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Plasma ghrelin concentrations in type 1 diabetic patients with autoimmune atrophic gastritis

¹ Department of Endocrinology and Nutrition, Hospital Universitari ‘Germans Trias i Pujol’, Ctra Canyet s/n, Badalona 08916, Barcelona, Spain² Department of Clinical Biochemistry,, Hospital Universitari ‘Germans Trias i Pujol’, Universitat Autònoma de Barcelona, Badalona, Barcelona, Spain³ Departments of Pathology and ⁴ Immunology (LIRAD-BST),, Hospital Universitari ‘Germans Trias i Pujol’, Badalona, Barcelona, Spain and ⁵ Departament de Medicina,, Hospital Universitari ‘Germans Trias i Pujol’, Universitat Autònoma de Barcelona, Badalona, Barcelona, Spain

(Correspondence should be addressed to N Alonso; Email: nalonso.germanstrias{at}gencat.net)

Objective: Type 1 diabetes mellitus patients (DM1) show increased prevalence of pernicious anaemia, the histological substrate of which is type A chronic atrophic gastritis (CAG) in the stomach corpus, the main source of ghrelin. We aimed to compare plasma ghrelin concentrations in DM1 patients with type A CAG (DM1-CAG), DM1 patients without type A CAG and healthy controls and in DM1-CAG group, to ascertain a possible relationship between ghrelin and biochemical markers of gastric mucosa atrophy and/or neuroendocrine (NE) cell hyperplasia and histological gastric biopsy findings.

Design and methods: Fifteen DM1-CAG patients were matched for age, sex and body mass index with 15 DM1 patients without type A CAG and 15 controls. Pepsinogen I, pepsinogen II, gastrin, parietal cell antibodies, chromogranin A (CgA) and ghrelin were determined in all subjects. In DM1-CAG patients, immunohistochemical analysis of gastric biopsies using antibodies to CgA and ghrelin was performed.

Results: Ghrelin concentrations differed among groups; however, paired comparisons between groups were not significant. In DM1-CAG, no correlation was found between ghrelin and gastric body atrophy markers, pepsinogen I and the pepsinogen I/II ratio. Immunohistochemical studies of DMI-CAG patients showed CgA staining in 12 and ghrelin staining in 6, which was confined to the foci of NE cell hyperplasia. Those patients who stained positive for ghrelin had higher ghrelin concentrations when compared with the negative patients.

Conclusions: Ghrelin concentrations are not decreased in DM1-CAG patients; thus, our data suggest that ghrelin is not a good marker of gastric mucosa atrophy in these patients, given the possible ghrelin synthesis in hyperplastic gastric endocrine/enterochromaffin-like cells.