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Biomedical subjects

S Vigneri

Publications and source records attributed to S Vigneri.

At least 19 recordsLinked to original sources
PubMed2006

Normal values of 24-h ambulatory intraluminal impedance combined with pH-metry in subjects eating a Mediterranean diet.

BACKGROUND AND AIMS: Multichannel intraluminal impedance combined with pH-metry is a novel technique for studying gastro-oesophageal reflux. As refluxes are particularly frequent after meals, we carried out this study in order to assess the impact of a Mediterranean diet on normal values of impedancemetry. METHODS: Twenty-five Italian healthy subjects (13 men, median age 29 years, range 22-67 years) without reflux symptoms were recruited for this study. They underwent oesophageal 24-h impedance + pH-metry. A Mediterranean diet was given to all subjects on the day of examination and its total energy intake was 9668.5 kJ (2300 kcal). RESULTS: A total of 1518 refluxes were recorded during 24 h with more upright than recumbent episodes (median 15 versus 0; p<0.01). The median total acid exposure time was 0.5% (range 0-4.2%). Acid and weakly acidic refluxes were equally reported (49% versus 51%). Weakly acidic episodes were more frequent than acid ones during 1-h postprandial periods (68% versus 32%; p<0.0001). Liquid-only and mixed refluxes reached the proximal oesophagus (15 cm above lower oesophageal sphincter) in 42.6% of cases. Median acid clearing time was longer than median bolus clearing time (28 s versus 12 s; p<0.01). CONCLUSIONS: This study provides normal values of pH-impedancemetry in Italian people eating a Mediterranean diet and are suitable for comparative pathophysiological investigations on reflux patients who have dietary habits similar to those of our country.

Adult↗
PubMed2005

An evaluation of the antireflux properties of sodium alginate by means of combined multichannel intraluminal impedance and pH-metry.

BACKGROUND: Alginate-based preparations act as mechanical antireflux barrier, which can reduce both acid and non-acid reflux events and limit the proximal migration of oesophageal refluxate. AIM: To evaluate all the above features with a novel technique, multichannel electrical impedance and pH-metry. METHODS: Ten reflux patients underwent stationary impedancemetry and pH-metry after eating a refluxogenic meal. They were studied 1 h in basal conditions and 1 h after taking 10 mL of Gaviscon Advance. In both sessions, measurements were obtained in right lateral and supine decubitus. RESULTS: Alginate preparation was able to decrease significantly (P < 0.05) the number of acid reflux events and the percentage time pH < 4.0 compared with baseline. There was no effect of the drug on non-acid refluxes. Gaviscon Advance was also significantly effective (P < 0.05) in reducing the height of proximal migration of reflux events compared with baseline in both decubitus positions. CONCLUSIONS: Our findings explain how Gaviscon Advance controls acid reflux episodes, limits the proximal migration of refluxed material and thereby decreases symptoms in clinical practice.

Adult↗
PubMed2005

Endoscopic treatment of gastroesophageal reflux disease.

Gastroesophageal reflux disease is a common chronic disorder which has a severe effect on the patient's quality of life. In view of the high cost of medical therapy and the limitations of surgery, a variety of endoscopic techniques have been developed for the treatment of this condition, and these have shown apparently encouraging results, at least in the short term. However, promising results have been obtained in only around two-thirds of patients over a short-term follow-up period of about 6 months. Moreover, several inconsistencies have emerged between the efficacy of this form of treatment in improving symptoms and quality of life and a lack of improvement of objective parameters, such as lower esophageal sphincter pressure and esophageal acid exposure. The authors strongly endorse the need for comprehensive evaluation of clinical evidence on this topic. After an extensive evaluation of existing literature, we suggest that controlled studies are urgently needed in order to clarify the potential of endoscopic therapy, either in terms of cost-effectiveness or in comparison with standard therapy. Meanwhile, with regard to current practice, the use of endoscopic treatment should be limited to clinical trials, which should incorporate the provision of comprehensive and unbiased information to study patients.

Catheter Ablation↗
PubMed2004

Carditis in patients with gastro-oesophageal reflux disease: results of a controlled study based on both endoscopy and 24-h oesophageal pH monitoring.

