METHODS: A study of all patients with significant GOER seen at the Paediatric Gastroenterology Unit, Queen Elizabeth Hospital for Children, Hackney Road, London, between December 1994 and August 1995.
RESULTS: The median age at referral was 16 months. Presenting symptoms were recurrent vomiting (72%), epigastric and abdominal pain (36%), feeding difficulties (29%), failure to thrive (28%) and irritability (19%). Continuous 24-h lower oesophageal pH studies performed in 57 children showed 20 (35%) had a reflux index of between 10% to 20%, 14 (25%) had a index > 20%, and six (11%) had a postprandial reflux index > 10%. Reflux was shown in 38 (62%) of 62 children who underwent barium studies. None had significant anatomical abnormalities, but in the 22 children who had a negative barium studies, six had severe reflux (reflux index > 20%). Upper gastrointestinal endoscopy performed in 47 children showed reflux oesophagitis in 29 (62%), oesophageal ulceration in three, and Barrett's oesophagus in one. All of the children were treated with standard medical therapy. Sixty-six per cent were able to discontinue medication within 12 months and remained well. Four children (6%) required Nissen's fundoplication for failure to respond to medical therapy.
CONCLUSIONS: Most infants with GOER have an uncomplicated course. False negative results were noted in both pH monitoring and barium meal. Up to 80% of children, with therapy, will improve within 12 months.
AIM: To assess the efficacy, safety and compliance of an H. pylori eradication regimen and examine clinical factors that potentially determine eradication.
METHODS: Consecutive outpatients from a multicultural, south east Asian, population with H. pylori infection, with or without peptic ulcer, were treated with lansoprazole 30 mg, amoxycillin 1 gm, clarithromycin 500 mg, twice a day for seven days. Eradication was assessed by either rapid urease, histology or urea breath test. Compliance and side effects were recorded. The eradication rate and effect of ethnicity, age, sex, usage of alcohol, smoking and non-steroidal anti-inflammatory drugs, history of ulcer and endoscopic diagnosis on eradication were examined by univariate and multivariate analysis.
RESULTS: Of 113 patients, the eradication rate by intention to treat was 98/113 (87%) (95% confidence interval [CI] 80-93%) and per protocol was 98/106 (92%) (95% CI 87-97%). Using Fisher's exact test, eradication was more successful in Chinese (intention to treat and per protocol respectively p=0.02 and p<0.001) compared to non-Chinese. By logistic regression analysis ethnicity was an independent factor associated with eradication success (p=0.0025). Side effects occurred in five (4.4%), resulting in cessation of treatment.
CONCLUSIONS: This one week eradication regimen is safe and effective in south east Asians. Chinese ethnicity may be associated with a higher likelihood of eradication success.
PATIENTS AND METHODS: Patients with unequivocal evidence of H. pylori infection based on culture, histology and rapid urease test of both antrum and corpus biopsies were recruited for the study. The study was a randomized, investigator-blind, comparative study. Patients received either omeprazole 20 mg o.m., clarithromycin 250 mg b.d. and amoxycillin 500 mg b.d. (OAC) or omeprazole 20 mg o.m., metronidazole 400 mg b.d. and clarithromycin 250 mg b.d. (OMC) for 1 week. Patients were assessed for successful eradication, which was defined as absence of bacteria in all tests (culture, histology and urease test on both antral and corpus biopsies), at least 4 weeks after completion of therapy.
RESULTS: Eighty-two patients were recruited for the study. Eradication rates on intention-to-treat analysis were--OAC: 36/41 (87.8%, 95% CI: 73.8, 95.9); OMC: 33/41 (80.5%, 95% CI: 65.1, 91.2). On per protocol analysis were--OAC: 36/40 (90%, 95% CI: 76.3, 97.2); OMC: 32/38 (84.2%, 95% CI: 68.7, 94.0). All side-effects encountered were mild and no patient discontinued treatment because of intolerance to medications. The most common side-effects were altered taste (OAC 31.7%, OMC 53.7%) and lethargy (OAC 14.6%, OMC 19.5%). Pre-treatment metronidazole resistance was encountered in 34/63 (54.0%) patients. No bacterial strains were found with primary resistance to clarithromycin. Metronidazole resistance did not significantly affect eradication rates. Emergence of resistance to clarithromycin was not seen post-therapy.
