Effect of Helicobacter pylori on gastric emptying in non-ulcer dyspepsia--evaluation of Helicobacter pylori by 13C-urea breath test]

AIM: Non-ulcer dyspepsia (NUD) is a common disorder in clinical field. The pathogenesis of NUD are still unclear especially the participation of Helicobacter pylori (H. pylori) in NUD is controversy. Aim of the present study was to clarify the effect of H. pylori at view of urea breath test on liquids and solids gastric emptying in patients with NUD. SUBJECTS AND METHODS: H. pylori positive (n = 24) and negative NUD subjects (n = 11), and H. pylori positive non-NUD subjects (n = 10) as control group were studied. Liquids and solids gastric emptying was evaluated according to the acetaminophen method and sulfamethzole modified method delta 13C-AUC was calculated as estimation of H. pylori by 13C-urea breath test. H. pylori positive NUD was classified into high delta 13C-AUC group (n = 11), median group (n = 8) and low group (n = 5). High delta 13C-AUC group (n = 6) and low delta 13C-AUC group (n = 4) group were treated by eradication therapy. In H. pylori positive NUD subjects, high and low delta 13C-AUC group were estimated the changes of liquids and solids gastric emptying, symptoms before and after eradication. RESULTS: H. pylori positive NUD group has higher liquids gastric emptying that H. pylori negative NUD group (7.6 +/- 2.8 vs. 4.9 +/- 1.4, p = 0.0022). No difference was observed between H. pylori positive and H. pylori negative group of solids gastric emptying. There was no significant difference in liquids gastric emptying among high-, median- and low-delta 13C-AUC group of H. pylori positive NUD subjects. Solids gastric emptying was significantly delayed in high delta 13C-AUC group compared with low delta 13C-AUC group (10.3 +/- 3.7 vs. 5.3 +/- 3.1, p = 0.014). delta 13C-AUC was not correlated to liquids gastric emptying, but to solids gastric emptying (r = -0.573. p = 0.006). In Non-NUD group as control group, delta 13C-AUC has not correlation to liquids and solids gastric emptying H. pylori positive NUD has higher delta 13C-AUC than Non-NUD group. Eradicated low delta 13C-AUC group did not show significant changes in liquids gastric emptying, but did improvement of solids gastric emptying and symptoms scores. Eradicated low delta 13C-AUC group did not show any significant changes. CONCLUSION: In non-ulcer dyspepsia patients H. pylori does not influence liquids gastric emptying, but does solids gastric emptying according to delta 13C-AUC of H. pylori, especially high delta 13C-AUC patients.     

Direct measurement of gastric H^＋／K^＋-ATPase activities in patients with or without Helicobacterpylori-associated chronic gastritis

AIM: The role of Helicobacter pylori (H pylori) infection in gastric acid secretion of patients with chronic gastritis remains controversial. This study was designed to elucidate the effect of H pylori on H+/K+-ATPase activities in gastric biopsy specimens. METHODS: Eighty-two patients with chronic gastritis who had undergone upper endoscopy were included in this study. H pylori infection was confirmed by rapid urease test and histology. Gastric H+/K+-ATPase activities and serum gastrin concentrations were measured by an enzymatic method and radioimmunoassay, respectively. For those patients who received triple therapy for eradicating H pylori, changes in the activity of gastric H+/K+-ATPase and serum gastrin levels were also measured. RESULTS: The mean gastric H+/K+-ATPase activity in Hpylori-positive group (42 patients) was slightly higher than that in Hpylori-negative group (29 patients) (169.65±52.9 and 161.38±43.85nmol P/(mg·h),respectively, P=0.301). After eradication of H pylori, the gastric H+/K+-ATPase activities slightly decreased compared to prior therapy (165.03±59.50 and 158.42±38.93 nmol P/(mg·h), respectively, P=0.805). The mean basal gastrin concentration was slightly higher in H pylori-positive patients than in H pylori-negative patients (87.92±39.65 pg/mL vs75.04±42.57 pg/mL, P= 0.228). The gastrin levels fell significantly after the eradication of H pylori. (Before treatment 87.00±30.78 pg/mL, after treatment 64.73±18.96 pg/mL, P=0.015). CONCLUSION: Gastric H+/K+-ATPase activities are not associated with H pylori status in patients with chronic gastritis.     