BACKGROUND: There are conflicting reports on the role of gastro-oesophageal reflux disease (GERD) and Helicobacter pylori infection in the aetiology of carditis. AIM: The role of reflux and H. pylori infection in causing carditis was assessed in 113 consecutive patients with GERD and in 25 controls. METHODS: All subjects underwent endoscopy and pH test and carditis was diagnosed on biopsies taken across the squamocolumnar junction. Helicobacter pylori was assessed by histology and rapid urease test. GERD was diagnosed by endoscopic oesophagitis or abnormal pH test. RESULTS: Carditis was detected in 53 of 71 GERD patients and in 15 of 20 controls. Among patients, 18 showed absent, 39 mild and 14 marked cardia inflammation and their H. pylori infection rates were 17, 23 and 57%, respectively (P < 0.025). Most patients with carditis (68%) lacked H. pylori infection. pH-metry was abnormal in 15 of 18 patients with normal cardia, 33 of 39 with mild carditis and 12 of 14 with marked inflammation. CONCLUSIONS: Carditis is a frequent finding in GERD and controls. Mild, non-active carditis is frequent in GERD patients. Marked inflammation is associated with both H. pylori and abnormal pH testing. Thus, both GERD and H. pylori infection may play a role in inducing carditis.

Adult↗
PubMed2003

Comparable Helicobacter pylori eradication rates obtained with 4- and 7-day rabeprazole-based triple therapy: a preliminary study.

BACKGROUND: Rabeprazole is a new proton pump inhibitor, which has been reported to induce a faster acid suppression than other drugs of the same category. This might be useful to reduce the duration of anti-Helicobacter therapies. AIMS: The aim of this study was to assess whether there is the possibility of shortening a rabeprazole-based triple therapy from 7 to 4 days without compromising its efficacy in the eradication of Helicobacter pylori infection. PATIENTS: A total of 128 consecutive dyspeptic patients with H. pylori infection were recruited for this controlled, randomized, open and parallel-group trial comparing the efficacy of two durations of the same rabeprazole-based triple therapy. METHODS: All patients were subdivided to receive a combination of rabeprazole 20 mg twice daily, clarithromycin 250 mg twice daily and metronidazole 500 mg twice daily (RCM) for 4 days (n = 63) and for 7 days (n = 65). At baseline, they underwent breath 13C-urea test and endoscopy with biopsies for rapid urease testing and histology to confirm infection with H. pylori. Eradication was determined by a negative 13C-urea breath test within 28-32 days after the end of therapy. RESULTS: Overall eradication rates were similar for patients treated with the 4- and the 7-day periods (intention-to-treat and per-protocol analyses showed a success rate of 81% versus 78% and 88% versus 85%, respectively; P = NS). Tolerance was similar in both groups. Most adverse events were mild to moderate, and only two patients were withdrawn because of them. CONCLUSIONS: The eradication rate of the 4-day regimen was equivalent to that of the same 7-day regimen based on rabeprazole plus clarithromycin and metronidazole. Therefore, the 4-day regimen of RCM seems to give us the possibility of adopting a shorter-than-usual duration of therapy against H. pylori.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2003

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.

Atrophy↗
PubMed2003

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.

Adolescent↗
PubMed2002

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.

Adult↗
PubMed2002

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.

Adult↗
PubMed2001

Improving opportunities for effective management of gastro-oesophageal reflux disease.

The recent introduction of proton pump inhibitors has extraordinarily improved the therapeutic approach to gastro-oesophageal reflux disease. The concept of decreasing gastric acid secretion and increasing the pH in the lower oesophagus has been demonstrated to be therapeutically effective and the higher the level of pH achieved, the better the results. In spite of the evident efficacy of these molecules, there are still many patients who will continue to have symptoms despite medical treatment. Proton pump inhibitors suppress gastric acidity, but this effect shows a remarkable interindividual variation depending on different reasons. Thus, it is still possible to optimise medical therapy for gastro-oesophageal reflux disease. Esomeprazole, the S-isomer of omeprazole, has an advantageous metabolism and this particular feature translates into superior clinical efficacy. Clinical trials for initial and long-term treatment across the gastro-oesophageal reflux disease spectrum, have clearly demonstrated the superiority of esomeprazole over omeprazole, even if tolerability and safety are very similar.

Anti-Ulcer Agents↗
PubMed2001

Clinical pharmacology and safety profile of esomeprazole, the first enantiomerically pure proton pump inhibitor.

Awareness of important differences in the pharmacological profile of individual optical isomers of chiral drugs led to the development of esomeprazole, the S-isomer of omeprazole, a new pharmacological entity designed to improve the clinical outcome of available proton pump inhibitors in the management of acid-related disorders. The superior acid control achieved by esomeprazole is mainly due to an advantageous metabolism compared with racemate omeprazole, leading to improved bioavailability and to enhanced delivery of the drug to the gastric proton pump.

