PubMed · 5688598
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E Hafter. 1968-07-13. [Meteorism].. https://pubmed.ncbi.nlm.nih.gov/5688598/
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Carboxypeptidase E deficiency as seen in the fat/fat mice is associated with reduced antral somatostatin content but tripling of the progastrin product. Thus, fat/fat mice are able to maintain normal tissue concentrations of bioactive alpha-amidated gastrin in spite of grossly attenuated progastrin processing. After induction of achlorhydria, however, neither the amount of alpha-amidated gastrin nor the total progastrin product increased in the fat/fat mice. This is contrary to what is seen in wild-type mice. Furthermore, the synthesis of antral somatostatin and fundic chromogranin A is also abnormal. Hence the results suggest a breakdown in the feedback loop that regulates gastric acid secretion.
BACKGROUND & AIMS: Helicobacter pylori is believed to predispose to gastric cancer by inducing gastric atrophy and hypochlorhydria. First-degree relatives of patients with gastric cancer have an increased risk of developing gastric cancer. The aim of this study was to determine the prevalence of atrophy and hypochlorhydria and their association with H. pylori infection in first-degree relatives of patients with gastric cancer. METHODS: H. pylori status, gastric secretory function, and gastric histology were studied in 100 first-degree relatives of patients with noncardia gastric cancer and compared with those of controls with no family history of this cancer. RESULTS: Compared with healthy controls, relatives of patients with gastric cancer had a higher prevalence of hypochlorhydria (27% vs. 3%) but a similar prevalence of H. pylori infection (63% vs. 64%). Relatives of cancer patients also had a higher prevalence of atrophy (34%) than patients with nonulcer dyspepsia (5%) matched for H. pylori prevalence. Among the relatives of cancer patients, the prevalence of atrophy and hypochlorhydria was increased only in those with evidence of H. pylori infection, was greater in relatives of patients with familial cancer than in relatives of sporadic cancer index patients, and increased with age. Eradication of H. pylori infection produced resolution of the gastric inflammation in each subject and resolution of hypochlorhydria and atrophy in 50% of the subjects. CONCLUSIONS: Relatives of patients with gastric cancer have an increased prevalence of precancerous gastric abnormalities, but this increase is confined to those with H. pylori infection. Consequently, prophylactic eradication of the infection should be offered to such subjects.
BACKGROUND: Gastric analysis is useful for diagnosing and monitoring the control of hypersecretory conditions and to distinguish appropriate from inappropriate causes of hypergastrinaemia. Pentagastrin, used to measure maximal acid output (MAO), is no longer available in the USA. METHODS: We examined the University of Pennsylvania Health System gastric analysis database, which includes demographic data, study indications, gastric analysis, and serum gastrin and secretin testing results according to referral indications, paying specific attention to discordant basal acid output (BAO) and MAO measurements. RESULTS: One hundred and twenty-four gastric analyses were performed in 103 patients (42 males, mean age 47.5 years, 14 with prior acid-decreasing surgery). Recurrent ulceration or pain unresponsive to antisecretory therapy was the indication in 42 patients. Twelve were hypersecretory, including three each with isolated elevations of BAO or MAO. Hypergastrinaemia was the indication in 35 patients. Five were hypersecretory (four with Zollinger-Ellison syndrome), three had isolated MAO elevations and 16 were hypo- or achlorhydric, indicating appropriate hypergastrinaemia. Of the seven patients with isolated MAO elevations, two had clear benefit from the stimulated portion of the study (four additional patients had equivocal benefit). CONCLUSIONS: Gastrin concentrations cannot be interpreted without knowledge of acid secretory capacity. MAO measurement has a small but significant benefit over measuring BAO alone.