The long-term efficacy of Helicobacter pylori eradication therapy in patients with idiopathic thrombocytopenic purpura

BACKGROUND AND AIM: A beneficial effect of Helicobacter pylori (H. pylori) eradication in patients with H. pylori-positive idiopathic thrombocytopenic purpura (ITP) has been reported by several investigators; however, it was not clear whether the recovered platelet count after H. pylori eradication was maintained for a long period. METHOD: Thirty-eight ITP patients who were examined for H. pylori infection were assessed. H. pylori-positive patients received a standard antibiotic therapy for H. pylori eradication. We investigated the long-term effect of H. pylori eradication on platelet recovery in patients with H. pylori-positive ITP. RESULTS: Of the 38 ITP patients, 26 (68.4%) were positive for H. pylori. The response rate of platelet recovery was 56.5% (13/23 patients). Twelve patients showed complete response (CR) and one showed partial response (PR). The mean platelet counts 6 months after eradication significantly increased from 31 x 10(9)/L to 129 x 10(9)/L in 23 H. pylori-eradicated patients (P < 0.001). The median platelet counts of responders 1, 2, 3, and 4 years after eradication were 168 x 10(9)/L (n = 10), 193 x 10(9)/L (n = 9), 168 x 10(9)/L (n = 7), and 243 x 10(9)/L (n = 4) after a mean follow-up of 25.8 months. CONCLUSION: Eradication therapy for H. pylori-positive patients with ITP was effective and a favorable effect was maintained for long periods.     

Does Helicobacter pylori infection affect gastric emptying in patients with functional dyspepsia?

The objectives of the study were first, to determine if gastric emptying was altered in patients with functional dyspepsia with and without Helicobacter pylori infection compared with normal healthy volunteers; and second, to determine if there were further alterations in gastric emptying when the infection was eradicated. Gastric emptying was measured using a ^99mtechnetium radiolabelled solid meal and gastric emptying time was measured as t_1/2, viz. time taken for half the radiolabelled meal to be emptied from the stomach. The mean gastric emptying time for H. pylori-positive patients (n= 20) was 56.4±24.8 min; H. pylori-negative patients (n= 19) 67.8±31.8 min; and normal controls (n= 20) 58.8 ± 18.8 min. No significant difference was obtained between the groups (ANOVA; P= 0.348). Thirteen of 18 H. pylori-positive patients successfully eradicated the infection following treatment with omeprazole 40 mg o.m. and amoxycillin 500 mg t.d.s. for 2 weeks. The mean difference in the gastric emptying time before and H. pylori eradication was 23.9 + 13.2 min (P= 0.556). There was no significant difference in the frequency of specific dyspeptic symptoms as well as the overall mean symptom score between the H. pylori-positive and -negative patients. Gastric emptying was not different between patients with functional dyspepsia and normal controls. Helicobacter pylori infection does not appear to affect gastric emptying in patients with functional dyspepsia.     

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.     

Influence of H pylori on plasma ghrelin in patients without atrophic gastritis

AIM:To determine the association between H pylori infection and serum ghrelin levels in patients without atrophic gastritis.METHODS:Fifty consecutive patients(24 males and 26 females)with either H pylori-positive gastritis(n = 34)or H pylori-negative gastritis(n = 16)with normal gastric acid secretion determined by 24-h pHmetry and without atrophic gastritis in histopathology were enrolled in this study.Thirty-four H pylori-infected patients were treated with triple therapy consisting of a daily regimen of 30 mg lansoprazole bid,1 g amoxicillin bid and 500 mg clarithromycin bid for 14 d,followed by an additional 4 wk of 30 mg lansoprazol treatment.H pylori infection was eradicated in 23 of 34(67.6%)patients.H pylori-positive patients were given eradication therapy.Gastric acidity was determined via intragastric pH catethers.Serum ghrelin was measured by radioimmunoassay(RIA).RESULTS:There was no signifficant difference in plasma ghrelin levels between H pylori-positive and H pylori-negative groups(81.10 ± 162.66 ng/L vs 76.51 ± 122.94 ng/L).In addition,there was no significant difference in plasma ghrelin levels and gastric acidity levels measured before and 3 mo after the eradication therapy.CONCLUSION:H pylori infection does not influence ghrelin secretion in patients with chronic gastritis without atrophic gastritis.     

