Marcello Bagnasco1,2, Daniele Saverino3,2, Francesca Pupo1,2, Manuela Marchiano1,2, Maria Grazia Alessio4, Wolfgang Schlumberger5, Antonio Antico6, Giampaola Pesce1,2, Nicola Bizzaro7. 1. Dipartimento di Medicina Interna, University of Genoa, Genoa, Italy. 2. Laboratory of Autoimmunology, Ospedale Policlinico San Martino, Genoa, Italy. 3. Dipartimento di Medicina Sperimentale, University of Genoa, Genoa, Italy. 4. Laboratory of Clinical Chemistry, Papa Giovanni Hospital XXIII, Bergamo, Italy. 5. Institute for Experimental Immunology, Euroimmun, Lübeck, Germany. 6. Laboratory of Clinical Pathology, Civic Hospital, Santorso, Italy. 7. Laboratory of Clinical Pathology, San Antonio Hospital, Tolmezzo, Italy.
Abstract
OBJECTIVES: Anti-parietal cell antibodies (APCA) are a serologic marker of autoimmune gastritis. Their prevalence in healthy individuals is not well defined. METHODS: We evaluated APCA prevalence in 515 healthy blood-donors by rat/primate tissue indirect immunofluorescence (IIF), enzyme-linked immunosorbent assay (ELISA), and immunoblot. RESULTS: Fifty-three of 515 (10.3%) subjects were positive for APCA by at least one method: 18 only by ELISA, 10 by rodent tissue IIF, and one by primate tissue IIF; 18 were positive by ELISA and primate tissue IIF, and one by ELISA and rodent tissue IIF. Two were positive by both IIF methods, and three were triple positive. APCA positivity was confirmed by immunoblot in 100% of ELISA positive, in 95.8% of positive primate tissue IIF, and in 50% of positive rat tissue IIF. CONCLUSIONS: A great discrepancy in APCA prevalence detected by different methods in this cohort was apparent. Thus, the results on APCA prevalence in healthy individuals are likely method-dependent.
OBJECTIVES: Anti-parietal cell antibodies (APCA) are a serologic marker of autoimmune gastritis. Their prevalence in healthy individuals is not well defined. METHODS: We evaluated APCA prevalence in 515 healthy blood-donors by rat/primate tissue indirect immunofluorescence (IIF), enzyme-linked immunosorbent assay (ELISA), and immunoblot. RESULTS: Fifty-three of 515 (10.3%) subjects were positive for APCA by at least one method: 18 only by ELISA, 10 by rodent tissue IIF, and one by primate tissue IIF; 18 were positive by ELISA and primate tissue IIF, and one by ELISA and rodent tissue IIF. Two were positive by both IIF methods, and three were triple positive. APCA positivity was confirmed by immunoblot in 100% of ELISA positive, in 95.8% of positive primate tissue IIF, and in 50% of positive rat tissue IIF. CONCLUSIONS: A great discrepancy in APCA prevalence detected by different methods in this cohort was apparent. Thus, the results on APCA prevalence in healthy individuals are likely method-dependent.