Annoyed with Haemorrhoids? Risks of the Emborrhoid Technique

Digestive Diseases and Sciences - Haemorrhoids, a common ailment afflicting mostly Western patients, can produce bothersome symptoms, in particular pain, pruritus, and bleeding. There is a wide...     

Isotope Ratio Mass Spectrometry (IRMS) Versus Laser-Assisted Ratio Analyzer (LARA)

This study was carried out to compare the measurements and the diagnostic accuracy of the traditional expensive IRMS and the new economical LARA system using two doses of [¹³C]urea + two different test meals in patients undergoing upper gastrointestinal endoscopy, both before and after anti-Helicobacter treatment. A total of 354 dyspeptic patients underwent endoscopy with gastric biopsies to diagnose H. pylori infection by CLO-test and histology. No patients had taken antibiotics, bismuth, or antisecretory drugs in the 4 weeks before testing. After overnight fasting, breath samples were collected simultaneously in both plastic and glass tubes at baseline and at 30 and 60 min after urea ingestion. In 237 patients 100 mg [¹³C]urea + Ensure and in 117 patients 75 mg [¹³C]urea + citric acid were given. The test was also performed with the two urea dosages and meals in 67 and 64 infected patients, respectively, four weeks after anti-Helicobacter therapy. H. pylori was considered eradicated when both biopsy-based tests were negative. A value >5 was considered positive. Breath samples with insufficient CO₂ levels at both 30 and 60 min were excluded from final analysis (N = 37 in pre- and N = 8 in posttreatment). There was excellent agreement between overall values of the two machines with both [¹³C]urea 100 mg + Ensure and [¹³C]urea 75 mg + citric acid. The 95% CI of the difference against the mean was wider with the former (mean –1.3, +6.3, and –9.4) than with the latter urea dosage and test meal (mean –1.2, +5.2 and –8.1). LARA and IRMS were equally effective (P = NS) in distinguishing infected from uninfected patients before therapy using both doses of [¹³C]urea and test meals (sensitivity ranged from 95% to 99% and specificity from 95% to 97%). This good performance was maintained in the posttreatment phase (sensitivity ranged from 90% to 100% and specificity from 90% to 97%), without any statistical difference among the various combinations (P = NS). The LARA system is a valid alternative to IRMS in the diagnosis of H. pylori infection. Both machines provide highly reliable results after 30 min, so that the 60 min sample can be avoided. The dose of 75 mg + citric acid suffices to ensure an accurate UBT. The test performed with both devices and [¹³C]urea dosages is very effective also for posttherapy evaluation of H. pylori status.     

Helicobacter pylori infection is not involved in the pathogenesis of either erosive or non-erosive gastro-oesophageal reflux disease

BACKGROUND: The majority of reflux patients have non-erosive reflux disease. AIM: To evaluate the influence of Helicobacter pylori on oesophageal acid exposure in patients with both non-erosive and erosive reflux disease and in a group of controls. The pattern and distribution of chronic gastritis were also assessed. METHODS: One hundred and twelve consecutive patients with symptoms of gastro-oesophageal reflux disease agreed to undergo both upper gastrointestinal endoscopy and 24-h oesophageal pH-metry. Patients were grouped as H. pylori-positive or H. pylori-negative on the basis of both CLO-test and histology, and as cases with or without oesophagitis on the basis of endoscopy. The controls consisted of 19 subjects without reflux symptoms and with normal endoscopy and oesophageal pH-metry. RESULTS: H. pylori was positive in 35 patients (31%) and in six controls (31%); oesophagitis was found in 44 patients (39%) and non-erosive reflux disease in 68 (61%). The prevalence of chronic gastritis in the antrum and corpus was higher in H. pylori-positive than in H. pylori-negative patients (P < 0.001), but was more frequently mild (P < 0.001) than moderate or severe. The percentage total time the oesophageal pH < 4.0 was higher in patients than in controls (P < 0.008-0.001), but there was no difference between H. pylori-positive and H. pylori-negative patients (12.3% vs. 12%, P = 0.43) or H. pylori-positive and H. pylori-negative controls (1.07% vs. 1.47%, P = 0.19). CONCLUSIONS: H. pylori infection had the same prevalence in reflux patients and in controls. It did not affect oesophageal acid exposure, as there was no difference between H. pylori-positive and H. pylori-negative individuals. The high prevalence of mild body gastritis in H. pylori-positive patients suggests that H. pylori eradication is unlikely to lead to gastric functional recovery, which might precipitate or worsen symptoms and lesions in patients with gastro-oesophageal reflux disease.     