Eradication of Helicobacter pylori restores the inhibitory effect of cholecystokinin on gastric motility in duodenal ulcer patients

BACKGROUND: Increased gastric emptying and defective action of endogenous cholecystokinin (CCK), that is known to inhibit this emptying, have been implicated in the pathogenesis of duodenal ulcer (DU). The aim of this double blind study was to assess whether CCK and somatostatin participate in the impairment of gastric motility in active DU patients before and after Helicobacter pylori eradication. METHODS: Tests were undertaken in 10 DU patients without or with elimination of the action of endogenous CCK using loxiglumide, a selective CCK-A receptor antagonist, before and 4 weeks after eradication of H. pylori with 1 week triple therapy that resulted in healing of all DUs tested. The gastric emptying rate after feeding was determined using the 13C-acetate breath test. Before each test, samples of gastric juice were obtained by aspiration using a nasogastric tube for determination of somatostatin using specific radioimmunoassay. RESULTS: Prior to H. pylori eradication gastric emptying half-time was 31 +/- 6 min in placebo-treated DU patients and this emptying rate was not significantly affected in tests after pretreatment with loxiglumide (10 mg/kg i.v.). Following eradication of H. pylori, in tests with placebo gastric emptying half-time was significantly longer (48 +/- 9 min) compared to that prior to H. pylori eradication. Pretreatment with loxiglumide in H. pylori eradicated DU patients significantly enhanced the gastric emptying rate with an emptying half-time of only 33 +/- 4 min. Eradication of H. pylori resulted in a significant increase in somatostatin concentration in gastric juice and loxiglumide significantly reduced this luminal somatostatin in H. pylori-eradicated subjects compared to values before anti-H. pylori therapy. CONCLUSIONS: 1) H. pylori infection in DU patients is accompanied by enhanced gastric emptying and reduction in luminal release of somatostatin; 2) the failure of loxiglumide to affect gastric emptying in H. pylori-infected DU patients might be attributed, at least in part, to the failure of endogenous CCK to control gastric motility due to deficient release of somatostatin; and 3) H. pylori-infected patients appear to exhibit a deficient somatostatin release by endogenous CCK that can be reversed by the eradication of H. pylori indicating that both CCK and somatostatin may contribute to normalization of gastric emptying following H. pylori eradication in DU patients.     

Eradication rates of helicobacter pylori infection with second-line treatment: non-ulcer dyspepsia compared to peptic ulcer disease

BACKGROUND/AIMS: Initial proton pump inhibitor (PPI)-based triple therapy for Helicobacter pylori (H. pylori) infection is less effective in patients with nonulcer dyspepsia (NUD) than those with peptic ulcer disease (PUD). To date, there have been no studies on the difference in eradication rates in NUD compared to PUD with regard to second-line therapy. Therefore, we retrospectively analyzed the difference in eradication rates of a second-line quadruple therapy for NUD and PUD patients. METHODOLOGY: Between June 2003 and December 2005, patients who failed to respond to initial PPI-based triple therapy, received 7 days of quadruple therapy (PPI b.i.d., bismuth 300mg q.i.d., metronidazole 500mg t.i.d., tetracycline 500mg q.i.d.) as a second-line treatment regimen. Four weeks after the completion of the course of medication, a 13C-urea breath test was performed for detection of H. pylori. RESULTS: A total of 87 patients received second-line quadruple therapy. Of these, 43 patients had NUD and 44 patients had PUD (19 gastric ulcers, 23 duodenal ulcers, 2 both ulcers). The eradication rates were 76.7% (33/43) in the NUD group and 90.9% (40/44) in the PUD group by per-protocol analysis. Therefore, the eradication rates in the NUD group were significantly lower than those in the PUD group (p = 0.034). CONCLUSIONS: A 7-day bismuth-based second-line quadruple therapy for H. pylori infection was less effective in patients with NUD than those with PUD. Therefore, a more potent second-line treatment regimen or extension of treatment duration of quadruple therapy should be considered for the eradication of H. pylori in patients with NUD.     

