Autoantibody "subspecificity" in type 1 diabetes: risk for organ-specific autoimmunity clusters in distinct groups
Autoimmune thyroid disease (AIT), celiac disease, and Addison's disease are characterized by the presence of autoantibodies: thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TGAb) in AIT, tissue transglutaminase antibody (TTGAb) in celiac disease, and 21-hydroxylase antibody (21-...
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| Veröffentlicht in: | Diabetes care 2005-04, Vol.28 (4), p.850-855 |
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| container_title | Diabetes care |
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| creator | Barker, Jennifer M Yu, Jeesuk Yu, Liping Wang, Jian Miao, Dongmei Bao, Fei Hoffenberg, Edward Nelson, Jerald C Gottlieb, Peter A Rewers, Marian Eisenbarth, George S |
| description | Autoimmune thyroid disease (AIT), celiac disease, and Addison's disease are characterized by the presence of autoantibodies: thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TGAb) in AIT, tissue transglutaminase antibody (TTGAb) in celiac disease, and 21-hydroxylase antibody (21-OHAb) in Addison's disease. The objective of this study was to define the prevalence of these autoantibodies and clinical disease in a population with type 1 diabetes.
We screened 814 individuals with type 1 diabetes for TPOAb, TGAb, TTGAb, and 21-OHAb. Clinical disease was defined by chart review. Factors related to the presence of autoimmunity and clinical disease including age at onset of type 1 diabetes, duration of diabetes, age at screening, sex, and the presence of autoantibodies were reviewed.
The most common autoantibodies expressed were TPOAb and/or TGAb (29%), followed by TTGAb (10.1%) and 21-OHAb (1.6%). Specific HLA DR/DQ genotypes were associated with the highest risk for expression of 21-OHAb (DRB1*0404-DQ8, DR3-DQ2) and TTGAb (DR3-DQ2- DR3-DQ2). The expression of thyroid autoantibodies was related to 21-OHAb but not to TTGAb. The presence of autoantibodies was associated with and predictive of disease.
In this large cohort of individuals with type 1 diabetes, the expression of organ-specific autoantibodies was very high. The grouping of autoantibody expression suggests common factors contributing to the clustering. |
| doi_str_mv | 10.2337/diacare.28.4.850 |
| format | Article |
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We screened 814 individuals with type 1 diabetes for TPOAb, TGAb, TTGAb, and 21-OHAb. Clinical disease was defined by chart review. Factors related to the presence of autoimmunity and clinical disease including age at onset of type 1 diabetes, duration of diabetes, age at screening, sex, and the presence of autoantibodies were reviewed.
The most common autoantibodies expressed were TPOAb and/or TGAb (29%), followed by TTGAb (10.1%) and 21-OHAb (1.6%). Specific HLA DR/DQ genotypes were associated with the highest risk for expression of 21-OHAb (DRB1*0404-DQ8, DR3-DQ2) and TTGAb (DR3-DQ2- DR3-DQ2). The expression of thyroid autoantibodies was related to 21-OHAb but not to TTGAb. The presence of autoantibodies was associated with and predictive of disease.
In this large cohort of individuals with type 1 diabetes, the expression of organ-specific autoantibodies was very high. The grouping of autoantibody expression suggests common factors contributing to the clustering.</description><identifier>ISSN: 0149-5992</identifier><identifier>DOI: 10.2337/diacare.28.4.850</identifier><identifier>PMID: 15793184</identifier><identifier>CODEN: DICAD2</identifier><language>eng</language><publisher>United States: American Diabetes Association</publisher><subject>Adolescent ; Antibody Specificity ; Autoantibodies ; Autoantibodies - blood ; Autoimmune Diseases - epidemiology ; Autoimmune Diseases - immunology ; Causes of ; Celiac Disease - blood ; Celiac Disease - immunology ; Child ; Child, Preschool ; Diabetes ; Diabetes Mellitus, Type 1 - blood ; Diabetes Mellitus, Type 1 - immunology ; Evaluation ; Female ; HLA Antigens - immunology ; Humans ; Iodide Peroxidase - immunology ; Lymphatic system ; Male ; Medical disorders ; Organ Specificity ; Prevalence ; Risk Factors ; Thyroglobulin - immunology ; Thyroiditis, Autoimmune ; Type 1 diabetes</subject><ispartof>Diabetes care, 2005-04, Vol.28 (4), p.850-855</ispartof><rights>COPYRIGHT 2005 American Diabetes Association</rights><rights>Copyright American Diabetes Association Apr 2005</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15793184$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Barker, Jennifer M</creatorcontrib><creatorcontrib>Yu, Jeesuk</creatorcontrib><creatorcontrib>Yu, Liping</creatorcontrib><creatorcontrib>Wang, Jian</creatorcontrib><creatorcontrib>Miao, Dongmei</creatorcontrib><creatorcontrib>Bao, Fei</creatorcontrib><creatorcontrib>Hoffenberg, Edward</creatorcontrib><creatorcontrib>Nelson, Jerald C</creatorcontrib><creatorcontrib>Gottlieb, Peter A</creatorcontrib><creatorcontrib>Rewers, Marian</creatorcontrib><creatorcontrib>Eisenbarth, George S</creatorcontrib><title>Autoantibody "subspecificity" in type 1 diabetes: risk for organ-specific autoimmunity clusters in distinct groups</title><title>Diabetes care</title><addtitle>Diabetes Care</addtitle><description>Autoimmune thyroid disease (AIT), celiac disease, and Addison's disease are characterized by the presence of autoantibodies: thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TGAb) in AIT, tissue transglutaminase antibody (TTGAb) in celiac disease, and 21-hydroxylase antibody (21-OHAb) in Addison's disease. The objective of this study was to define the prevalence of these autoantibodies and clinical disease in a population with type 1 diabetes.
