improve Markedly Following Eradication of Helicobacter pylori,Although Less So Than Patients with Ulcers

Background: It is well documented that dyspepsia in patients with peptic ulcer disease (PUD) improves markedly after eradication of Helicobacter pylori, while rarely does it improve in patients with functional dyspepsia. There is a large group of H. pylori -infected patients who do not qualify for either diagnosis, but in whom eradication may be considered. The aim of this study was to compare symptom severity, change in gastrointestinal symptoms 1 year after eradication and satisfaction with therapy between PUD patients and patients with endoscopic diagnoses of gastritis and/or duodenitis (G/D patients). Methods: The patients were randomized to one of four triple regimens containing ranitidine bismuth and metronidazole, and either oxytetracycline or spiramycine. Eradication was assessed with the 14 C-urea breath test. GI symptoms were evaluated using the Gastrointestinal Symptom Rating Scale (GSRS) and the Ulcer Esophagitis Subjective Symptoms Scale (UESS) questionnaires. Results: One-hundred-and-eighty-three patients were recruited from GI outpatient clinics. Patients with PUD and G/D had similar severity of symptoms before eradication therapy. One year after H. pylori eradication, 99% of the PUD patients and 75% of the G/D patients felt better regarding their main upper GI complaint. Abdominal pain score decreased by 48% as measured by GSRS and by 78% as measured by UESS in the PUD group and by 25% and 47%, respectively, in the G/D group. Reflux symptoms decreased by 41% and 63% in PUD patients and by 28% and 45% in G/D patients; indigestion by 30% and 47% in PUD and by 20% and 34% in G/D; eating discomfort by 60% in PUD and by 35% in G/D. Sleep quality score improved by 68% in PUD and by 41% in NU patients. Constipation decreased by 22% in the PUD group. All these differences in symptoms were highly significant compared to baseline. Diarrhoea was unchanged. Conclusions: Abdominal pain, reflux symptoms, indigestion and the ability to eat and sleep improved in both PUD and G/D patients 1 year after H. pylori eradication. Chronic diarrhoea was not induced. Abdominal pain improved significantly more in PUD than in G/D patients. Further study of the effect of H. pylori eradication in G/D patients is warranted.     

Helicobacter pylori Reinfection Rate, in Patients with Cured Duodenal Ulcer

Objective: To determine the reinfection rate of the gastric mucosa in patients previously cured of duodenal ulcers, following the eradication oi Helicobacter pylori . Only those remaining H. pylori-negative beyond 12 months of follow-up were studied, to minimize the potential inclusion of patients with H. pylori recrudescence. Methods: Patients with endoscopically proven duodenal ulcers who had heen treated with triple therapy, resulting in documented eradication of H. pylori and cure of the ulcer for at least 4 years, were recalled and had their H. pylori status determined by the ¹⁴C-urea breath test. Those found positive for H. pylori underwent endoscopic confirmation of the infection. Results: Of the 94 patients restudied, with a follow-up period range of 48–96 months or a total of 549.8 yr, only two (2.2%) were again H. pylori positive. This gives an effective reinfection rate of 0.36% per patient year. In the two H. Pylori -positive patients, one had normal mucosa endoscopically, whereas duodenitis without active ulceration was present in the other. The former was asymptomatic, whereas the latter patient was using ranitidine daily for symptom control. Conclusion: In the Australian setting, following cure of duodenal ulcer disease by eradication of H. pylori , subsequent reinfection is an unusual phenomenon. We conclude that efforts aimed at eradication of H. pylori in duodenal ulcer are justified and are worthwhile.     

Non-Invasive Histologic Markers of Liver Disease in Patients With Chronic Hepatitis B

Background:

An exact histologic staging of liver fibrosis is essential for identifying the best therapeutic strategy and determining the disease prognosis in patients with chronic hepatitis B (CHB). While liver biopsy has a vital role in the management of liver diseases, it also sustains some limitations hampering its widespread use.

Objectives:

In this study, we evaluated and compared several available indices of the severity of liver diseases in patients with hepatitis.

Patients and Methods:

Exclusion criteria were as follows: decompensated liver disease, alcoholic liver disease or alcohol intake of 40 g or more per week; co-infection with human immunodeficiency virus, hepatitis C virus, or hepatitis D virus.

Results:

Results showed that AST to platelet ratio index (APRI) (odds ratio = 2.35, P = 0.01) and age (odds ratio = 1.04, P = 0.007) were independently predictive of the presence of significant liver necrosis and inflammation. On the other hand, AARPRI (odds ratio = 3.8, P = 0.07), age (odds ratio = 1.04, P = 0.02), and ALT levels (odds ratio = 1.01, P = 0.007) were predictive of a significant liver fibrosis. Further analysis with receiver-operating curve showed that none of these predictors had a fair diagnostic value (area under the curve < 70).

Conclusions:

The APRI had the highest sensitivity and specificity (64% and 71%, respectively) for prediction of the presence of liver disease. We suggest that APRI may be applicable for the detection of a severe liver disease.     

十二指肠溃疡与血浆促胃动素和β内啡肽关系的临床研究

目的探讨十二指肠溃疡(DU)与血浆促胃动素(MTL)和p内啡肽(β-EP)的关系.方法用放射免疫法测定活动期DU、疤痕期DU患者及健康对照组的血浆MTL和β-EP浓度,并进行比较分析.结果活动期DU及疤痕期DU患者的血浆MTL浓度均明显低于正常对照组(活动期DU153.79ng/L±42.20ng/L,疤痕期DU154.96ng/L±46.32ng/L,正常对照组190.49ng/L±36.54ng/L).活动期DU患者的血浆β-EP浓度明显高于正常对照组,而疤痕期DU患者的血浆β-EP浓度与正常对照组无显著差异(活动期DU12.56ng/L±4.62ng/L,疤痕期DU9.11ng/L±4.09ng/L,正常对照组8.92ng/L±3.45ng/L).结论DU患者的血浆MTL浓度降低和β-EP浓度升高可能参与DU发生、发展的病理生理过程.     

Helicobacter pylori Infection and Peptic Ulcer Disease in Cirrhosis

An increased frequency of peptic ulcer diseaseis noted in patients with cirrhosis, but the role of H.pylori in this disorder remains to be determined. Thediagnosis of cirrhosis was confirmed by a combination of clinical, biochemical, radiological, andhistological methods. The severity of cirrhosis wasassessed by Pugh's modification of Child's criteria.Upper gastrointestinal endoscopy was performedconsecutively to evaluate the presence of varices andgastroduodenal mucosa. H. pylori status was assessed byhistology, urease test, and serology. In all, 130patients with cirrhosis were recruited into the study;there were 86 males and 44 females with a mean (SD)age of 54.4 (12.7) years. The H. pylori prevalence was76.2% . There was no difference in age between the H.pylori-positive and -negative cirrhotics (P = 0.29). The H. pylori prevalence revealed no differenceamong cirrhotics with Child A (77.8%), Child B (72.9%),and Child C (78.6%) (P = 0.8), and neither was there adifference in H. pylori prevalence in cirrhotics with and without congestive gastropathy (77% vs73.7% , P = 0.84). The prevalence of H. pylori incirrhotics with and without varices did not show astatistical difference (75% vs 81.8%, P = 0.68). There also was no difference in the H. pyloriprevalence between cirrhotic patients with and withoutpeptic ulcers (84.4% vs 69.7% , P = 0.09). Inconclusion, the prevalence of H. pylori or peptic ulceris independent of the severity of cirrhotic liver disease. Theassociation between H. pylori infection and peptic ulcerdisease is weak in cirrhosis.