Altered hypothalamic cholinergic responses in patients with nonulcer dyspepsia: a study of pyridostigmine-stimulated growth hormone release

OBJECTIVE: Acetylcholine plays a central and peripheral role in regulating gastric motility. In the hypothalamus, it is a key neuroendocrine modulator; acting through somatostatin, it brings about the release of growth hormone (GH). We measured hypothalamic cholinergic receptor sensitivity in patients with nonulcer dyspepsia (NUD) by examining GH release in response to cholinergic challenge. METHODS: Forty patients with NUD and 40 healthy comparison subjects were administered pyridostigmine (the acetylcholinesterase inhibitor, 120 mg), and GH release over a 3-h period was monitored. RESULTS: Calculating response as the maximum GH relative to baseline (delta GH), the mean +/- SEM response in the patients was 11.9 +/- 1.9 U/L and in the healthy subjects 6.7 +/- 0.7 mU/L (t = 2.1, df = 78, p = 0.03). Helicobacter pylori status had no appreciable impact on GH response with H. pylori-positive patients having a mean response of 10.5 +/- 2.1 mU/L and negative patients a mean response of 13.2 +/- 3.4 mU/L. Overall, patients with NUD release more GH in response to pyridostigmine challenge than healthy subjects. CONCLUSIONS: Patients with NUD may have a pathophysiological disturbance involving central cholinergic systems.     

Transfer of metronidazole to gastric juice: impact of Helicobacter pylori infection and omeprazole

BACKGROUND: The effects of Helicobacter pylori infection associated with inhibition of gastric acid secretion on the distribution of medications used for H. pylori eradication are poorly understood. The aim of this study was to investigate the effects of a 7-day administration of 20 mg omeprazole on the transfer of metronidazole from plasma to the gastric juice of individuals with and without H. pylori infection. METHODS: Fourteen H. pylori-positive and 14 H. pylori-negative male volunteers were enrolled in a study with an open, randomized, two-period crossover design with a 21-day washout period between phases. Plasma, salivary, and gastric juice concentrations of metronidazole in subjects with and without omeprazole treatment were measured with reversed-phase high-performance liquid chromatography/liquid chromatography. RESULTS: Metronidazole peak concentration (Cmax) was similar in plasma and saliva and was approximately threefold higher in gastric juice in all groups. Omeprazole treatment increased gastric pH and did not affect metronidazole Cmax or the time required for this to be reached (tmax) in plasma, saliva, or gastric juice. However, omeprazole significantly reduced metronidazole transfer from plasma to gastric juice in H. pylori-positive but not H. pylori-negative subjects, as shown by statistical analysis of AUC(0-2 h). CONCLUSION: Short-term treatment with omeprazole in H. pylori- positive volunteers reduces the amount of metronidazole transferred from plasma to gastric juice. This seems to occur in a pH-independent form.     

Transfer of clarithromycin to gastric juice is enhanced by omeprazole in Helicobacter pylori-infected individuals.

