24-hour study of intragastric acidity in duodenal ulcer patients and normal subjects using continuous intraluminal pH-metry

Savarino, Vincenzo; Mela, Giuseppe Sandro; Scalabrini, P.; Sumberaz, Alessandro; Fera, G.; Celle, G

doi:10.1007/bf01535781

Cited by 65 publications

(21 citation statements)

References 15 publications

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“…Consequently it has been reported that N is the least reproducible reflux parameter, and the most reproducible is % [12,13]. Gastric acid secretion is known to be greatest in the early part of the night as a continuation of evening meal stimulated output, decreasing to near-normal subject basal levels by halfway through the night [14][15][16]. This may explain the predominance of gastroesophageal acid reflux in the first half of the night.…”

Section: Discussionmentioning

confidence: 94%

Determinants of Abnormal Supine Reflux in 24-Hour pH Recordings

et al. 2007

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A previous study showed that supine gastroesophageal reflux occurs mainly in the early nighttime period and is greater if the patient retires within 2 hr of a meal. We analyzed 306 consecutive esophageal pH studies between January and July 2003. Ninety-two patients had abnormal supine reflux. The recumbent period was divided into quarters (Q1-Q4) and reflux parameters were calculated for each period. Reflux was maximal in Q1, and decreased progressively from Q1 to Q4 (P<0.001). Median time between evening meal and retiring was no different from that for 44 upright gastroesophageal reflux patients. Patients retiring within 2 hr of a meal had a higher percentage supine reflux time (P=0.012), but no increase in reflux was observed in those retiring within 3 hr. Supine reflux occurs maximally in the early nighttime period. Although not fully explained as a postprandial phenomenon, these patients should avoid going to bed within 3 hr of a meal.

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Section: Discussionmentioning

confidence: 94%

Determinants of Abnormal Supine Reflux in 24-Hour pH Recordings

et al. 2007

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“…In contrast to the slight alkalinity of the fasting python's stomach, mammals maintain a highly acidic environment (pH 1.1-3) within their stomachs between bouts of digestion (Youngberg et al, 1985;Evans et al, 1988;Cilluffo et al, 1990;Viani et al, 2002). Whereas pythons experience a dramatic postprandial decrease in gastric pH, the luminal pH of mammal stomachs increases rapidly after feeding to range between 3 and 6, presumably as the ingested meal buffers the gastric acid (Savarino et al, 1988;McLauchlan et al, 1989;Cilluffo et al, 1990). Within a few hours after feeding, intragastric pH of mammals drops as acid production, which has increased 20-fold, overwhelms the buffering capacity of the food, which is then being passed through the pyloric sphincter into the small intestine (Fordtran and Walsh, 1973).…”

Section: Gastric Phmentioning

confidence: 99%

Gastric function and its contribution to the postprandial metabolic response of the Burmese pythonPython molurus

Secor

2003

Journal of Experimental Biology

139

141

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SUMMARY The large intact prey ingested by Burmese pythons require considerable processing by the stomach before passage into the small intestine. To investigate the function and cost of gastric digestion and its contribution to postprandial metabolic response for the Burmese python, I examined the rate of gastric digestion, the postprandial profile of gastric pH and the effects of decreasing gastric workload on the metabolic cost of digestion, referred to as specific dynamic action (SDA). Ingested meal mass (equivalent to 25% of snake body mass) was reduced by 18% within 1 day postfeeding, by which time intragastric pH had decreased from 7.5 to 2. Gastric pH was maintained at 1.5 for the next 5–7 days, after which it returned to 7.5. The SDA generated by digesting an intact rat meal was reduced by 9.1%, 26.0%, 56.5% and 66.8%,respectively, when pythons were fed steak, ground rat, liquid diet or ground rat directly infused into the small intestine. The production of HCl and enzymes and other gastric functions represent an estimated 55% of the python's SDA generated from the digestion of an intact rodent meal. Additional contributors to SDA include protein synthesis (estimated 26%),gastrointestinal upregulation (estimated 5%) and the activities of the pancreas, gallbladder, liver, kidneys and intestines during digestion(estimated 14%). Operating on a `pay before pumping' principle, pythons must expend endogenous energy in order to initiate acid production and other digestive processes before ingested nutrients can be absorbed and channeled into metabolic pathways.