We screened 814 individuals with type 1 diabetes for TPOAb, TGAb, TTGAb, and 21-OHAb. Clinical disease was defined by chart review. Factors related to the presence of autoimmunity and clinical disease including age at onset of type 1 diabetes, duration of diabetes, age at screening, sex, and the presence of autoantibodies were reviewed.
The most common autoantibodies expressed were TPOAb and/or TGAb (29%), followed by TTGAb (10.1%) and 21-OHAb (1.6%). Specific HLA DR/DQ genotypes were associated with the highest risk for expression of 21-OHAb (DRB1*0404-DQ8, DR3-DQ2) and TTGAb (DR3-DQ2- DR3-DQ2). The expression of thyroid autoantibodies was related to 21-OHAb but not to TTGAb. The presence of autoantibodies was associated with and predictive of disease.
In this large cohort of individuals with type 1 diabetes, the expression of organ-specific autoantibodies was very high. The grouping of autoantibody expression suggests common factors contributing to the clustering.</description><subject>Adolescent</subject><subject>Antibody Specificity</subject><subject>Autoantibodies</subject><subject>Autoantibodies - blood</subject><subject>Autoimmune Diseases - epidemiology</subject><subject>Autoimmune Diseases - immunology</subject><subject>Causes of</subject><subject>Celiac Disease - blood</subject><subject>Celiac Disease - immunology</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Type 1 - blood</subject><subject>Diabetes Mellitus, Type 1 - immunology</subject><subject>Evaluation</subject><subject>Female</subject><subject>HLA Antigens - immunology</subject><subject>Humans</subject><subject>Iodide Peroxidase - immunology</subject><subject>Lymphatic system</subject><subject>Male</subject><subject>Medical disorders</subject><subject>Organ Specificity</subject><subject>Prevalence</subject><subject>Risk Factors</subject><subject>Thyroglobulin - immunology</subject><subject>Thyroiditis, Autoimmune</subject><subject>Type 1 diabetes</subject><issn>0149-5992</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkb1r3jAQhzW0JGmSvVMR79DNjmTJstTtJaRtINClmY0sn4xSW3L1Mbz_fRWSLCXccHA89_DjDqHPlLQdY8PN7LTREdpOtryVPfmALgjlqumV6s7Rp5SeCCGcS3mGzmk_KEYlv0DxWHLQPrspzCd8SGVKOxhnnXH5dMDO43zaAVNc9RNkSN9wdOkPtiHiEBftmzce62py21Z83cRmLSlDTM-G2aXsvMl4iaHs6Qp9tHpNcP3aL9Hj97vftz-bh18_7m-PD83CKMsNgJYCJBso8M4KYidFpOZKdJqzfrCkn6VgQjElmeUzE1pwBfPAJ2aEIAO7RF9fvHsMfwukPG4uGVhX7SGUNIqhF4yIZ_DwH_gUSvQ129h1jPSUSlmh5gVa9Aqj8zbkqM0CHqJegwfr6vhIa_R6V9FXvn2HrzXD5sy7C19eU5Rpg3nco9t0PI1vv2L_ABMklPE</recordid><startdate>200504</startdate><enddate>200504</enddate><creator>Barker, Jennifer M</creator><creator>Yu, Jeesuk</creator><creator>Yu, Liping</creator><creator>Wang, Jian</creator><creator>Miao, Dongmei</creator><creator>Bao, Fei</creator><creator>Hoffenberg, Edward</creator><creator>Nelson, Jerald C</creator><creator>Gottlieb, Peter A</creator><creator>Rewers, Marian</creator><creator>Eisenbarth, George S</creator><general>American Diabetes Association</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7RV</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0K</scope><scope>M0R</scope><scope>M0S</scope><scope>M0T</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>7X8</scope></search><sort><creationdate>200504</creationdate><title>Autoantibody "subspecificity" in type 1 diabetes: risk for organ-specific autoimmunity clusters in distinct groups</title><author>Barker, Jennifer M ; Yu, Jeesuk ; Yu, Liping ; Wang, Jian ; Miao, Dongmei ; Bao, Fei ; Hoffenberg, Edward ; Nelson, Jerald C ; Gottlieb, Peter A ; Rewers, Marian ; Eisenbarth, George