BACKGROUND: The effects of proton-pump inhibitors and Helicobacter pylori infection on the distribution of drugs employed for the eradication of H. pylori are poorly understood. The aim of this study was to investigate the effects of a 7-day oral administration of 20 mg omeprazole on the distribution of clarithromycin in the gastric juice of individuals with H. pylori infection. METHODS: Eighteen H. pylori-infected dyspeptic male volunteers without endoscopic lesions were enrolled in a study with an open, randomized, two-period crossover design and a 21-day washout period between phases. Plasma and gastric juice concentrations of clarithromycin in subjects with and without omeprazole pretreatment were measured by means of liquid chromatography coupled to tandem mass spectrometry. RESULTS: The maximum concentration of clarithromycin (Cmax) and the area under the time-concentration curve from 0 to 2 h (AUC0-2h) were significantly higher in gastric juice than in plasma. Omeprazole treatment further augmented clarithromycin Cmax and AUC0-2h in gastric juice approximately 2-fold (P < 0.05). CONCLUSIONS: Short-term treatment with omeprazole in H. pylori-positive volunteers increases the amount of clarithromycin transferred to the gastric juice, confirming a synergism between these drugs. Our results suggest the presence of an active transport mechanism for clarithromycin from plasma to the gastric lumen, which is influenced by omeprazole.     

Helicobacter pylori eradication can induce platelet recovery in chronic idiopathic thrombocytopenic purpura

We prospectively investigated the prevalence of Helicobacter pylori (H. pylori) infection in a cohort of 54 adult Serbian patients with chronic idiopathic thrombocytopenic purpura (ITP), and examined the effects of its eradication on their platelet counts. H. pylori infection was diagnosed in 39/54 (72.2%) patients, using the 14C-urea breath test; and was significantly higher than in the healthy Serbian population (55% P < 0.05). H. pylori-positive patients were significantly older than H. pylori-negative patients (P = 0.006), though there were no significant differences regarding gender, disease duration, mean platelet counts, previous therapies and spleen status between H. pylori-positive and H. pylori-negative patients. Successful eradication was confirmed in 23/30 (77%) treated patients. Stable platelet recovery was registered in 6/23 eradicated patients (26.1%) and maintained for 18 months. Complete and partial remissions were achieved in two and four patients, respectively, including one highly refractory patient. A significant mean platelet recovery was seen 6 months after successful H. pylori eradication in the group of 23 patients (P < 0.05). No platelet recovery was registered in either H. pylori-negative (n = 15), untreated H. pylori-positive patients (n = 9) or H. pylori-positive non-eradicated patients (n = 7). Even though the pathogenetic mechanisms of H. pylori-induced thrombocytopenia remain obscure, the results of this small prospective study support the use of H. pylori eradication as an effective non-immunosuppressive treatment for chronic ITP.     

The impact of B(12) treatment on gastric emptying time in patients with Helicobacter pylori infection

GOALS: The role that vitamin B12 deficiency plays in upper gastrointestinal motor dysfunction is not clear. The aim of this study was to determine whether B12 replacement therapy improves prolonged gastric emptying time in dyspeptic patients with Helicobacter pylori infection. MATERIALS AND METHODS: The study included 34 H. pylori-positive patients who had low serum levels of B12 but had no other factors associated with altered gastric motility. Each patient underwent a radionuclide gastric emptying study before and after 3 months of B12 replacement therapy. Dyspepsia scores were calculated pretherapy and posttherapy using a semiquantitative scale. A vitamin B12 preparation (1000 microg/d) was given intramuscularly for the first 10 days and then orally for 80 days. H. pylori eradication therapy was delayed for 3 months until the posttreatment radionuclide study was completed. RESULTS: The mean gastric emptying time before B12 treatment was significantly longer than that after treatment (230 +/- 190 minutes vs. 98 +/- 29 minutes, respectively; P < 0.0001). The mean dyspepsia score was also significantly improved by treatment (5.4 +/- 1.0 vs. 1.2 +/- 1.0, respectively; P < 0.0001). CONCLUSION: Vitamin B12 deficiency appears to play an important role in the development of gastric dysmotility and its clinical consequences. Replacement therapy will improve gastric emptying in some patients with dyspepsia.     