Anti-Ulcer Agents↗
PubMed2001

Negative effect of ranitidine on the results of urea breath test for the diagnosis of Helicobacter pylori.

OBJECTIVES: In analogy with proton pump inhibitors, H2-antagonists may also be responsible for false-negative results on urea breath test for the detection of Helicobacter pylori. In this study we assessed the frequency and duration of false-negative urea breath tests in patients given different doses of ranitidine. METHODS: A total of 120 consecutive dyspeptic patients infected with H. pylori on the basis of concomitant positive results of CLO-test, histology and urea breath test were recruited for this prospective, open, parallel-group study performed in an urban university gastroenterological clinic. They were randomized to receive an acute treatment with either ranitidine 300 mg once a day in the evening, ranitidine 300 mg once a day in the morning, ranitidine 150 mg b.i.d., or ranitidine 300 mg b.i.d. for 14 days. The urea breath test was performed on day 14 while patients were still taking ranitidine, and on day 21, 1 wk after completion of therapy. The test was repeated on day 28 in those patients who were still negative on day 21. Duplicate breath samples were collected after ingestion of 75 mg 13C-urea plus citric acid. A delta value >5/1000 was considered positive. RESULTS: Of 118 patients infected with H. pylori, 15 (13%) had a negative urea breath test on day 14. The false-negative results were equally distributed among the four groups of ranitidine dosage. Nine of these patients reverted to positive at 7 days and the remaining six at 14 days after completion of therapy. CONCLUSIONS: Our study shows that ranitidine negatively affects the results of urea breath testing, independent of the given dosage. Patients undergoing this examination for H. pylori diagnosis should discontinue use of H2-antagonists 2 wk before testing.

Breath Tests↗
PubMed2001

Endothelial perturbation in children and adolescents with type 1 diabetes: association with markers of the inflammatory reaction.

OBJECTIVE: The progression of diabetic angiopathy is, in most cases, unpredictable. The aim of this study was to investigate early events that could influence the development of diabetic angiopathy. RESEARCH DESIGN AND METHODS: Circulating levels of von Willebrand factor (vWF) and tissue-plasminogen activator (tPA), defining endothelial perturbation, were measured in 40 young patients with type 1 diabetes. Patients were divided into two groups according to the duration of diabetes (group A, <1 year; group B, >1 year) and compared with a control group of age- and sex-matched healthy individuals. Prothrombin fragment 1 and 2 (F(1+2)), tumor necrosis factor-alpha (TNF-alpha), and C-reactive protein (CRP) levels were also determined as markers of a prothrombotic state and inflammatory response. A total of 16 of the 20 children in group A were re-examined after 12 months. RESULTS: Compared with either normal subjects or patients in group B, children in group A showed increased levels of vWF, tPA, F(1+2), TNF-alpha, and CRP. Significant direct correlations between TNF-alpha or CRP and either vWF, tPA, or F(1+2) were observed. Endothelial perturbation was shown in 70% of group A and 20% of group B. After 1 year, 16 of the 20 patients in group A showed a significant reduction in vWF, tPA, F(1+2), TNF-alpha, and CRP levels, whereas endothelial perturbation was reversed in 5 of these patients. CONCLUSIONS: Endothelial perturbation represents an early and, in some cases, reversible event in the chronology of type 1 diabetes in children. A correlation might exist between the initial inflammatory reaction and the appearance of endothelial perturbation.

Adolescent↗
PubMed2000

Circadian gastric acidity and Helicobacter pylori infection in patients with chronic pancreatitis.

A high prevalence of duodenal ulcer has been reported in patients with chronic pancreatitis. Data from previous studies on gastric acid secretion in these patients have provided conflicting results, and the potential role of H. pylori infection has been poorly investigated. The aim of this study was to assess the circadian pattern of gastric acidity and the prevalence of H. pylori infection in a group of patients suffering from this disease. Thirty-five patients with chronic pancreatitis ascertained by means of pancreatic calcifications or ductal alterations revealed by ERCP were recruited for this prospective study. They underwent 24-hr gastric pH-metry with glass minielectrodes positioned in the gastric corpus, and their profile of gastric acidity was compared with that of 35 healthy subjects, matched for age and sex. H. pylori infection was diagnosed by means of serology. There was no statistical difference (P = NS) in gastric pH of circadian, nocturnal, daytime, and postprandial periods between healthy subjects and patients with chronic pancreatitis. The prevalence of H. pylori infection was rather low (31%) in our patients and similar to that of a comparable control population (37%) in our geographical area. In conclusion, our study shows that patients with chronic pancreatitis have a circadian pattern of gastric acidity similar to that of normal subjects. Moreover, the prevalence of H. pylori infection is low in this population. These findings greatly differentiate the ulcer diathesis in chronic pancreatitis from that of patients with ordinary duodenal ulcer and suggest that other factors are implicated in the ulcerogenic process.

