Effects of Helicobacter pylori infection on gastric emptying rate in patients with non-ulcer dyspepsia

AIM: The pathogenesis of delayed gastric emptying in patients with non-ulcer dyspepsia (NUD) remains unclear. We aimed to examine whether gastric emptying rate in NUD patients was associated with Helicobacter pylori (H pylori) infection and whether it was affected by eradication of the infection. METHODS: Gastric emptying rate of a mixed solid-liquid meal was assessed by the paracetamol absorption method in NUD patients and asymptomatic controls (n=17). H pylori status was assessed by serology and biopsy urease test. H pylori-positive NUD patients (n=23) received 10-day triple eradication therapy. H pylori status was re-assessed by biopsy urease test four weeks later, and if eradication was confirmed, gastric emptying rate was re-evaluated. RESULTS: Thirty-three NUD patients and 17 controls were evaluated. NUD patients had significantly delayed gastric emptying compared with controls. The mean maximum plasma paracetamol concentration divided by body mass (Cmax/BM) was 0.173 and 0.224 mg/L.kg respectively (P=0.02), the mean area under plasma paracetamol concentration-time curve divided by body mass (AUC/BM) was 18.42 and 24.39 mg.min/L.kg respectively (P=0.01). Gastric emptying rate did not differ significantly between H pylori-positive and H pylori-negative NUD patients. The mean Cmax/BM was 0.172 and 0.177 mg/L.kg respectively (P=0.58), the mean AUC/BM was 18.43 and 18.38 mg.min/L.kg respectively (P=0.91). Among 14 NUD patients who were initially H pylori-positive, confirmed eradication of the infection did not significantly alter gastric emptying rate. The mean Cmax/BM was 0.171 and 0.160 mg/L.kg before and after Hp eradication, respectively (P=0.64), the mean AUC/BM was 17.41 and 18.02 mg.min/L.kg before and after eradication, respectively (P=0.93). CONCLUSION: Although gastric emptying is delayed in NUD patients compared with controls, gastric emptying rate is not associated with H pylori status nor it is affected by eradication of the infection.     

The effect of Helicobacter pylori eradication on symptoms and gastric emptying in patients with nonulcer dyspepsia.

BACKGROUND/AIMS: This study was undertaken to evaluate the effect of eradication therapy on the symptoms of Helicobacter pylori positive non-ulcer dyspepsia patients. METHODS: Twenty-four patients participated in the study and the symptoms of daytime epigastric pain, night or hunger pain, nausea, vomiting, regurgitation, bloating, belching, early satiety and anorexia were scored at the beginning, the 15th day after starting eradication therapy (amoxicillin 2 gr bid, clarithromycin 2 gr bid and omeprazole 40 mg daily for two weeks) and during the third and sixth months. Gastric emptying of radiolabelled solid meal was determined at baseline and during the third month. RESULTS: The Helicobacter pylori eradication rate was 79% and symptom scores significantly decreased during the follow-up period in both of the groups, irrespective of Helicobacter pylori status. The mean symptom scores of the 24 patients at baseline, day 15 and and months three and six were as follows: 1.275, 0.274, 0.496 and 0.238 respectively. Symptom scores for the 19 patients with Helicobacter pylori eradication were 1.084, 0.263, 0.347 and 0.215 respectively while in the five patients in whom Helicobacter pylori eradication therapy failed it was 2.0, 0.314, 1.06 and 0.32 respectively. Of the 16.6% Helicobacter pylori positive non-ulcer dyspepsia patients who had delayed gastric emptying of solids, there was no change after eradication therapy. Nine patients, including all of those in whom eradication therapy failed, required further medication (antacids/prokinetics) for continuing symptoms one month after completion of treatment. CONCLUSIONS: The results of this study suggest that Helicobacter pylori is a causal factor in symptoms of non-ulcer dyspepsia and that eradication therapy improves symptoms and endoscopic findings but has no effect on gastric emptying.     