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“…A previous study concluded that omeprazole produces profound gastric anacidity or achlorhydria over 24 h [6, 7]. However, the gastric aspiration techniques used in this study pooled secretions collected over the previous hour, thereby obscuring the temporal pH variations observed during ambulatory, 24-hour, single-electrode recordings of gastric pH [8, 9, 10]as well as the regional, intragastric variations detected in multi-electrode studies [10, 11]. Such regional differences in the pH of gastric contents might also explain, in part, the marked variations in response observed with omeprazole therapy in individual patients with gastro-esophageal reflux disease since acidic material could reflux into the esophagus from localized pockets low pH, thereby producing esophageal mucosal damage.…”

Section: Introductionmentioning

confidence: 88%

Effect of Omeprazole on Regional and Temporal Variations in Intragastric Acidity

Viani

Verdú²,

Idström³

et al. 2002

Digestion

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Background: Conventional techniques for measuring gastric acidity have demonstrated the decrease in gastric acidity produced by proton pump inhibitors (PPI); however, such techniques do not detect transient or localized pH changes which may modify the intragastric environment without affecting the therapeutic efficacy of PPIs. Aim: To investigate local and temporal variations in intragastric pH and to test the hypothesis that omeprazole produces prolonged, generalized gastric anacidity (pH >6). Methods: A single-blind study was conducted with triple-point 24-hour gastric pH-metry on days 7, 14 and 21 in 14 healthy, Helicobacter pylori-negative volunteers (7 M; 20–46 years) who received placebo for 7 days, followed by omeprazole 20 mg daily for 14 days. Results: Omeprazole increased the median 24-hour pH significantly in the distal corpus (placebo: 1.3 (95% CI 1.1 to 1.6); omeprazole week 1: 4.0 (2.6–5.0); omeprazole week 2: 4.0 (2.8–4.6)) and at all other gastric recording sites (p < 0.01). At both corpus sites, nocturnal pH was lower and mealtime pH was higher than the non-meal daytime pH during placebo and both omeprazole administration periods; in the antrum, however, the major difference noted was that meal-time pH was higher than non-meal daytime pH. Antral pH was lower during meals and higher at night than proximal corpus pH. During placebo, gastric pH >6.0 was observed at 1 site only for 1.7% (median; 95% CI 0.4–3.3%), at 2 sites simultaneously for 0.24% (0.0–1.0%) and at 3 sites for 0.0% (0.0–0.28%), respectively, of the recording periods; during the second week of omeprazole, the equivalent results were 7.7% (1.4–14.0%), 4.9% (0.21–15.7%) and 4.7% (0.0–9.9%), respectively. Conclusions: Omeprazole, 20 mg daily, does not produce gastric anacidity despite significant increases in median 24-hour pH values. The time-, meal- and site-related variations in gastric pH observed under normal physiological conditions are seen to persist, with prolonged periods of low pH throughout the stomach and preservation of the normal, meal-related rise and nocturnal fall in gastric pH during omeprazole administration.

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24-hour study of intragastric acidity in duodenal ulcer patients and normal subjects using continuous intraluminal pH-metry

Cited by 65 publications

References 15 publications

Determinants of Abnormal Supine Reflux in 24-Hour pH Recordings

Determinants of Abnormal Supine Reflux in 24-Hour pH Recordings

Gastric function and its contribution to the postprandial metabolic response of the Burmese pythonPython molurus

Effect of Omeprazole on Regional and Temporal Variations in Intragastric Acidity

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