Comparison of the main oesophageal pathophysiological characteristics between short- and long-segment Barrett's oesophagus

AIM: To assess the oesophageal manometric characteristics and 24-h pH profiles of patients with both short-segment and long-segment Barrett's oesophagus and compare them with those of patients with reflux oesophagitis and controls. METHODS: Seventy-nine patients who had undergone upper digestive endoscopy were recruited: 16 had short-segment Barrett's oesophagus, 13 had long-segment Barrett's oesophagus, 25 had grade III oesophagitis according to the Savary-Miller classification and 25 were used as controls. The diagnosis of Barrett's oesophagus was based on the histological detection of specialized intestinal metaplasia, which extended < 3 cm into the oesophagus in patients with short-segment disease and > 3 cm in patients with long-segment disease. All subjects underwent oesophageal manometry and basal 24-h oesophageal pH monitoring. RESULTS: The lower oesophageal sphincter pressure was significantly lower in patients with reflux oesophagitis and short-segment and long-segment Barrett's oesophagus than in controls (P=0.0004-0.0001), but there was no difference among the three reflux groups. The peristaltic wave amplitude of patients with long-segment Barrett's oesophagus was significantly lower than that of controls (P=0.002) and patients with short-segment Barrett's oesophagus (P=0.02), but was no different from that of patients with reflux oesophagitis. The percentage of non-propagated wet swallows was significantly higher in patients with reflux oesophagitis and short-segment and long-segment Barrett's oesophagus when compared with that of controls (P=0.0004-0.0001). The total percentage of time the oesophagus was exposed to pH < 4.0 was significantly higher in patients with reflux oesophagitis and short-segment and long-segment Barrett's oesophagus (P=0.0001) than in controls, and was higher in patients with long-segment disease than in those with short-segment disease (P=0.01). CONCLUSIONS: Long-segment Barrett's oesophagus is characterized by a greater impairment of peristaltic wave amplitude and a higher oesophageal acid exposure than is short-segment Barrett's oesophagus. However, both forms are linked to increased acid reflux.     

Effect of Helicobacter pylori Eradication on 24-Hour Gastric pH and Duodenal Gastric Metaplasia

Published data on the regression of the extent of duodenal gastric metaplasia (DGM) after the eradication of Helicobacter pylori infection and the normalization of the organism-induced alterations in gastric physiology are scanty and controversial. Therefore, we decided to assess the circadian pattern of gastric acidity and the degree of DGM before and one year after H. pylori eradication in a group of duodenal ulcer patients. Fifteen consecutive H. pylori-positive patients with endoscopically proven duodenal ulcer were recruited for this study. The diagnosis of H. pylori infection was based on CLO-test and histology, and DGM was assessed on four bulb biopsies taken before and one year after H. pylori eradication. At the same time, gastric pH was measured by 24-hr continuous intraluminal recording. H. pylori eradication was ascertained by means of concomitant negative CLO-test and histology performed both four weeks after the end of the eradicating treatment and at the one-year endoscopic control. After successful cure, all patients discontinued any antiulcer medication. The mean 24-hr gastric pH was 1.7 ± 0.4 before and 1.6 ± 0.4 after one year of H. pylori eradication (P = 0.75). DGM improved in three cases, worsened in four cases, and was unchanged in eight cases at the one-year control (P = 0.87). No correlation was found between 24-hr gastric pH and DGM (P = NS) both at baseline and one year after eradication. Our results show that neither circadian gastric acidity nor DGM change significantly one year after H. pylori eradication in duodenal ulcer patients. Thus, the disappearance of H. pylori infection does not determine any increase in gastric pH and any reversal of gastric-type epithelium in the duodenum.     

Circadian pattern of intragastric acidity in patients with non-erosive reflux disease (NERD)

BACKGROUND: Most patients with gastro-oesophageal reflux disease have non-erosive reflux disease. Proton pump inhibitors are less effective than expected in these patients, but no previous study has measured their 24-h gastric pH values. AIMS: To evaluate whether there are differences in 24-h intragastric acidity between reflux patients with and without oesophagitis and controls. The influence of Helicobacter pylori on the gastric pH of reflux patients was also assessed. METHODS: Sixty-three consecutive patients with gastro-oesophageal reflux disease symptoms who agreed to undergo endoscopy and 24-h pH-metry were recruited. Twenty-five (39%) had erosive oesophagitis and 38 (61%) did not. H. pylori was diagnosed by CLO test, histology and 13C-urea breath test. Gastric pH was also measured in 30 controls without digestive symptoms. RESULTS: H. pylori was found in seven of the 25 (28%) patients with oesophagitis and 14 of the 38 (37%) patients with non-erosive reflux disease. Oesophageal pH-metry was abnormal in 21 of the 25 (84%) patients with oesophagitis and in 32 of the 38 (84%) patients with non-erosive reflux disease. The median gastric pH did not differ between patients with and without oesophagitis or between them and controls during the 24 h (P = 0.8) and other time intervals (P = 0.2-0.4). The gastric pH did not differ between infected and non-infected patients with oesophagitis (P = 0.2-0.4) or non-erosive reflux disease (P = 0.3-0.8). CONCLUSIONS: The circadian pattern of intragastric acidity does not differ between patients with non-erosive reflux disease and oesophagitis. Moreover, the study confirms that H. pylori infection does not affect the gastric pH in either group of reflux patients.     