Helicobacter pylori eradication therapy is more effective in peptic ulcer than in non-ulcer dyspepsia.

AIM: To evaluate whether eradication therapy is more effective in peptic ulcer disease (PUD) than in non-ulcer dyspepsia (NUD). METHODS: We retrospectively studied 481 patients with NUD (183 patients) or PUD (298 patients) infected with Helicobacter pylori included in several prospective clinical trials. Three eradication regimens were given: (1) proton pump inhibitor (PPI) plus clarithromycin, plus either amoxycillin or metronidazole for 7 days (297 patients); (2) ranitidine bismuth citrate (RBC) plus clarithromycin plus amoxycillin for 7 days (79 patients); and (3) RBC plus clarithromycin plus amoxycillin plus metronidazole for 5 days (105 patients). H. pylori eradication was defined as a negative 13C-urea breath test 4 weeks after completing treatment. RESULTS: H. pylori eradication rates were 82% (95% CI 78-87%) with PPI plus two antibiotics for 7 days, 85% (95% CI 75-91%) with RBC plus two antibiotics for 7 days, and 91% (95% CI 86-97%) with RBC plus three antibiotics for 5 days (P < 0.05 compared with the first regimen). Overall, the H. pylori eradication rate in patients with NUD was 78% (95% CI 71-84%), while in patients with PUD it was 89% (95% CI 86-93%) (P < 0.001). Both the combination of PPI plus two antibiotics for 7 days and the combination of RBC plus three antibiotics for 5 days were more effective in PUD than in NUD patients. However, RBC plus clarithromycin plus amoxycillin for 7 days was equally effective in both diseases. RBC plus two antibiotics for 7 days achieved better results than the same therapy with PPI only in NUD patients (84% v. 59%, P < 0.01), but both regimens were similar when prescribed in PUD patients (86% v. 88%). In the multivariate analysis, the type of therapy, the diagnosis (NUD v. PUD), and the product variable of therapy (with RBC plus 2 antibiotics for 7 days) and diagnosis (interaction variable) were the only variables that influenced H. pylori eradication. The odds ratio (OR) for the effect of RBC versus PPI plus two antibiotics for 7 days in patients with NUD was 4 (95% CI 1.7-9.7; P < 0.01), whereas in patients with PUD no statistical significance was achieved (OR 0.79; 95% CI 0.2-3.9). CONCLUSION: Overall, H. pylori eradication therapy is more effective in PUD than in NUD patients. This advantage of eradication therapies in PUD patients seems to be observed with 7-day PPI-based triple regimens, and with 5-day RBC-based quadruple therapy, while the 7-day RBC-based triple regimen seems to be equally effective in both diseases.     

Presence of Helicobacter pylori in patients with non-ulcer dyspepsia revealing normal antral histological characteristics

Two hundred consecutive patients suffering from non-ulcer dyspepsia were studied for the presence of Helicobacter pylori in antral gastritis and normal antral mucosa, using the combination of culture, modified Giemsa stain and a sensitive immunoperoxidase stain as means of detection. H. pylori gastritis was present in 56% of the cases. The bacterium was present in 75% of cases of normal antral mucosa, however, in low numbers. It is concluded that 87% of patients with non-ulcer dyspepsia are H. polory-positive implying a larger role for the micro-organism as initially thought.     

Comparison of clinical, serological and histological findings between non-ulcer dyspepsia patients with and without Helicobacter pylori infection

