Decrease Of Intragastric Acidity Research Articles

817 DCLK1 Labels Adult Pancreatic Progenitor and Cancer Initiating Cells

G A A b st ra ct s secretion volume despite significant decrease in intragastric acidity. Gastric secretion accumulates on the top of the liquid meal forming a "floating" layer. We assume that this layer is the correlate for the so called "acid pocket", which has previously been assumed according to several pH pull-through studies− the term "pocket" therefore being an unfavourable description. This phenomenon may be an important factor in the pathogenesis of GERD and in the persistence of GERD symptoms under PPI.

815 An Insertion of Eight Amino Acids in HLA-DQA1 and Three Amino Acid Substitutions in HLA-DQA1 and HLA-DQB1 Confer Risk to Idiopathic Achalasia

G A A b st ra ct s secretion volume despite significant decrease in intragastric acidity. Gastric secretion accumulates on the top of the liquid meal forming a floating layer. We assume that this layer is the correlate for the so called acid pocket, which has previously been assumed according to several pH pull-through studies− the term pocket therefore being an unfavourable description. This phenomenon may be an important factor in the pathogenesis of GERD and in the persistence of GERD symptoms under PPI.

Intragastric acidity and circadian rhythm

Most patients with peptic ulcers or gastroesophageal reflex disease develop subjective symptoms of epigastralgia and retrosternal pain during the period of time from the middle of the night to the early dawn (nocturnal pain). Such pain often disappears before breakfast. Disturbed circadian rhythm of gastric acid secretion may have a close relationship with the onset and aggravation of acid-related diseases. On the other hand, Hefcobacter pylori has been considered to be an etiological agent of duodenal ulcer, and H. pylori eradication has been conducted in patients with gastritis and peptic ulcers. However, such eradication therapy sometimes results in the onset or deterioration of gastroesophageal reflux diseases. In this context, the question of whether the circadian rhythm of gastric acid secretion varies in accordance with the presence or absence of H. pylori infection is of interest. In the present study, we examined the fluctuation in intragastric acidity via a portable pH meter in 10 H. pylori-positive and 10 H. pylori-negative subjects. As a result, a significant difference in the circadian rhythmicity was observed between the H. pylori-negative and the H. pylori-positive group, with mean values for each parameter of 28.1 and 13.3 for amplitude, 22.7 and 12.4 for the midline-estimating statistic of rhythm (MESOR), and 324.0 and 321.0 for acrophase, respectively ( P < 0.001). In both H. pylori-positive and negative groups, a tendency was observed toward an increase in intragastric acidity during the time period from the middle of the night to the early dawn, and toward a decrease in intragastric acidity during the early morning. In the H. pylori-positive group, the values for intragastric acidity over time were lower, and the degree of amplitude was smaller as compared to the H. pylori-negative group. Further, H. pylori-positive individuals were at a more advanced stage of the disease.

Treatment of chronic gastroduodenal ulcers associated with Helicobacter Pylori-infection

Treatment of chronic gastroduodenal ulcers remains one of the most difficult and unsolved problems. The main difficulty that they try to overcome is their recurrent course. Nowadays the main directions of medical therapy of peptic ulcer disease are the decrease of intragastric acidity and sanation of gastroduodenal mucosa from Helicobacter Pylori. Treatment aimed at the destruction of Helicobacter Pylori allows to reduce the relapse rate to almost zero, provided it is successfully suppressed.

Decrease of intragastric acidity following low doses of ranitidine

Methods: Twenty-four healthy males, mean age 23 years (range 20 to 29 years) took part in the study. Each subject took one tablet of antacid (Maalox TC TM) on the first study day and on subsequent study days received single oral doses of ranitidine 25mg, 75mg and 125mg (as the hydrochloride) and matching placebo, in accordance with a random code. The doses of study drug were administered 45 minutes after lunch and intmgastric pH was recorded for 9 hours after dosing. Each dose was separated by a two-week washout period.

Degrees of acid suppression and ulcer healing: dosage considerations

The human stomach has a normal circadian rhythm of intragastric acidity characterized by increasing acidity during the day and peaks in the early hours of the morning. Eating causes a transient decrease of intragastric acidity. Acid appears to be the permissive factor in peptic ulcer disease and to be responsible for symptoms; the patient with duodenal ulcer may secrete too much acid. Pharmacological control of gastric acid secretion will speed ulcer healing. Modern regimens, which typically use a bedtime dose of an H2-receptor antagonist, produce a pulse of decreased acidity. Intragastric acidity is decreased during the night and early morning, leaving a normal profile of acidity during the day and early evening. Higher or more frequent doses of an antisecretory agent can produce a more profound decrease of 24-h intragastric acidity. Theoretical problems associated with a sustained or profound decrease of 24-h intragastric acidity include the threat of enteric infection and infestation, potential bacterial overgrowth with possible N-nitrosamine formation, and drug-induced hypergastrinaemia. In light of these potential problems, for the management of simple peptic ulceration, it appears sensible to use the minimum intervention required. Bedtime H2-receptor blockade is one such regimen. The more potent antisecretory regimens can be used for difficult clinical problems such as the Zollinger-Ellison syndrome, intractable duodenal ulceration, and severe oesophagitis.

Pharmacokinetics and bioavailability of omeprazole after single and repeated oral administration in healthy subjects.

1. Ten healthy subjects were given 20 mg omeprazole EC (enteric coated) granules once daily for 8 days. An i.v. tracer dose of [14C]-omeprazole was given simultaneously with the first and last oral doses and blood sampling was performed thereafter. In order to study the extent of absorption at minimal acid exposure, a single dose of 20 mg omeprazole was also given as a buffered solution, before and after the treatment with EC granules. 2. Kinetic parameters of omeprazole after the i.v. tracer dose were unchanged on repeated dosing while AUC increased by approximately 40% for the solution and 60% for the EC granules. 3. The increased AUC is caused by an increased systemic availability, which may be explained by a decreased first-pass elimination during repeated treatment and/or by a reduced degradation of omeprazole in the stomach secondary to the profound decrease in intragastric acidity caused by the drug. 4. The implication of these findings is that the antisecretory effect of therapeutic doses of omeprazole must be studied during repeated administration and not judged from studies using single doses only.

24-HOUR CONTROL OF INTRAGASTRIC ACIDITY BY CIMETIDINE IN DUODENAL-ULCER PATIENTS

The effects of two dose regimens of cimetidine on 24 h intragastric acidity were investigated in six patients with duodenal ulcer. They received placebo capsules on the first day and cimetidine on the second day. Cimetidine 0·8 g/day decreased 24 h mean H + activity by 55% but 1·6 g/day decreased it by 67%, the difference being due to a greater nocturnal decrease in the high-dose group. Intragastric pH remained below 2·0 for much of the treatment day but similar values were found in four post-vagotomy patients. Cimetidine 0·8-1·6 g/day results in a decrease of intragastric acidity that is compatible with successful medical treatment of duodenal ulceration.