Stool antigen assay (HpSA) is less reliable than urea breath test for post-treatment diagnosis of Helicobacter pylori infection

BACKGROUND: The diagnostic yield of the stool antigen test (HpSA) in evaluating the results of Helicobacter pylori eradication therapy is controversial, but many studies have used only the 13C-urea breath test (13C-UBT) as a gold standard which has greatly reduced their relevance. AIM: To compare the reliability of HpSA and 13C-UBT in patients post-treatment using biopsy-based methods as reference tests. METHODS: A total of 100 consecutive dyspeptic patients (42 male and 58 female; mean age, 56 +/- 18 years) were enrolled in our study. All patients were H. pylori positive on the basis of at least two biopsy-based methods, and underwent 1 week of treatment with various triple therapies. They were again endoscoped 4 weeks after completing therapy and six biopsy specimens were taken from the gastric antrum and corpus for rapid urease test, histology and culture. HpSA and 13C-UBT were also performed within 3 days of the second endoscopy. RESULTS: On the basis of biopsy-based tests, infection was eradicated in 77 patients but continued in 23. Three false negatives were observed with HpSA and two with 13C-UBT. In contrast, the number of false positives was significantly higher (P < 0.01) with HpSA than with 13C-UBT (nine vs. one), confirming the lower specificity of the former test. The overall accuracy of HpSA was 88% vs. 97% for 13C-UBT (P < 0.02). CONCLUSIONS: HpSA has lower diagnostic value than 13C-UBT in the evaluation of the outcome of anti-H. pylori therapy. 13C-UBT remains the first-line diagnostic method to monitor eradication results. The use of HpSA should be reserved for those settings in which 13C-UBT is not available.     

The impact of antibiotic resistance on the efficacy of three 7-day regimens against Helicobacter pylori

BACKGROUND: Antibiotic resistance affects the success of anti-Helicobacter pylori therapies and varies greatly from country to country. AIM: To compare the efficacy of three short-term triple regimens in relation to H. pylori primary resistance in our region. METHODS: We enrolled 210 H. pylori-positive dyspeptic patients for this randomized, open, parallel-group study. Three arms of 70 patients each received the following 1-week regimens: (1) ranitidine bismuth citrate 400 mg b.d. + clarithromycin 250 mg b.d. + metronidazole 500 mg b.d. (RCM); (2) bismuth subcitrate 240 mg b.d. + amoxycillin 1000 mg b.d. + metronidazole 500 mg b.d. (BAM); (3) omeprazole 20 mg o.d. + clarithromycin 250 mg b.d. + metronidazole 500 mg b.d. (OCM). H. pylori was assessed by CLO-test and histology before and 4 weeks after therapy. Antibiotic resistance was assessed by E-test. RESULTS: On intention-to-treat analysis RCM was more effective than OCM (84% vs. 69%; P < 0.03) and BAM (84% vs. 63%; P < 0.004). MIC determination was successful in 117 out of 210 patients (55%); metronidazole resistance was present in 52 out of 117 patients (44%) and clarithromycin resistance was present in 17 out of 117 patients (14%). Excellent cure rates were achieved when strains were sensitive to both antibiotics (100% with RCM and BAM and 90% with OCM), whereas RCM was superior to OCM (P=0.009) and BAM (P=0.001) with respect to overall resistant strains (94% vs. 57% and 38%, respectively). CONCLUSIONS: One-week RCM is the best regimen to eradicate H. pylori in our geographical area. This seems to be linked to the better ability of RCM compared to OCM and BAM in overcoming the high prevalence of H. pylori resistance to both metronidazole and clarithromycin in our region.     

Impact of long-term ranitidine and pantoprazole on accuracy of [13C]urea breath test

No previous study has analyzed the impact of long-term antisecretory drugs on the precision of [¹³C]urea breath test (UBT). We assessed the rate of UBT conversion from positive to negative results during 60-day therapy with standard doses of ranitidine and pantoprazole. For this purpose, we recruited 60 dyspeptic patients with H. pylori infection ascertained on the basis of the concomitant results of CLO-test, histology, and UBT. Our patients were randomly assigned to receive ranitidine 300 mg at night or pantoprazole 40 mg in the morning for 60 days. UBT was performed at baseline and on days 14, 30, and 60, while patients were still taking antisecretory drugs. Patients with false-negative UBT on day 60 repeated the test every 3 days until conversion. After overnight fasting, duplicate breath test samples were taken from each patient before and 30 min after ingestion of 75 mg [¹³C]urea dissolved in 150 ml of 0.033 mol/liter citric acid. Four patients dropped out of the study. Both drugs induced similar false-negative UBTs on day 14 of dosing (P = 0.5). Afterwards, the three false-negative UBTs in the ranitidine group again became positive during therapy and particularly on day 30 of dosing. Of the four false-negative UBTs in the pantoprazole group at day 60, one became positive after 3 and three after 9 days of therapy cessation. Our findings show that the long-term use of ranitidine and pantoprazole at standard doses has different effects on the results of UBT. In the pantoprazole group patients again became positive within 3–9 days after stopping 60-day therapy, whereas in the ranitidine group patients reverted to positive on day 30 of dosing while they were still on treatment and this was likely due to development of tolerance. Therefore, patients taking pantoprazole need at least a 10-day withdrawal before UBT testing, while those taking ranitidine for at least 30 days can undergo UBT without the necessity of a wash-out period.