BACKGROUND AND AIMS: The role of Helicobacter pylori (H. pylori) infection in non-ulcer dyspepsia (NUD) remains controversial. This study investigates the clinical, serological and histological differences between patients with H. pylori-positive and -negative NUD. METHODS: One hundred and eighty consecutive patients with NUD were enrolled from January to December 1998. The severity of symptoms was evaluated by the Tucci's scoring system. The histological changes of gastric mucosa were assessed according to the Updated Sydney System, and a fasting blood sample was obtained to test the serum gastrin and pepsinogen I levels. RESULTS: The H. pylori-positive NUD patients were notably older than H. pylori-negative NUD patients (48.2 +/- 15.9 vs 39.8 +/- 15.7 years, P= 0.001). There were no differences in other clinical factors between the two NUD groups. The serum pepsinogen I levels were considerably higher in H. pylori-positive NUD patients than in H. pylori-negative NUD patients (78.9 +/- 42.2 vs 61.5 +/- 43.3 ng/mL, P<0.01). However, no significant differences in serum gastrin levels were discovered between the two groups. The antrum histological scores for chronic inflammation, acute inflammation, gland atrophy and lymphoid follicles were higher in H. pylori-positive NUD patients than in H. pylori-negative NUD patients (2.09 vs 1.01, P<0.001; 1.22 vs 0.36, P<0.001; 0.76 vs 0.36, P<0.01; 0.33 vs 0.13, P<0.01, respectively). CONCLUSIONS: The present study discovered marked differences in age, serum pepsinogen I levels, histological grades of acute inflammation, chronic inflammation, gland atrophy and lymphoid tissue formation between H. pylori-positive and H. pylori-negative NUD patients. Further investigation of the clinical prognosis of the two groups of patients is necessary.     

Histological changes in the gastric mucosa after Helicobacter pylori eradication

BACKGROUND AND AIM: Correa described a stepwise model of changes in the gastric mucosa after Helicobacter pylori infection, from the normal gastric epithelium to chronic gastritis, atrophy, intestinal metaplasia, dysplasia and adenocarcinoma. The aim of this study is to assess the reversibility of these mucosal changes after H. pylori eradication. METHODS: The study sample consisted of 89 patients who underwent at least two gastric biopsies from 1990 to 2000, with a positive finding for H. pylori in the first and a negative finding in the second. Specimens were evaluated for acute and chronic inflammation, lymphoid aggregates, proliferation, mucosal atrophy, intestinal metaplasia, dysplasia, and MUC5AC and MUC6 expression using histochemical and immunohistochemical methods. RESULTS: The average time between biopsies was 23.15 +/- 26.30 months. There was a significant decrease in acute and chronic inflammation scores, from 1.48 +/- 1.10 to 0.23 +/- 0.63 and from 2.67 +/- 0.68 to 1.44 +/- 1.04, respectively (P < 0.001), and in a number of lymphoid follicles, from 42.68% to 21.95% of cases (P < 0.008). The number of glands increased from 39.08 +/- 16.67/mm to 48.86 +/- 17.93/mm after eradication (P = 0.062). Intestinal metaplasia was found in 17.07% of the cases, with no change over time. Dysplasia appeared in one case 2 years after eradication. In 27 patients, the Ki67 labeling index decreased significantly after eradication, while MUC5AC and MUC6 expression increased. CONCLUSION: Our findings, although not conclusive for arrest of the malignant potential, support the importance of H. pylori eradication in the prevention of gastric cancer.     

幽门螺杆菌感染与胃不同部位组织学病变的关系

目的 明确幽门螺杆菌(Helicobacter pylori,H,pylori)感染与胃不同部位粘膜组织学病变的关系。方法 在215例胃镜受检者胃窦、角、体三点取材进行组织学检查，Giemsa染色明确H.pylori感染情况，HE染色计量观察组织学病变情况，分析两者的相关关系。结果 从胃窦到胃角、胃体，炎症程度(单个核细胞浸润)、活动度(中性粒细胞浸润)、糜烂及淋巴滤泡形成均递减，H.pylori阳性者积分高于阴性者。在胃窦和胃角部，H.pylori感染更常引起近腔面上皮分泌下降，而在胃体部无此发现，H.pylori感染在三个部位均可引起腺体萎缩。结论 H.pylori感染是胃多部位组织学病变如淋巴细胞、中性粒细胞浸润、糜烂和淋巴滤泡形成与粘膜萎缩的病因，在胃窦和胃角引起的病变重于胃体。     

Helicobacter pylori infection and non-ulcer dyspepsia: the effect of treatment with colloidal bismuth subcitrate.