CONCLUSIONS: Both the OAC and the OMC regimens were convenient and well-tolerated treatments for H. pylori. However, eradication rates were lower than anticipated.
DESIGN: Prospective study.
PATIENTS AND METHODS: Patients were followed up endoscopically at 3, 6, 12 and 24 months after successful H. pylori eradication and duodenal ulcer healing. H. pylori status was determined by culture, rapid urease test, Gram's stain of a fresh tissue smear and histological examination of antral biopsies and rapid urease test and histological examination of corpus biopsies.
MAIN OUTCOME MEASURES: Duodenal ulcer healing, H. pylori reinfection.
RESULTS: Thirty-eight patients with duodenal ulcer disease (35 active, 3 healed) had successfully eradicated H. pylori following treatment with omeprazole/amoxycillin (n = 11), omeprazole/amoxycillin/metronidazole (n = 16) and colloidal bismuth subcitrate/ amoxycillin/metronidazole (n = 11). All patients with active duodenal ulcer had healed ulcers at the end of therapy. Thirty-five of 38 patients were seen according to schedule up to 2 years; two patients were seen up to 12 months and one up to 6 months only. Reinfection with H. pylori was not recorded in any of our patients. Shallow duodenal ulcers were noted in three patients at 1-year follow-up, two of whom admitted to taking non-steroidal anti-inflammatory drugs (NSAIDs); H. pylori status was negative in all three. Subsequent follow-up revealed spontaneous healing of the ulcers in all three patients. At 2 years, one patient whose H. pylori status was negative had recurrence of duodenal ulcer. All of the three patients who defaulted subsequent to follow-up were negative for H. pylori and had healed ulcers on follow-up endoscopy at 6 and 12 months.
CONCLUSION: Reinfection rate with H. pylori was zero in a group of South-East Asian patients who had successfully eradicated the infection. Duodenal ulcer relapse was also low (2.9%) in this group of patients at 2 years.
METHODS: Twenty-eight male Wistar rats were randomly assigned to four groups of seven rats. The two control groups were administered vitamin-free palm oil (vehicle) and the two treatment groups were given omeprazole (20 mg/kg) or tocotrienol (60 mg/kg) by oral gavage. After 28 d of treatment, rats from one control group and both treated groups were subjected to WIRS one time for 3.5 h. Gastric lesions were measured and gastric tissues were obtained to measure vascular endothelial growth factor (VEGF), epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), and transforming growth factor-alpha (TGF-α) mRNA expression.
RESULTS: Rats exposed to WIRS for 3.5 h demonstrated the presence of considerable ulcers in the form of gastric erosion. The lesion index in the stressed control (S) group was increased (P < 0.001) compared to the tocotrienol treated and omeprazole treated groups. Stress led to a decrease in gastric VEGF (P < 0.001), bFGF (P < 0.001) and TGF-α (P < 0.001) mRNA levels and caused an increase in EGF mRNA (P < 0.001) that was statistically significant compared to the non-stressed control group. Although both treatment agents exerted similar ulcer reducing ability, only treatment with tocotrienol led to increased expression of VEGF (P = 0.008), bFGF (P = 0.001) and TGF-α (P = 0.002) mRNA.
CONCLUSION: Tocotrienol provides gastroprotective effects in WIRS-induced ulcers. Compared to omeprazole, tocotrienol exerts a similar protective effect, albeit through multiple mechanisms of protection, particularly through up-regulation of growth factors that assist in repair of gastric tissue injuries.
OBJECTIVE: The purpose of this study was to investigate the influence of P-gp modulation on the efficacy of treatment regimen.
METHOD: P-gp modulation in rats was performed by using P-gp inducer (150 mg/kg rifampicin) and P-gp inhibitor (10 mg/kg cyclosporine A) for 14 days prior to be infected with Helicobacter pylori (H. pylori). The rats were further divided into groups, which were normal control, vehicle control, antibiotics and omeprazole, antibiotics only and omeprazole only for another 2 weeks of treatment. The ulcer formation and P-gp expression were determined by using macroscopic evaluation and western blot analysis, respectively.
RESULTS: The highest P-gp expression was shown in the induced P-gp rats (2.00 ± 0.68) while the lowest P-gp expression was shown in the inhibited P-gp rats (0.45 ± 0.36) compared to the normal P-gp rats. In all groups, the rats which were infected with H. pylori, had a significant increase (p