gastrins and Bacterial-Infections

This paper reviews the relationship between gastric acid secretion and infection and the protective role of gastric acid as a primary bactericidal barrier and modulator of gastrin section. Gastric acid is bactericidal at pH 3 or less, but reduction of acidity predisposes to infection with a wide variety of bacteria. Bacterial infections or hyperpyrexia may be associated with a marked reduction in gastric acid secretion, and Campylobacter pylori has been suggested as one cause of epidemic hypochlorhydria. Achlorhydria is also associated with hypergastrinaemia with levels 20-fold higher in pernicious anaemia patients than normal subjects. Treatment with antisecretory drugs is associated with hypergastrinaemia with gastrin levels 2- to 5-fold higher than with placebo, and the gastrin levels correlate with the degree of acid suppression. The possible relationship among infection, acid suppression, hypergastrinaemia, and the development of enterochromaffin cell hyperplasia and possible carcinogenesis is reviewed.

Topics: Achlorhydria; Bacterial Infections; Campylobacter Infections; Gastric Acid; Gastrins; Humans; Hydrogen-Ion Concentration

Proton pump inhibitors (PPI) remain the leading therapy for acid-related disorders. Long-term PPI use increases the risk of pneumonia and enteric bacterial infections and of nosocomial Clostridium difficile-associated diarrhoea. PPIs do not lead to vitamin B12 or iron deficiencies and do not induce malignancies or increase the risk of major birth defects. Prolonged PPI use may be a weak risk factor for certain fractures and results in hypergastrinaemia and parietal cell hyperplasia leading to rebound acid hypersecretion, which may induce symptoms on withdrawal of therapy.

Topics: Anti-Ulcer Agents; Bacterial Infections; Congenital Abnormalities; Dyspepsia; Fractures, Bone; Gastrins; Gastroenteritis; Gastroesophageal Reflux; Heartburn; Humans; Neoplasms; Omeprazole; Pneumonia; Proton Pump Inhibitors; Risk Factors; Time Factors; Vitamin B 12 Deficiency

Proton pump inhibitors (PPIs) have become the mainstay of therapy in acid-related upper gastrointestinal disorders including gastroesophageal reflux disease and peptic ulcer disease. Alltough these medications are generally accepted as safe, the long-term clinical consequences of the inducing hypochlorhydria are not completely clear. Gastric acid production is mainly controlled by the hormone gastrin through a negative feedback in which hypochlorhydria induces an increase in serum gastrin. PPIs have been shown to increase serum gastrin levels. Gastric endocrine cell hyperplasia can occur in 10 to 30% of patients without carcinoid tumors. Recent studies indicate no association between PPI use and the risk of colorectal and gastric cancers. Proton pump inhibitor-associated gastric polyps are totally benign tumors that should not be followed. There is an association between PPIs-induced acid suppression and an increased risk of enteric infection. PPIs do not inhibit intestinal absorption of lipids, iron, phosphorus, magnesium or zinc from food but can affect vitamin B12 status in older patients. Despite the undoubted benefits of PPIs, the practitioner always needs to consider risks and benefits before initiating them.

Topics: Bacterial Infections; Colonic Neoplasms; Gastric Acid; Gastrins; Humans; Polyps; Proton Pump Inhibitors; Vitamin B 12 Deficiency

Topics: Acute Disease; Age Factors; Bacterial Infections; Calcium; Dysentery; Gastrins; Humans; Infant; Intestinal Diseases; Islets of Langerhans; Pancreas; Trypsin

The effect of bombesin (BBS) in modulating the secretion of specific Aeromonas antibodies in rat intestine was determined. Rats were immunized with the culture supernatant of Aeromonas hydrophila, isolate SSU. This culture supernatant contained a number of toxins that may be considered virulence factors. After 24 days of immunization, rats were anesthetized and a 10-cm intestinal segment was perfused with phosphate-buffered saline. The effluents were collected for measurement of IgA and IgG by the enzyme-linked immunosorbent assay. When compared with the effect of intravenous administration of normal saline in the control group, intravenous injection of BBS (20 micrograms/kg) in the experimental group caused a significant increase in rat intestinal IgA and IgG in perfusates. The stimulatory effects of BBS on the presence of IgA and IgG were depressed partially by proglumide, a receptor antagonist of cholecystokinin (CCK) and gastrin. Treatment with pentagastrin (250 micrograms/kg) accelerated intestinal secretion of IgA, but failed to stimulate intestinal IgG secretion. In addition, intravenous injection of CCK-8 (120 ng/kg) evoked the intestinal secretion of either IgA or IgG. These findings demonstrated that BBS, gastrin, and CCK can stimulate antibody secretion in rat intestine and the stimulatory effect of BBS may be mediated partially via release of CCK and gastrin. These results suggest that neuropeptides such as BBS and gastrointestinal hormones, eg, CCK and gastrin, may participate in the regulation of intestinal secretion of IgA and IgG antibodies, respectively, in rats.

Topics: Aeromonas; Animals; Antibodies, Anti-Idiotypic; Antibodies, Bacterial; Bacterial Infections; Bombesin; Cholecystokinin; Enzyme-Linked Immunosorbent Assay; Gastrins; Immunoglobulin A; Immunoglobulin G; Intestinal Mucosa; Intestines; Male; Pentagastrin; Proglumide; Rats; Rats, Inbred Strains; Sincalide