A study was undertaken to determine the role of Helicobacter pylori in non-ulcer dyspepsia (NUD) and to determine the efficacy of colloidal bismuth subcitrate (CBS) in the treatment of NUD. Seventy-one patients were randomly allocated (double blind) to CBS or placebo, two tablets twice daily for 4 weeks. The severity of dyspepsia was scored and endoscopies performed before and after treatment, and antral biopsy specimens were taken for bacteriologic and histologic examination. Forty patients had H. pylori infection, and all had changes of chronic active gastritis. H. pylori was cleared from 17 to 21 patients (81%) treated with CBS, whereas none of the 19 patients treated with placebo cleared the bacteria. Improvement in histology was noted in 15 of 21 patients (71.4%) treated with CBS, whereas no improvement was noted in any of the placebo controls. Thirty-one patients were negative for H. pylori. All had either normal gastric histology or minor degrees of inflammation. Seventeen of these patients received CBS, and 14 received placebo. All groups reported improvement in the symptom score; however, the H. pylori-positive, CBS-treated group recorded a significantly higher improvement than the other groups (p less than 0.001). Relapse of H. pylori infection after initial clearance of the bacteria was high. Twelve of 16 patients evaluated relapsed 1 month after withdrawal of CBS.     

根除幽门螺杆菌对胃黏膜肠化的影响

目的　幽门螺杆菌 (Hp)感染可导致慢性活动性胃炎进一步发展为慢性萎缩性胃炎、胃黏膜肠化、最终发展成肠型胃癌。通过 5年随访 ,探讨根除Hp是否对胃黏膜肠化逆转、发生及发展有影响。方法　将 1996年快速尿素酶试验及组织学方法检测Hp均为阳性的 398例病人随机分为治疗组和对照组。治疗组 2 0 1例 ,进行根除Hp治疗 ;对照组 197例 ,给予安慰剂 ;服药前及 5年后分别从胃窦部及胃体部取材检测胃炎、胃炎活动性及肠化。结果　 5年后治疗组中 15 1/2 0 1例Hp为阴性 ,对照组中 16 1/197例Hp为阳性 ;治疗组中Hp被根除的病人胃炎活动性的检出率明显减少 ,与对照组持续Hp感染者比较 ,差异有显著性 (P <0 .0 0 0 1) ;对照组中持续Hp感染者 5年后肠化检出率与自身 5年前、治疗组成功根除Hp者 5年前和 5年后比较均增高 ,差异有显著性 (P均 <0 .0 0 1) ,治疗组根除Hp的病人 5年前后比较差异无显著性 ;对照组中持续Hp感染者胃窦部 5年后肠化检出率与自身 5年前、治疗组根除Hp者 5年前和 5年后比较均增高 ,差异有显著性 (分别为P <0 .0 0 1,P <0 .0 0 1和P<0 .0 1) ,治疗组根除Hp感染的病人 5年前后比较差异无显著性 ;对照组持续Hp感染的病人与治疗组根除Hp感染的病人胃窦部肠化新增及新减情况比较无差异。 结论　 5年     

Surface hydrophobicity of gastric mucosa in Helicobacter pylori infection: effect of clearance and eradication.