根除幽门螺杆菌对功能性消化不良疗效的研究

背景:功能性消化不良(FD)的患病率始终居高不下,目前就幽门螺杆菌(H.pylori)阳性的FD患者是否需根除H.pylori尚存在争议。目的:探讨根除H.pylori对H.pylori阳性FD患者的疗效。方法:200例H.pylori阳性FD患者随机分为治疗组(100例.予以枸橼酸铋雷尼替丁400mg+阿莫西林1000mg+克拉霉素250mg,2次/d,疗程1周)和对照组(100例,予以铝碳酸镁1000mg,3次/d,疗程1周)。随访结束后评估H.pylori根除率和FD症状改善情况。结果:治疗组的H.pylori根除率分别为87.5%(PP分析)和84.0%(ITT分析),对照组H.pylori根除率为0%。H.pylori根除亚组FD症状改善的总有效率显著高于H.pylori未根除亚组和对照组(90.5%对41.7%和45.9%,P0.01)。结论:部分H.pylori阳性FD患者根除H.pylori后,其症状可长期缓解,因此对部分H.pylori阳性FD患者根除H.pylori是一种值得推广的有效治疗手段。     

Helicobacter pylori eradication lowers esophageal sphincter pressures in functional dyspepsia patients

BACKGROUND/AIMS: Helicobacter pylori infection is the most common cause of gastroduodenal diseases. The role H. pylori eradication in functional dyspepsia patients is contradictory. We performed this study to determine the effects of H. pylori eradication in functional dyspepsia patients with respect to physiological and histological parameters including esophageal sphincter functions. METHODOLOGY: We studied 20 functional dyspepsia patients, whose H. pylori infection was confirmed by histology and urease test. We also confirmed eradication using the same methods after three months. We performed 24-hour esophageal pH monitoring, esophageal manometry, meal stimulated gastrin release test and measured dyspepsia severity score and gastric emptying time before and three months after eradication. Eradication regimen consisted of omeprazol 20 mg b.i.d., clarithromycin 500 mg b.i.d. and metranidazol 500 mg b.i.d., for two weeks. Gastric inflammation and H. pylori density within biopsy samples from the antrum (n = 4), corpus (n = 4), cardia (n = 2), fundus (n = 2), duodenum (n = 2) and distal esophagus (n = 1) were assessed. RESULTS: Dyspepsia severity score (P < 0.001), meal stimulated gastrin levels, upper (P = 0.01) and lower (P = 0.06) sphincter pressures were decreased after eradication irrespective of gastric histology; but gastric emptying times (P = 0.87) and pH < 4.5% reflux (P = 0.91) were not changed significantly. CONCLUSIONS: H. pylori eradication results in decreased esophageal sphincter pressures irrespective of gastric histology in functional dyspepsia patients. These decreases are not associated with increased objective reflux or reflux symptomatology. The clinical significance of these finding deserves further evaluations.     

How to eradicate Helicobacter pylori using amoxicillin and omeprazole in the remnant stomach

BACKGROUND/AIMS: We previously investigated the effects of amoxicillin/omeprazole combined therapy on patients who were Helicobacter pylori (H. pylori) positive after gastrectomy for the treatment of gastric cancer, and we determined the difference in amoxicillin dosage between the therapeutic successes and failures. In the present study, assuming that amoxicillin dosage should be determined on the basis of body weight of each patient, we examined whether the eradication of H. pylori would be improved by using this novel dose-selection method. METHODOLOGY: We have previously reported about eradication of H. pylori of remnant stomach as follows. Patients who underwent gastrectomy for the treatment of gastric cancer were enrolled if H. pylori was detected in their remnant stomach after the operation. Of these patients, 22 were treated with amoxicillin at 750 mg/day for 2 weeks and omeprazole at 20 mg/day for 8 weeks. For the evaluation of H. pylori eradication, endoscopic examination and 13C-urea breath test were performed 12 weeks after the initiation of the treatment. The amoxicillin dosage in the therapeutic successes was compared with that in the therapeutic failures, and we found that the dosage was 14.1 +/- 1.5 and 12.5 +/- 1.5 mg/kg/day in the successes and the failures, respectively. Following these results, another 10 H. pylori-positive patients were treated with amoxicillin greater than 16 mg/kg/day for 2 weeks and omeprazole at 20 mg/day for 8 weeks, and H. pylori eradication was evaluated as mentioned above. The efficacy of the drug therapy on H. pylori infection was compared between the two groups that one group (Group A) is treated with amoxicillin 750 mg/day for 2 weeks and omeprazole at 20 mg/day for 8 weeks and the other group (Group B) is treated with 1250 mg/day for 2 weeks and omeprazole at 20 mg/day for 8 weeks. RESULTS: The eradication rate of H. pylori in Group B (84.6%) was higher than that in Group A (42.1%). There was significant difference between the two groups (p = 0.028). CONCLUSIONS: We assumed that the optimal dosage of amoxicillin was over 15.6 mg/kg/day for omeprazole-amoxicillin combined therapy for gastrectomized patients who were H. pylori positive, and the favorable therapeutic effects could be obtained by applying this amoxicillin dosage to the eradication of H. pylori.     

