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Title: Somatostatin Secretion into the Gastric Juice Enhanced, Basal Acid Output Recovered Following Helicobacter Pylori Eradication in Gastric Ulcers

URL: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=R
Retrieve&db=PubMed&list_uids=12702041&dopt=Abstract

J Gastroenterol Hepatol 2003 May;18:5:505-511. "Enhanced somatostatin secretion into the gastric juice with recovery of basal acid output after Helicobacter pylori eradication in gastric ulcers"
05/06/2003 10:41:03 AM
By David Ball

Gastric ulcer patients in the early phase of Helicobacter pylori eradication experience improved antral neutrophil infiltration and an increase in basal and gastrin- stimulated somatostatin-containing cell activity, say Japanese researchers. Recovery of gastric basal acid output (BAO) is not caused by an increase in parietal cell volume or a change in atrophy, but rather by an improvement in corpus neutrophil infiltration, they suggest. This study, undertaken by T. Hayakawa and colleagues at the Aichi Medical University School of Medicine, Aichi Cancer Center Hospital and Nagoya University School of Medicine, investigated the effect of eradication on gastric acid, somatostatin secretion and mucosal histology in gastric ulcer patients with H. pylori infection. They point out that antral somatostatin is known to interact with gastric acid secretion. H.pylori-positive gastric ulcers were treated with dual therapy in 21 male and 7 female patients. Assessments were made of the histology of biopsy specimens, BAO and maximal acid output (MAO) after stimulation with tetragastrin before therapy and at 4 and 8 weeks. Radioimmunoassay was used to measure somatostatin concentration in the gastric juice. Somatostatin output was also examined during either the basal or gastrin-stimulated period. H.Pylori eradication was found to be successful in 22 subjects. Acid and somatostatin output before treatment were seen to be inversely related to the severity of neutrophil infiltration in the corpus and antrum, respectively. The researchers report improvement of histological inflammation and an increase in BAO, basal and gastrin- stimulated somatostatin output following successful eradication. No effect was seen by eradication on atrophy and MAO. Irrespective of H. pylori infection, they found a positive correlation between gastric acid and somatostatin output in the basal or stimulated condition.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=R
Retrieve&db=PubMed&list_uids=12702041&dopt=Abstract

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