Surface hydrophobicity of the gastric mucosa is reduced in peptic ulcer disease and Helicobacter pylori infection. This abnormality may be caused by H. pylori or may be an inherent defect. The aim of the present study was to clarify the relationship between H. pylori infection and mucosal hydrophobicity by examining the effect of eradication of the organism. H. pylori-positive patients with (n = 42) or without (n = 42) duodenal ulcer were randomized to receive ranitidine, bismuth, or bismuth plus antibiotics. Surface hydrophobicity of gastric mucosa was assessed by measurement of plateau-advancing contact angle. Measurements were performed at presentation, end of treatment, and 1 month later. Contact angle was unchanged after ranitidine (55 degrees vs. 56 degrees) but increased with bismuth (57 degrees-62 degrees; P < 0.05) and bismuth plus antibiotics (56 degrees-67 degrees; P < 0.0001). One month after treatment ended, contact angles in patients in whom H. pylori was not eradicated were not different from those before treatment (56 degrees vs. 56 degrees) but increased to a value similar to H. pylori-negative controls in patients in whom H. pylori was eradicated (56 degrees-69 degrees; P < 0.0001). It is concluded that reduced mucosal hydrophobicity in peptic ulcer disease is secondary to H. pylori infection and that this impaired mucosal defense provides a possible mechanism whereby H. pylori infection predisposes to acid/peptic digestion.     

Association between cag-pathogenicity island in Helicobacter pylori isolates from peptic ulcer, gastric carcinoma, and non-ulcer dyspepsia subjects with histological changes

AIM: To investigate the presence of the cag-pathogenicity island and the associated histological damage caused by strains with complete cag-PAI and with partial deletions in correlation to the disease status. METHODS: We analyzed the complete cag-PAI of 174 representative Helicobacter pylori (H pylori ) clinical isolates obtained from patients with duodenal ulcer, gastric ulcer, gastric cancer, and non-ulcer dyspepsia using eight different oligonucleOtide primers viz cagA1, cagA2, cagAP1, cagAP2, cagE, cagT, LEC-1, LEC-2 spanning five different loci of the whole cag-PAI by polymerase chain reaction (PCR). RESULTS: The complete screening of the genes comprising the cag-PAI showed that larger proportions of subjects with gastric ulcer (97.8%) inhabited strains with complete cag-PAI, followed by gastric cancer (85.7%), non-ulcer dyspepsia (7.1%), and duodenal ulcer (6.9%), significant differences were found in the percentage distribution of the genes in all the clinical groups studied. It was found that strains with complete cag-PAI were able to cause severe histological damage than with the partially deleted ones. CONCLUSION: The cag-PAI is a strong virulent marker in the disease pathogenesis as it is shown that a large number of those infected with strain with complete cag-PAI had one or the other of the irreversible gastric pathologies and interestingly 18.5% of them developed gastric carcinoma. The presence of an intact cag-PAI correlates with the development of more severe pathology, and such strains were found more frequently in patients with severe gastroduodenal disease. Partial deletions of the cag-PAI appear to be sufficient to render the organism less pathogenic.     

非溃疡性消化不良患者幽门螺杆菌感染和病理的相关性

[目的]研究非溃疡性消化不良（NUD）患者幽门螺杆菌（Hp）感染的患病率，Hp感染和胃黏膜组织病理的相关性。[方法]入选者为门诊接受胃镜检查的132例临床诊断NUD患者，排除消化性溃疡、胃食管反流病等疾病，胃黏膜组织用Warthin-Starry染色半定量诊断Hp感染，并对胃黏膜组织按慢性炎症、活动性炎症、萎缩、肠化进行病理评价。[结果]NUD患者Hp感染率为54．5％（67／132），Hp感染和病理诊断慢性炎症及活动性炎症有相关性，分别P〈0．001，〈0．048，相关系数分别为0．324和0．167。[结论]NUD患者Hp感染和病理诊断胃黏膜慢性炎症及活动性炎症相关，提示Hp感染在慢性胃炎中的致病作用。     

A study of Helicobacter pylori in north Indian subjects with non-ulcer dyspepsia.

A prospective case control study was conducted in 50 patients with non-ulcer dyspepsia (NUD) and 10 age and sex matched controls to determine the prevalence of Helicobacter pylori in patients with NUD and to correlate symptoms, histology and presence of H pylori in gastric biopsies. Endoscopic biopsies from antrum and fundus were subjected to urease test and histological examination. On histology, H pylori was identified in 27 (54%) NUD patients and in one of 10 controls. Urease test was positive in 31 (62%) antral and 21 (42%) fundal biopsies in patients with NUD and in only one (10%) of 10 antral biopsies in the control group. On histology, gastritis was present in the antrum in 46 (92%) NUD patients and in the fundus in 40 (80%) cases; of these, 27 (54%) and 15 (30%) had H pylori in antral and fundal biopsies respectively. The severity of antral gastritis correlated with the density of H pylori (p < 0.05).     