Adult↗
PubMed2000

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.

Adult↗
PubMed2000

Review article: is Helicobacter pylori status relevant in the management of GORD?

There is growing interest in the relationship between H. pylori infection and gastro-oesophageal reflux disease (GORD). However, this relationship is complex, as yet not fully elucidated, and probably based on a multiplicity of factors. The prevalence of H. pylori infection in patients with GORD is similar, more often lower than in matched controls. There is a negative correlation between H. pylori infection and the severity of GORD. There are many hypothetical mechanisms by which H. pylori infection may protect from the development of GORD. Conversely, there are many possible mechanisms by which H. pylori infection could theoretically foster the GORD. Patients after H. pylori eradication may develop GORD, and this seems to suggest a protective role of H. pylori infection, but other possible explanations include weight gain after H. pylori eradication, changes in dietary habits and smoking, and pre-existing GORD. H. pylori infected patients treated by various acid-inhibiting therapies such as proton pump inhibitors (PPIs), H2-receptors antagonists (H2-RA) or vagotomy, have an increase of their corpus gastritis severity, both in the activity of inflammation and in the density of organisms. Long-term therapy of GORD in H. pylori infected may lead to rapid progression of atrophic gastritis intestinal metaplasia and dysplasia, and increase the risk of developing gastric cancer. More recently it has been shown that H. pylori infection may interfere with the acid suppressive therapies used for treating GORD. In our opinion the progression of gastritis depends on the threshold of acid output at which H. pylori can 'flourish'. Recently interest is growing on gastric transitional zones and Helicobacter ecology. Any decrease of acid secretion changes the behaviour of H. pylori: the activity of gastritis improves in the antrum, but it deteriorates in the body. During proton pump inhibitor treatment, H. pylori redistribution occurs within the stomach, from an antral to a corpus or fundus prevalent pattern; corpus-fundus gastritis, exacerbated by PPI therapy, may result both in a diminished acid secretion and gastro-oesophageal reflux. The interest in Barrett's oesophagus is growing due to the associated risk of adenocarcinoma. The literature seems to demonstrate that the prevalence of H. pylori infection of the stomach in Barrett's oesophagus patients is not different from that exhibited by controls, roughly one-third of the subjects. Intestinal metaplasia of the gastric cardia seems to be equally frequent in patients with and without GORD. Finally, it appears unlikely that a causal relationship exists between H. pylori infection and Barrett's-associated adenocarcinoma.

Animals↗
PubMed2000

Effect of gastric acid suppression on 13C-urea breath test: comparison of ranitidine with omeprazole.

BACKGROUND: The assessment of the effect of H2 antagonists on the results of the urea breath test has produced controversial results. AIM: To assess whether standard doses of both omeprazole and H2 blockers can adversely influence the accuracy of the urea breath test. METHODS: Sixty dyspeptic patients with ascertained Helicobacter pylori infection were recruited for this prospective, open study. They were randomized to receive either omeprazole 20 mg at 08:00 hours (n = 30) or ranitidine 300 mg at 22:00 hours (n = 30) for 14 days. The urea breath test was performed at baseline, on day 14, while patients were still taking the antisecretory drugs, and on day 21, 1 week after their cessation. Duplicate breath samples were collected after ingestion of 75 mg 13C-urea + citric acid. A delta value > 5 per thousand was considered positive. RESULTS: On day 14 the median delta values had declined, but not significantly (P = 0. 07) compared to baseline (13.79 vs. 22.39) with omeprazole, while they had increased (P = 0.27) with ranitidine (27.21 vs. 19.46). On the same day there were five out of 30 (17%) and five out of 28 (18%) false-negative results in the omeprazole and ranitidine groups, respectively. All these cases became positive again on day 21. However, in eight cases treated with omeprazole and 13 treated with ranitidine, there was an increase of 14-day delta values compared to baseline. CONCLUSIONS: Our study shows that both omeprazole and ranitidine at standard doses are able to negatively affect the results of the urea breath test. Their adverse effect resolves within 7 days of drug cessation and therefore the withdrawal of these drugs 7 days before testing seems to be sufficient to avoid false-negative results. The surprising finding that both antisecretory drugs reduce delta values in one group and increase them in another group of patients deserves further study.

Anti-Ulcer Agents↗