Abstract
BackgroundSerum gastrin concentration can help diagnose gastrinomas in dogs if >3–10× the upper reference limit (URL), but antisecretory therapy and other conditions can also cause hypergastrinemia. Effects of antisecretory therapy (famotidine or ranitidine, omeprazole) on serum gastrin concentration in dogs with chronic enteropathy (CE) and its biological variation (BV) are unknown. Aim of the study was to evaluate serum gastrin in acid-suppressant-treated or -naïve CE dogs; test the association between serum gastrin and histopathologic findings in acid-suppressant-naïve CE dogs; and evaluate the BV of serum gastrin in dogs not receiving any gastric acid suppressive therapy. Samples from 231 dogs were used and serum gastrin was measured by chemiluminescence assay. Gastric and duodenal histologic lesions were evaluated and graded. BV of serum gastrin was evaluated in serial samples.ResultsSerum gastrin concentrations were significantly higher in acid-suppressant-treated than acid-suppressant-naïve dogs (P = 0.0245), with significantly higher concentrations in proton pump inhibitor (PPI)- than H2-antihistamine-treated patients (P = 0.0053). More PPI- than H2-antihistamine-treated dogs had gastrin concentrations above URL (P = 0.0205), but not >3× nor >10× the URL. Serum gastrin concentrations correlated with the severity of gastric antral epithelial injury (P = 0.0069) but not with any other lesions or the presence/numbers of spiral bacteria in gastric biopsies. Intra- and inter-individual BV were 43.4 and 21.6%, respectively, in acid-suppressant-naïve dogs, with a reciprocal individuality index of 0.49 and a critical difference of ≥29.5 ng/L.ConclusionsAntisecretory (particularly PPI) treatment leads to hypergastrinemia in CE dogs, but the concentrations seen in this study are unlikely to compromise a diagnosis of gastrinoma. Use of a population-based URL for canine serum gastrin and a URL of ≤27.8 ng/L are appropriate.
Highlights
Serum gastrin concentration can help diagnose gastrinomas in dogs if >3–10× the upper reference limit (URL), but antisecretory therapy and other conditions can cause hypergastrinemia
While no differences in plasma gastrin concentrations were seen between dogs colonized with Helicobacter spp. and specific-pathogen-free, Helicobacter spp.-free dogs [14], an enhanced basal gastrin release from canine antral G cells was detected after incubation with Helicobacter pylori extracts [15], and an increase in gastrin-mRNA expression in the fundus of the stomach has been demonstrated in dogs harboring virulent strains of Helicobacter heilmannii [16]
This study evaluated serum gastrin concentrations in acid-suppressant-naïve chronic enteropathy (CE) dogs and CE dogs receiving gastric acid-suppressive therapy, and it is reasonable to assume that the findings of this study are likely to translate to other species
Summary
Serum gastrin concentration can help diagnose gastrinomas in dogs if >3–10× the upper reference limit (URL), but antisecretory therapy and other conditions can cause hypergastrinemia. Effects of antisecretory therapy (famotidine or ranitidine, omeprazole) on serum gastrin concentration in dogs with chronic enteropathy (CE) and its biological variation (BV) are unknown. Gastrin is a small peptide hormone that is produced by gastric and proximal duodenal G cells [1]. Serum gastrin concentrations were approximately twice as high in a small group of dogs with moderate to severe chronic lymphocytic-plasmacytic enteritis (LPE) compared to a group of dogs without gastrointestinal disease, and were higher in dogs with severe microscopic lesions in the Heilmann et al BMC Veterinary Research (2017) 13:321 stomach [13]. Effects of gastric Helicobacter spp. on gastrin expression and release in dogs have not been definitively elucidated. While no differences in plasma gastrin concentrations were seen between dogs colonized with Helicobacter spp. and specific-pathogen-free, Helicobacter spp.-free dogs [14], an enhanced basal gastrin release from canine antral G cells was detected after incubation with Helicobacter pylori extracts [15], and an increase in gastrin-mRNA expression in the fundus of the stomach has been demonstrated in dogs harboring virulent strains of Helicobacter heilmannii [16]
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