basal acid output , BAO (skrót)

Secretions were obtained for 60 minutes for estimation of basal acid output.

Basal acid output was calculated by taking the mean of all three 15 minute samples before gastrin releasing peptide infusion.

Further studies will be necessary to determine which factor - the ulcer crater or H pylori - is reponsible for the increased basal acid output.

Increased basal acid output and increased peak acid output are important features in patients with DU.

Basal acid output per hour was calculated by doubling the acid output during the 30 minutes of infusion of saline only.

Figure 2 shows that after eradication of H pylori there was a reduction of basal acid output in eight patients and no change in one patient.

After eradication of H pylori in the duodenal ulcer patients both their basal acid output and basal gastrin fell by 50%.

Though gastrin is considered to be the main mediator of food stimulated acid secretion, its role in the regulation of basal acid output is unclear.

Despite a fall in the basal plasma gastrin concentration, however, it has not been shown previously that eradication of H pylori can significantly decrease the basal acid output.

The basal acid output in the one duodenal ulcer subject in whom H pylori infection was not eradicated was similar before (3.7) and after (4.8) the triple treatment.

We also found the basal acid output to be significantly greater in patients with duodenal ulcers and with H pylori than in patients with duodenal ulcers without this infection.

When six patients with duodenal ulsers in whom H pylori had been eradicated were retested after 12 months, we found that the median basal acid output fell by about 40%, although the change was not significant.

This may be explained by the fact that the increased basal acid output in duodenal ulcer patients was due to their combination of increased basal gastrin and exaggerated acid response to gastrin.

Two previous studies, one by outselves in patients with duodenal ulcers and another by Mountbriand et al in dyspeptic patients showed no significant change in basal acid output after anti- H pylori treatment.

Though basal gastrin was increased to a similar extent in H pylori positive healthy volunteers and H pylori positive duodenal ulcer patients the first did not have a significantly increased basal acid output.

The remaining subject was achlorhydric during rhe first intubation study (basal acid output 0 mEq/h, stimulated acid output 0.36 mEq/h), and a further test after histamine receptor blockade was not therefore undertaken.

Achord noted that the basal acid output decreased after healing of an ulcer by drugs that do not eradicate H pylori, implying that the ulcer crater is itself associated with increased basal acid secretion.

Results were expressed as basal acid output (BAO), defined as the mean of the last two recordings during the basal collection, and peak acid output (PAO) defined as the highest mean obtainable from two consecutive recordings during the stimulated period.

Increased basal and nocturnal acid output are also important features of duodenal ulcer disease and in this study the median basal acid output of the H pylori positive duodenal ulcer patients was five times that of the H pylori negative healthy volunteers.