Aim. To assess the predictive value for chronic autoimmune gastritis (AIG) of the combined assay of anti-parietal-cell antibodies (PCA), anti-intrinsic-factor antibodies (IFA), anti-Helicobacter pylori (Hp) antibodies, and measurement of blood gastrin. Methods. We studied 181 consecutive patients with anemia, due to iron deficiency resistant to oral replacement therapy or to vitamin B12 deficiency. Results. 83 patients (45.8%) tested positive for PCA and underwent gastroscopy with multiple gastric biopsies. On the basis of the histological diagnosis, PCA-positive patients were divided into 4 groups: (1) 30 patients with chronic atrophic gastritis; they had high concentrations of PCA and gastrin and no detectable IFA; (2) 14 subjects with metaplastic gastric atrophy; they had high PCA, IFA, and gastrin; (3) 18 patients with nonspecific lymphocytic inflammation with increased PCA, normal gastrin levels, and absence of IFA; (4) 21 patients with multifocal atrophic gastritis with “borderline” PCA, normal gastrin, absence of IFA and presence of anti-Hp in 100% of the cases. Conclusions. The assay of four serological markers proved particularly effective in the diagnostic classification of gastritis and highly correlated with the histological profile. As such, this laboratory diagnostic profile may be considered an authentic “serological biopsy.” 1. Introduction Chronic autoimmune gastritis (AIG), also known as type A chronic atrophic gastritis, is an organ-specific disease that causes malabsorption of essential elements and pernicious or microcytic anemia, and it is a predisposing factor to carcinoid tumour and gastric adenocarcinoma. It is generally asymptomatic up to an advanced stage of atrophy and/or dysplasia of the mucosa [1, 2]. Histologically, it is characterised by a chronic inflammatory disorder of the gastric body and the fundus, sustained by a cell-mediated aggression by CD4+CD25- Th1 lymphocyte effectors. The main target of immunological injury is the H+/K+-adenosine-triphosphate enzyme (ATPase), a protein of the membrane that coats the secretory canaliculi of the parietal cells and is responsible for the secretion of the hydrogen ions in exchange for the potassium ions (proton pump) [3, 4]. Induced by a triggering factor not yet entirely identified, the CD4+CD25？？？T-cells, together with macrophages and B lymphocytes, infiltrate the submucosa, the lamina propria, and the gastric glands causing the loss of parietal, principal, and ghrelin-producing cells or P/D1 cells [5, 6]. The damage of the body and fundus mucosa results in [3,
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