Does the depth of gastric ulceration influence a modified dual therapy with amoxicillin and lansoprazole for Helicobacter pylori-associated gastric ulcer?

PURPOSE: To clarify whether the depth of ulceration evaluated by endoscopic ultrasonography (EUS) influences a modified dual therapy with amoxicillin and lansoprazole for the treatment of Helicobacter pylori-positive patients with gastric ulcer. PATIENTS AND METHODS: Twenty-two consecutive cases of gastric ulcer (nine superficial ulcers and 13 deep ulcers) in H pylori-positive patients were studied. Ten of 22 patients received a two-week eradication therapy with amoxicillin 1500 mg/day, lansoprazole 30 mg/day and a new antiulcer agent with features in common with sucralfate, ecabet sodium, 2.0 g/day. They continued to receive the same doses of lansoprazole and ecabet sodium for the next six weeks. The other 12 patients received the same therapy except for those who underwent the four-week amoxicillin treatment. All patients underwent EUS both at the start of the study and eight weeks later. They then received ecabet sodium alone for the next six months as a maintenance therapy, followed by a six-month interval with no treatment. The final endoscopy was done one year after H pylori eradication therapy was completed to evaluate H pylori status and ulcer recurrence. RESULTS: The rates of endoscopic healing and H pylori eradication in the nine patients with superficial ulcer were 100%, irrespective of the period of amoxicillin treatment. In contrast, the rates of endoscopic evidence of healing and H pylori eradication in the 13 patients with deep ulcer were different for each period of amoxicillin treatment; that is, the rates of reduction in ulcer determined by echo and H pylori eradication in the four patients treated with the two-week amoxicillin course were significantly lower (P=0.03) than those in the nine patients treated with the four-week course. CONCLUSION: Ulcer depth is likely to influence the success of amoxicillin treatment for H pylori-positive patients with gastric ulcer.     

Gastric electrical activity and gastrointestinal hormones in dyspeptic patients

AIMS: To explore the patterns of gastric electrical activity, gastric emptying and gastrointestinal hormones in dyspeptic patients and relate them to Helicobacter pylori status. METHODS: Twenty-two patients with functional dyspepsia and 29 healthy volunteers underwent cutaneous electrogastrography and dynamic ultrasound before and after a test meal. All dyspeptic patients underwent endoscopy and biopsy; all subjects were examined for the presence of antibodies to H. pylori, and the plasma levels of gastrin, neurotensin, cholecystokinin, and pancreatic polypeptide were measured. RESULTS: The area under the curve (AUC) of the normal slow wave percentage was lower in dyspeptic patients than controls (Kruskal-Wallis p = 0.016; Dunn's test: H. pylori-positive patients: 21,235.5 [19,101.0-22,688.8] vs. H. pylori-negative controls: 22,532.0 [20,133.0-23,755.0], p < 0.05). The AUC of the tachygastria percentage was higher in dyspeptic patients than controls (p = 0.0001; H. pylori-positive patients: 2,173.5 [325.8-3,055.3] vs. H. pylori-negative controls: 682.0 [118.5-1,902.4], p < 0.05; H. pylori-negative patients: 1,843.0 [1,107.0-4,277.0] vs. H. pylori-negative controls: 682.0 [118.5-1,902.4], p < 0.05). The AUC of gastrin was higher in H. pylori-positive than H. pylori-negative subjects (p = 0.0002; H. pylori-positive patients: 16,146.5 [11,368.8-33,141.7] vs. H. pylori-negative controls: 11,250.0 [5,674.0-17,448.0], p < 0.05; H. pylori-positive controls: 20,250.0 [12,070.0-64,430.0] vs. H. pylori-negative controls: 11,250.0 [5,674.0-17,448.0], p < 0.05). In the total group of dyspeptic patients and in the H. pylori-positive patients, a negative correlation was found between the AUC of neurotensin and the total score for postprandial fullness (dyspeptic patients r = -0.51, p = 0.01; H. pylori-positive patients r = -0.66, p = 0.02). CONCLUSIONS: In dyspeptic patients, alterations in gastric electrical activity were not related to H. pylori infection. Nevertheless, H. pylori infection induces higher gastrin levels in both patients and asymptomatic subjects.     

