Maho Iwamoto

Usefulness of rectally administering [1-13C]-butyrate for breath test in patients with active and quiescent ulcerative colitis

Objective. Impaired butyrate metabolism plays a part in ulcerative colitis (UC). To assess the usefulness of measuring butyrate metabolism as an indication of inflammatory activity, we investigated the rate of butyrate metabolism by breath test after administering [1-13C]-butyrate rectally to patients with UC. Material and methods. Thirty-eight UC patients (22 active, 16 quiescent) and 15 healthy controls were given [1-13C]-butyrate enemas. The 13CO2 production rate was measured by breath test using an infrared spectrometric analyzer. Results. The quantity of expired 13CO2 was significantly lower in the active than in the quiescent UC and control groups. Cumulative 13CO2 production at 240 min showed significant negative correlations with the clinical activity index (r= −0.65, p<0.0001), endoscopic activity index (r= −0.63, p=0.0001) and histology (r= −0.71, p<0.0001) in the active UC group. The 13CO2 production rate was significantly increased in the quiescent stage as compared with the active stage in six UC patients, in whom clinical remission was achieved, in accordance with improvements in the clinical activity index, the endoscopic activity index, histology and fecal butyrate concentrations. Significant inverse correlations between the cumulative 13CO2 production rate and these three parameters were seen in these six UC patients assessed in both the active and quiescent stages. Conclusions. Measurement of expired 13CO2 after rectally administering [1-13C]-butyrate in active and quiescent UC appears to be a promising and reliable method for evaluating disease activity and metabolic changes associated with amelioration of inflammation.

Helicobacter pylori eradication reduces platelet count in patients without idiopathic thrombocytopenic purpura.

Discrepant outcomes of Helicobacter pylori eradication in patients with idiopathic thrombocytopenic purpura have been reported. Here patients with dyspepsia and no other complications underwent gastroendoscopic examination and evaluation for Helicobacter pylori infection. Helicobacter pylori-infected patients with gastritis and gastric ulcer received eradication therapy: lansoprazole (60 mg/day), clarithromycin (400 mg/day), and amoxicillin (1500 mg/day) for 1 week. Lansoprazole 30 mg/day was administrated additional 7 weeks. Peripheral platelets were counted before treatment, 8 weeks after initiation of therapy, and at follow-up periods. Platelet counts in patients with both gastritis and gastric ulcer were evaluated with reference to the presence of Helicobacter pylori infection. Eighty-seven patients with gastritis and 35 of those with gastric ulcer underwent successful eradication therapy. Peripheral platelet counts in patients with gastritis decreased from 235+/−55 to 228+/−58 (103/µL) (p = 0.0337), and those with gastric ulcer decreased from 248+/−60 to 232+/−48 (103/µL) (p = 0.020) 8 weeks after initiation of therapy. Non-eradicated patients did not show such a tendency. Helicobacter pylori eradication reduced peripheral platelet counts in patients with gastritis and gastric ulcer. Amelioration of thrombocytopenia by eradicating Helicobacter pylori appears to involve mechanisms specific to idiopathic thrombocytopenic purpura.

Long term changes in platelet counts after H. pylori eradication in non-ITP patients

Helicobacter pylori eradication is becoming a first-line therapy against idiopathic thrombocytopenic purpura (ITP) and its long term efficacy has already been reported. In contrast, eradication therapy reduced peripheral platelets in non-ITP patients 8 weeks later. To confirm the long term efficacy of Helicobacter eradication on platelet counts in non-ITP patients, we evaluated changes in peripheral platelet counts in endoscopically diagnosed patients with Helicobacter infection. Endoscopically diagnosed patients with Helicobacter infection received eradication therapy using amoxicillin (1500 mg/day), clarithromycin (400 mg/day) and lansoprazole (60 mg/day). The changes in platelet counts after Helicobacter eradication were serially evaluated for as long as 3 years or more. In total, 294 patients were enrolled: 243 patients successfully received eradication therapy and 51 were unsuccessfully treated. As a whole, peripheral platelet counts significantly decreased after Helicobacter eradication, being reduced by more than 1.0 × 109/l by 5–6 months, 1 year, 2 years and 3 years or more (from 24.2+/−5.6 to 23.1+/−5.0, 23.0+/−5.0, 22.1+/−4.5, 22.4+/−5.6, and 21.6+/−5.3 × 109/l: p = <0.0001, <0.0001, 0.0001, 0.0052, and <0.0001, respectively). Helicobacter pylori eradication finally reduced peripheral platelet counts around 2.0 × 109/l in non-ITP patients. There was a definite difference in platelet regulation by Helicobacter pylori between ITP and non-ITP patients. These bivalent effects, upregulation and downregulation, on the peripheral platelet induced by Helicibacter pylori infection appeared to originate from quite different mechanisms.

Helicobacter pylori Upregulates Peripheral Platelet Counts Mainly in Female Patients

To evaluate the influence of Helicobacter pylori and sex difference on peripheral platelet counts, dyspeptic patients without immunohaematologic disorders were evaluated. H. pylori infection was verified with the rapid urease test and serum anti-H. pylori IgG antibody. Platelet counts were analysed with a reference to H. pylori infection and sex difference. Among H. pylori-eradicated patients, changes in platelet counts were separately evaluated. Totally, 655 patients were enrolled: 340 patients were infected with H. pylori and 178 patients received eradication therapy, with a success rate of 88.2% (157/178). Females with H. pylori infection definitely manifested elevated platelet counts (infected vs. uninfected 244 ± 57 vs. 219 ± 54 × 109/l; p < 0.0001). H. pylori eradication reduced peripheral platelets by 8 weeks, 5–6 months, 1, 2 and ≧3 years after eradication in females from 248 ± 54 to 237 ± 49, 237 ± 54, 229 ± 48, 238 ± 61 and 232 ± 50 × 109/l (p = 0.0003, 0.0182, 0.0041, 0.0398 and 0.0289), respectively. In males, the reduction was verified by 8 weeks, 1 year and ≧3 years from 226 ± 52 to 217 ± 47, 214 ± 44 and 200 ± 49 × 109/l (p = 0.0464, 0.0164 and 0.0016), respectively. In conclusion, H. pylori infection upregulates platelet counts mainly in females, and eradication reduced peripheral platelets in both sexes. Females appeared more susceptible to H. pylori infection than males with regard to upregulation of platelet counts.

Evaluation of gastro-oesophageal flap valve is useful for diagnosing gastro-oesophageal reflux disease: GEFV FOR DIAGNOSIS OF GERD

Gastro‐oesophageal flap valve (GEFV) grade correlated with endoscopic reflux oesophagitis (RE) prevalence.