Applicability of a short/rapid 13C-urea breath test for Helicobacter pylori: retrospective multicenter chart review study

<p>Abstract</p> <p>Background</p> <p>Carbon labeled urea breath tests usually entail a two point sampling with a 20 to 30-minute gap. Our aim was to evaluate the duration of time needed for diagnosing <it>Helicobacter pylori </it>by the BreathID^®System.</p> <p>Methods</p> <p>This is a retrospective multicenter chart review study. Test location, date, delta over baseline, and duration of the entire test were recorded. Consecutively ¹³C urea breath tests results were extracted from the files over a nine year period.</p> <p>Results</p> <p>Of the 12,791 tests results, 35.1% were positively diagnosed and only 0.1% were inconclusive. A statistically significant difference in prevalence among the countries was found: Germany showing the lowest, 13.3%, and Israel the highest, 44.1%. Significant differences were found in time to diagnosis: a positive diagnosis had the shortest and an inconclusive result had the longest. Overall test duration averaged 15.1 minutes in Germany versus approximately 13 minutes in other countries. Diagnosis was achieved after approximately 9 minutes in Israel, Italy and Switzerland, but after 10 on average in the others. The mean delta over baseline value for a negative diagnosis was 1.03 ± 0.86, (range, 0.9 - 5), versus 20.2 ± 18.9, (range, 5.1 - 159.4) for a positive one.</p> <p>Conclusions</p> <p>The BreathID^®System used in diagnosing <it>Helicobacter pylori </it>can safely shorten test duration on average of 10-13 minutes without any loss of sensitivity or specificity and with no test lasting more than 21 minutes.</p

Prolonged Survival and Cytoplasmic pH Homeostasis of Helicobacter pylori at pH 1

In the presence of urea, Helicobacter pylori survived for at least 3 h at pH 1. Under these conditions, the cells maintained their cytoplasmic pH at 5.8. De novo protein synthesis during acid shock was not essential for survival of H. pylori at pH 1

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

New inhibitors of Helicobacter pylori urease holoenzyme selected from phage-displayed peptide libraries.

Urease is an important virulence factor for Helicobacter pylori and is critical for bacterial colonization of the human gastric mucosa. Specific inhibition of urease activity has been proposed as a possible strategy to fight this bacteria which infects billions of individual throughout the world and can lead to severe pathological conditions in a limited number of cases. We have selected peptides which specifically bind and inhibit H. pylori urease from libraries of random peptides displayed on filamentous phage in the context of pIII coat protein. Screening of a highly diverse 25-mer combinatorial library and two newly constructed random 6-mer peptide libraries on solid phase H. pylori urease holoenzyme allowed the identification of two peptides, 24-mer TFLPQPRCSALLRYLSEDGVIVPS and 6-mer YDFYWW that can bind and inhibit the activity of urease purified from H. pylori. These two peptides were chemically synthesized and their inhibition constants (Ki) were found to be 47 microM for the 24-mer and 30 microM for the 6-mer peptide. Both peptides specifically inhibited the activity of H. pylori urease but not that of Bacillus pasteurii