Relevance of underlying disease and bacterial vacA and cagA status on the efficacy of Helicobacter pylori eradication

AIM: To study the effects of Helicobacter pylori associated diseases and the bacterial vacA and cagA statuses on the efficacy of H. pylori eradication. METHODS: A prospective study in a consecutive series of outpatients of a gastroenterological institution and of a primary practice. A series of 146 H. pylori positive patients with peptic ulcer disease (PUD; n = 40) or nonulcer dyspepsia (NUD; n = 106) were evaluated. H. pylori vacA genotpyes and cagA status were determined directly in gastric biopsy specimens by polymerase chain reaction. The patients were treated with triple-therapy regimens consisting of a proton pump inhibitor and two antibiotics twice daily for 7 days. Reevaluation of H. pylori was determined 4-5 weeks later by endoscopy or 13C urea breath test. RESULTS: 123 patients completed the study. In 8 patients, colonization with two or more H. pylori strains was found. The overall cure rate was 84.6% (104/123). The eradication rates were significantly higher in patients with PUD (94.4%, 34/36) than in those with NUD (81.6%, 71/87; p < 0.05). In patients with cagA-positive H. pylori strains, the eradication rate was 89.0% (73/82) as compared with 78.8% (26/33) in those with cagA-negative strains (p = 0.15). The vacA genotype had no effect on the efficacy of H. pylori eradication. CONCLUSION: Using 1-week triple-therapy regimens, treatment of H. pylori infection is more effective in patients with PUD than in those with NUD.     

Effect of Helicobacter pylori eradication on gastroesophageal function

BACKGROUND: To elucidate the cause of possible occurrence of reflux esophagitis after Helicobacter pylori eradication, gastric and esophageal function among H. pylori infected Japanese patients were evaluated both before and after eradication therapy. METHODS: Nine H. pylori-positive patients were studied before and 6 months after successful H. pylori eradication. Studies included gastric emptying, esophageal manometry, gastric and esophageal pH monitoring as well as measuring serum levels of gastrin, pepsinogen I and pepsinogen II. RESULTS: Helicobacter pylori eradication was associated with a significant change in serum gastrin and pepsinogen levels, consistent with the improvement in mucosal inflammation. There was no significant change in gastric emptying, fasting or postprandial lower esophageal sphincter (LES) pressure, esophageal primary peristaltic contractions, frequency of transient LES relaxation, or gastroesophageal reflux, as assessed by 24 h pH monitoring. The percent time of the gastric pH>4 at night decreased significantly. A 41-year-old male developed erosive gastroesophageal reflux disease (GERD) (Los Angeles Classification Grade A) after eradication. Physiological studies showed he had abnormal esophageal motility prior to H. pylori eradication. CONCLUSIONS: With the exception of gastric pH at night, most patients did not experience a significant change in gastric or esophageal function after H. pylori eradication. Development of GERD post H. pylori eradication likely reflects an increase in the acidity of the refluxate superimposed on pre-existing abnormalities in gastroesophageal motility.