{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T02:27:20Z","timestamp":1790908040054,"version":"4.1.0"},"reference-count":16,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2022,9,30]],"date-time":"2022-09-30T00:00:00Z","timestamp":1664496000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Diabetes Invest"],"published-print":{"date-parts":[[2023,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Aims\/Introduction<\/jats:title><jats:p>This study aimed to investigate the clinical significance and antigen specificity of autoantibodies to insulinoma\u2010associated antigen\u20102 (IA\u20102A) by radioimmunoassay (RIA; IA\u20102A\u2010RIA) and enzyme\u2010linked immunosorbent assay (ELISA; IA\u20102A\u2010ELISA) in Japanese patients with type\u20091 diabetes.<\/jats:p><\/jats:sec><jats:sec><jats:title>Materials and Methods<\/jats:title><jats:p>A total of 338 type\u20091 diabetic patients were enrolled, including 38 fulminant type\u20091 diabetes, 168 acute\u2010onset type\u20091 diabetes and 137 slowly\u2010progressive type\u20091 diabetes (SPIDDM). The concordance, correlation of autoantibody titer, and the relationship between IA\u20102A and progression to the insulin\u2010deficient state were examined. Also, competitive assay was used to examine the antigen specificity.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The prevalence of IA\u20102A\u2010ELISA was 4\u20135% lower than that of IA\u20102A\u2010RIA in both the acute\u2010onset type\u20091 diabetes and SPIDDM, but the diagnostic sensitivities of both subtypes, when measured in combination with glutamic acid decarboxylase autoantibody, were comparable. The diagnosis of type\u20091 diabetes using either the RIA or ELISA methods showed substantial agreement with the exponential correlation of autoantibody titers detected by RIA and ELISA. Among the SPIDDM patients, the fasting C\u2010peptide for IA\u20102A\u2010positive cases by ELISA, but not the RIA method, was significantly lower than in the negative cases (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.05). Furthermore, IA\u20102A\u2010ELISA proved superior to the RIA method in predicting the progression to insulin deficiency in SPIDDM. Competitive analysis showed that even sera with discrepant results by RIA and ELISA have IA\u20102\u2010specific autoantibodies.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>These results suggest that IA\u20102A\u2010ELISA is a reliable marker not only for the diagnosis of type\u20091 diabetes, but also for the prediction of future insulin dependency; that is, detection of IA\u20102A\u2010ELISA helps identify a subtype of SPIDDM patients who would likely progress onto insulin\u2010deficient state.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jdi.13910","type":"journal-article","created":{"date-parts":[[2022,9,30]],"date-time":"2022-09-30T09:09:24Z","timestamp":1664528964000},"page":"58-66","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Comparing the clinical significance and antigen specificity of insulinoma\u2010associated antigen\u20102 autoantibodies between radioimmunoassay and <scp>enzyme\u2010linked<\/scp> immunosorbent assay in Japanese patients with type\u20091 diabetes"],"prefix":"10.1111","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7434-4744","authenticated-orcid":false,"given":"Eiji","family":"Kawasaki","sequence":"first","affiliation":[{"name":"Diabetes Center Shin\u2010Koga Hospital  Kurume Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3954-4983","authenticated-orcid":false,"given":"Akira","family":"Shimada","sequence":"additional","affiliation":[{"name":"Department of Endocrinology and Diabetes, School of Medicine Saitama Medical University  Iruma Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4213-3229","authenticated-orcid":false,"given":"Akihisa","family":"Imagawa","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine (I) Osaka Medical and Pharmaceutical University  Takatsuki 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Diabetes and Endocrinology Showa University School of Medicine  Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5115-1111","authenticated-orcid":false,"given":"Junnosuke","family":"Miura","sequence":"additional","affiliation":[{"name":"Division of Diabetology and Metabolism, Department of Internal Medicine Tokyo Women's Medical University School of Medicine  Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6966-496X","authenticated-orcid":false,"given":"Kazuki","family":"Yasuda","sequence":"additional","affiliation":[{"name":"Department of Diabetes, Endocrinology, and Metabolism Kyorin University  Mitaka Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3742-9268","authenticated-orcid":false,"given":"Hisafumi","family":"Yasuda","sequence":"additional","affiliation":[{"name":"Division of Health Sciences, Department of 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