Helicobacter pylori infection and gastric function in patients with chronic idiopathic dyspepsia.

Helicobacter pylori infection, histological features of the gastric mucosa, and gastric motor and secretory functions were evaluated in 45 consecutive patients with chronic idiopathic dyspepsia. H. pylori infection was found in 60% of dyspeptic patients, compared with 33% of 15 healthy controls (P = 0.1). No difference was detected in basal or stimulated gastric acid secretion between dyspeptic patients and healthy controls. Gastric emptying was significantly (P less than 0.01) delayed in dyspeptic patients compared with healthy controls when standardized for age and sex. Delayed gastric emptying was associated with a low frequency of H. pylori infection, female gender, and young age. Epigastric pain or burning and postprandial fullness were, respectively, more severe in patients with H. pylori infection (P less than 0.02) and in those with delayed gastric emptying (P less than 0.01). These findings support the existence of separate subsets of patients with chronic idiopathic dyspepsia. Despite the presence of overlaps, there appear to be partially different functional derangements and clinical features in different subgroups of dyspeptic patients.     

Helicobacter pylori infection and histological changes in siblings of young gastric cancer patients

Background and Aim: Helicobacter pylori infection is a risk factor for gastric cancer. We evaluated whether H. pylori infection and premalignant histological changes are more prevalent in siblings of young gastric cancer patients. Methods: Young (age ≤ 40) gastric cancer patients (n = 185), their young siblings (n = 130), and young control participants (n = 287) were recruited. H. pylori infection and histological changes were assessed using the updated Sydney system in biopsy specimens from three regions. We analyzed the association of H. pylori infection and histological changes with gastric cancer using logistic regression analysis. Results: The H. pylori infection rate was significantly higher in young cancer patients than their siblings (odds ratio [OR] = 2.42, P = 0.001) or control participants (OR = 3.60, P < 0.001). In H. pylori‐infected subjects, corpus gastritis and premalignant changes of the corpus lesser curvature (LCv) were also more prevalent in patients than in siblings or controls. In terms of the antrum, intestinal metaplasia was more prevalent in H. pylori‐infected patients than in siblings or controls, while atrophy was not affected. Siblings also had a higher H. pylori infection rate (OR = 1.60, P = 0.046) and higher prevalence of intestinal metaplasia at the corpus LCv (OR = 2.88, P = 0.027) than control participants. Conclusions: Even in young adults, H. pylori infection is a risk factor for gastric cancer. Young adults with histological findings including corpus predominant gastritis, corpus atrophy, or intestinal metaplasia are at increased risk. Since young siblings share risk factors, screening and treatment should be considered for these family members.     

Prevalence of gastric metaplasia in the duodenal bulb is low in Helicobacter pylori positive non-ulcer dyspepsia patients.

BACKGROUND: Gastric metaplasia in duodenum is a common phenomena in duodenal ulcer patients. However, the role of gastric metaplasia in patients with non-ulcer dyspepsia is not clear. It is not known either whether Helicobacter pylori infected non-ulcer patients who are CagA-seropositive have gastric metaplasia in duodenum more often than CagA-negative patients. AIMS: To compare prevalence of gastric metaplasia in duodenum in non-ulcer dyspepsia patients according to Helicobacter pylori status. PATIENTS AND METHODS: A series of 400 unselected dyspeptic patients in primary care were investigated. Patients with no endoscopic evidence of organic disease (n=236) were enrolled in the study. Duodenal bulb and gastric biopsies were collected, as well as blood samples for Helicobacter pylori determination. RESULTS: There were no differences between CagA-seropositive and -seronegative Helicobacter pylori infected patients as far as concerns gastric metaplasia in duodenal bulb (20% vs 25%). Helicobacter pylori negative non-ulcer patients more often had gastric metaplastic changes (46%, p<0.0001) in duodenum. CONCLUSION: Helicobacter pylori infection has no major role in development of gastric metaplasia in duodenal bulb in non-ulcer dyspeptic patients. Furthermore, it does not result in positive CagA-serology, an increased risk for gastric metaplasia compared with CagA-seronegative cases.     

