A new endoscopic method of gastric acid secretory testing

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Gastroesophageal reflux disease (GERD) is a common disease, in which the reflux of gastric acid causes mucosal damage of the esophagus and/or troublesome symptoms. Esomeprazole, a proton pump inhibitor, has been used for treatment of GERD in Japan since 2011; namely, only little is known about its effect on gastric acid secretion in Japanese. We, therefore, assessed the relationship between dose and timing of esomeprazole administration and gastric acid inhibition in 11 healthy male Japanese volunteers by directly examining gastric acid secretion capacity. In this randomized, open-label, three-way crossover study, the subjects were dosed with esomeprazole 10 mg or 20 mg once a day (q.

Section: Discussionmentioning

confidence: 99%

“…Gastric acid secretion capacity was measured by EGT, as described previously (Iijima et al 1998). After fasting for at least 10 h, the subjects were intramuscularly injected with 6 µg/kg of pentagastrin (Sigma, St. Louis, MO, USA).…”

Section: Measurement Of Gastric Acid Secretion Capacitymentioning

confidence: 99%

Esomeprazole Inhibits the Pentagastrin-Stimulated Secretion of Gastric Acid in Healthy Japanese Volunteers

Maejima

Koike

Nakagawa

et al. 2015

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“…The procedure of these invasive tests causes significant distress to the patients and is time consuming. To estimate gastric acid secretion easily and rapidly, we previously devised an endoscopic method of gastric acid secretory testing (endoscopic gastrin test: EGT), which is a simple modification of the conventional gastrin-stimulated maximal acid output test (Iijima et al 1998). However, the endoscopic procedure still causes some discomfort in the subjects, hence repeating EGT is not always easy.…”

Section: Introductionmentioning

confidence: 99%

Calcium Carbonate Breath Test for Non-Invasive Estimation of Gastric Acid Secretion

Shinkai

Iijima

Koike

et al. 2014

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Gastric acid measurement is useful in assessing the effectiveness of antisecretory drugs, however, the conventional tests involve invasive nasogastric intubation. Orally administered 13 C-labeled calcium carbonate (Ca 13 CO 3 ) reacts with gastric acid to produce 13 C-labeled carbon dioxide ( 13 CO 2 ), which is then excreted in the breath. The objective of this study was to evaluate the suitability of Ca 13 CO 3 breath test for estimating gastric acid secretion in human noninvasively. First, the Ca 13 CO 3 breath test and the measurement of pooled gastric acid under a fasting condition were performed in 6 healthy volunteers to evaluate the correlation between the two parameters. Next, endoscopic gastric acid collection and the Ca 13 CO 3 breath test were performed on different days after pentagastrin injection in 20 subjects to evaluate the correlation between the tests and the reproducibility. Finally, the same studies were repeated in 4 subjects before and after 1-week rabeprazole, a proton pump inhibitor, administration. The maximum 13 CO 2 concentration (Cmax) correlated very well with the amount of pooled gastric acid (r = 0.95), suggesting that Ca 13 CO 3 breath test values well reflected the fasting intragastric acidity. The 13 CO 2 concentration after pentagastrin injection correlated well with pentagastrin-stimulated maximal acid output (r = 0.79 at 20 min). The reproducibility of the Ca 13 CO 3 breath test under pentagastrin-stimulation was good (coefficient of variation = 0.11). Rabeprazole administration markedly reduced the values of the Ca 13 CO 3 breath test, suggesting that it can sensitively assess the efficacy of rabeprazole. The Ca 13 CO 3 breath test can potentially be a useful method for non-invasive estimation for gastric acid secretion in human.

“…The acid output in the 10-min period was calculated by multiplying the volume by the H + concentration, and the EGT value was expressed as mEq/10 min. We previously determined that the EGT values correlate very well with the peak acid outputs, as determined by conventional methods (correlation coefficient = 0.92), and have a high reproducibility (coefficient of variation = 5.6%) (Iijima et al 1998). …”

Section: Assessment Of Gastric Acid Secretionsmentioning

confidence: 99%

“…The details of the EGT have been reported previously (Iijima et al 1998(Iijima et al , 2009. Briefly, subjects were injected intramuscularly with pentagastrin (Sigma, St. Louis, MO, USA) at a dose of 6 µg/kg at approximately 15 min before endoscopy.…”

Section: Gastric Aspiration Using the Endoscopic Gastrin Test Techniquementioning

confidence: 99%

Increased Gastric Mucus Secretion Alleviates Non-Steroidal Anti-Inflammatory Drug-Induced Abdominal Pain

Iwabuchi

Iijima

Ara

et al. 2013

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Non-steroidal anti-inflammatory drugs (NSAIDs) can cause dyspeptic symptoms, including abdominal pain. Gastric mucus is important as the first line of defense against luminal irritants. In the present study, we investigated whether gastric mucus secretion could influence the severity of gastric mucosal injuries or NSAID-induced dyspeptic symptoms. Fifteen Helicobacter pylori-negative, healthy males were administered two types of NSAIDs, a non-selective cyclooxygenase inhibitor, naproxen (300 mg, twice a day), or a cyclooxygenase-2-selective inhibitor, etodolac (200 mg, twice a day), for 1 week in a crossover study, with an interval of ≥ 4 weeks. Study participants underwent endoscopic examinations before and after treatment. Pentagastrin-stimulated gastric secretions were collected for 10 min during endoscopic examinations, and were analyzed for gastric acid levels (mEq/10 min) and mucus output (mg hexose/10 min). The grade of gastric mucosal injury was assessed endoscopically. Among 29 subjects who completed the crossover study, 11 individuals reported abdominal pain following the administration of naproxen or etodolac for 1 week, as judged by elevated pain scores, while 18 individuals did not report abdominal pain. The occurrence of symptoms was not associated with the type of NSAIDs administered or the occurrence of erosive injury visualized by endoscopy. Gastric mucus secretion was significantly increased in subjects without drug-induced abdominal pain (P < 0.05), whereas it was significantly reduced in those with drug-induced abdominal pain (P < 0.05). In conclusion, the occurrence of NSAID-induced abdominal pain is associated with reduced levels of gastric mucus secretion rather than the occurrence of endoscopic mucosal injury.