Intragastric acidification reduces the occurrence of false-negative urea breath test results in patients taking a proton pump inhibitor

The aim of this study was to investigate whether reducing intragastric pH, at the time of urea ingestion, decreases the likelihood of false-negative (FN) urea breath test (UBT) results in patients taking a proton pump inhibitor (PPI). Methods : Patients with active Helicobacter pylori infection underwent a baseline 14 C-UBT (UBT-1) followed by treatment with lansoprazole 30 mg/day for 14 to 16 days. On day 13, patients returned for a repeat standard UBT (UBT-2). Between days 14 to 16, patients underwent a modified UBT (UBT-3), which included consuming 200 ml of 0.1 N citrate solution 30 min before and at the time of 14 C-urea administration. Breath samples were collected 10 and 15 min after 14 C-urea ingestion. Mean 14 CO 2 excretion and the number of FN and equivocal UBT results were compared for the three UBTs. Results : A total of 20 patients completed the study. Lansoprazole caused a significant decrease in mean breath 14 CO 2 excretion (disintegrations per minute) between UBT-1 (2.96 ± 0.23) and UBT-2 (2.08 ± 0.52, p < 0.05 ). Lansoprazole caused six (30%) FN and eight (40%) equivocal UBT-2 results. Mean breath 14 CO 2 excretion for UBT-3 (677 ± 514) was greater than for UBT-2 (234 ± 327, p = 0.001 ). UBT-3 caused only two (10%) FN and three (15%) equivocal results. The 15-min breath sample caused fewer FN and equivocal results than the 10-min sample for both UBT-2 and UBT-3. Conclusions : Giving citrate before and at the time of 14 C-urea administration increases mean breath 14 CO 2 excretion and decreases FN and equivocal UBT results in patients taking a PPI. These observations suggest that it may be possible to design a UBT protocol that will remain accurate in the face of PPI therapy.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/71971/1/j.1572-0241.2001.03687.x.pd

Treatment of irritable bowel syndrome: beyond fiber and antispasmodic agents

Irritable bowel syndrome (IBS) is a chronic functional disorder of the gastrointestinal tract of unknown etiology. The diagnosis of IBS is made clinically, using symptom-based criteria such as the Manning or Rome criteria. Medical therapy for this condition has traditionally been directed towards symptom relief, using fiber or antispasmodic agents. In recent years, emerging data have confirmed the efficacy of antidepressants, psychological therapies, 5-HT3 antagonists, 5-HT4 agonists, and probiotics in the short-term treatment of IBS, although whether these therapies influence the long-term course of the disease is unknown. Increasing knowledge regarding the pathophysiological mechanisms underlying IBS has resulted in a number of novel molecular treatments, which show promise. These include therapies targeting gastrointestinal mucosal chloride channels and guanylate cyclase-C receptors, as well as highly selective agents influencing serotonergic transmission that, at the time of writing, do not appear to have any severe deleterious effects. In this article we provide a summary of current and emerging therapies in this field