FD患者Hp感染对胃排空的影响

目的探讨幽门螺杆菌（Ｈｐ）感染在功能性消化不良（ＦＤ）患者胃排空功能障碍中的作用．方法采用放射性同位素γ－照相法观测了５６例ＦＤ患者胃固－液体排空情况，并用胃窦粘膜印片Ｇｉｅｍｓａ染色及石蜡切片ＨＥ，Ｗ＿Ｓ银染色镜检Ｈｐ．结果ＦＤ患者餐后３０，６０及９０ｍｉｎ时的胃排空率均显著低于正常对照组（Ｐ＜００５－００１）；ＦＤ患者Ｈｐ感染率无明显增高（Ｐ＞００５），Ｈｐ阳性组与阴性组在３个时相的胃排空率差异均无显著性（Ｐ＞００５）结论ＦＤ患者胃排空功能与Ｈｐ感染无关     

根除幽门螺杆菌对胃黏膜及肠化、不典型增生的影响

目的探讨根除幽门螺杆菌（Hp）后慢性胃炎的胃黏膜炎症及肠上皮化生、不典型增生的变化。方法选择172例伴有Hp感豢的慢性活动性胃炎病人分为两组：阴性组（68例）和阳性组（104例），观察阴性组治疗后的变化并与阳性组进行比较，并观察阴性组肠上皮化生和不典型增生在治疗前后的变化。结果阴性组的胃黏膜炎症有28例（41．2％）好转，2例（2．9％）治愈，明显高于阳性组（P〈0.01），其伴有的肠上皮化生有2例（25％）治愈，4例（50％）好转，不典型增生有7例（38．9％）好转，6例（33．3%）治愈。结论Hp感染阴转后慢性胃炎的治疗效果明显优于阳性者，其伴有的肠化和不典型增生亦能好转或治愈。因此，根除Hp是治疗Hp相关性胃炎和防止发生胃癌的重要措施。     

Helicobacter pylori infection and gastric emptying in cirrhotic patients with symptoms of dyspepsia

BACKGROUND/AIMS: Chronic gastric Helicobacter pylori infection is common in patients with dyspeptic symptoms. The effect of H. pylori infection on gastric emptying, in cirrhotic patients with dyspeptic symptoms, has never been studied. Therefore, we investigated the incidence of H. pylori infection and its relationship with gastric emptying in cirrhotic patients with dyspepsia. METHODOLOGY: A solid-phase gastric emptying study and 14C urea breath test were performed in 80 cirrhotic patients with dyspepsia. The severity of cirrhosis was assessed according to Child-Pugh's classification. RESULTS: The overall incidence of delayed gastric emptying was 75%. Delayed gastric emptying incidences according to severity of cirrhosis were 71.4% for Child-A, 73.1% for Child-B, and 80.8% for Child-C. The differences were not significant. The incidence of H. pylori infection was 52.5% overall. H. pylori infection rates were 46.4% for Child-A, 42.3% for Child-B, and 69.2% for Child-C. Although there was a tendency for the infection rate to increase with the severity of liver cirrhosis, the difference was not significant. In addition, there were no significant differences in the incidences of H. pylori infection among patients with normal and delayed gastric emptying. CONCLUSIONS: Delayed gastric emptying is common in cirrhotic patients with dyspepsia. However, the status of H. pylori infection does not seem to play a role in delayed gastric emptying in these patients.