S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-g313t-eea86e8371e42f60fb908a4962a4357f05d863693983f4d36a649ed74b3c66073</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adolescent</topic><topic>Antibody Specificity</topic><topic>Autoantibodies</topic><topic>Autoantibodies - blood</topic><topic>Autoimmune Diseases - epidemiology</topic><topic>Autoimmune Diseases - immunology</topic><topic>Causes of</topic><topic>Celiac Disease - blood</topic><topic>Celiac Disease - immunology</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Type 1 - blood</topic><topic>Diabetes Mellitus, Type 1 - immunology</topic><topic>Evaluation</topic><topic>Female</topic><topic>HLA Antigens - immunology</topic><topic>Humans</topic><topic>Iodide Peroxidase - immunology</topic><topic>Lymphatic system</topic><topic>Male</topic><topic>Medical disorders</topic><topic>Organ Specificity</topic><topic>Prevalence</topic><topic>Risk Factors</topic><topic>Thyroglobulin - immunology</topic><topic>Thyroiditis, Autoimmune</topic><topic>Type 1 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Barker, Jennifer M</creatorcontrib><creatorcontrib>Yu, Jeesuk</creatorcontrib><creatorcontrib>Yu, Liping</creatorcontrib><creatorcontrib>Wang, Jian</creatorcontrib><creatorcontrib>Miao, Dongmei</creatorcontrib><creatorcontrib>Bao, Fei</creatorcontrib><creatorcontrib>Hoffenberg, Edward</creatorcontrib><creatorcontrib>Nelson, Jerald C</creatorcontrib><creatorcontrib>Gottlieb, Peter A</creatorcontrib><creatorcontrib>Rewers, Marian</creatorcontrib><creatorcontrib>Eisenbarth, George S</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>eLibrary</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Agricultural Science Database</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Healthcare Administration Database</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Science Database</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><jtitle>Diabetes care</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Barker, Jennifer M</au><au>Yu, Jeesuk</au><au>Yu, Liping</au><au>Wang, Jian</au><au>Miao, Dongmei</au><au>Bao, Fei</au><au>Hoffenberg, Edward</au><au>Nelson, Jerald C</au><au>Gottlieb, Peter A</au><au>Rewers, Marian</au><au>Eisenbarth, George S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Autoantibody "subspecificity" in type 1 diabetes: risk for organ-specific autoimmunity clusters in distinct groups</atitle><jtitle>Diabetes care</jtitle><addtitle>Diabetes Care</addtitle><date>2005-04</date><risdate>2005</risdate><volume>28</volume><issue>4</issue><spage>850</spage><epage>855</epage><pages>850-855</pages><issn>0149-5992</issn><coden>DICAD2</coden><abstract>Autoimmune thyroid disease (AIT), celiac disease, and Addison's disease are characterized by the presence of autoantibodies: thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TGAb) in AIT, tissue transglutaminase antibody (TTGAb) in celiac disease, and 21-hydroxylase antibody (21-OHAb) in Addison's disease. The objective of this study was to define the prevalence of these autoantibodies and clinical disease in a population with type 1 diabetes.
We screened 814 individuals with type 1 diabetes for TPOAb, TGAb, TTGAb, and 21-OHAb. Clinical disease was defined by chart review. Factors related to the presence of autoimmunity and clinical disease including age at onset of type 1 diabetes, duration of diabetes, age at screening, sex, and the presence of autoantibodies were reviewed.
The most common autoantibodies expressed were TPOAb and/or TGAb (29%), followed by TTGAb (10.1%) and 21-OHAb (1.6%). Specific HLA DR/DQ genotypes were associated with the highest risk for expression of 21-OHAb (DRB1*0404-DQ8, DR3-DQ2) and TTGAb (DR3-DQ2- DR3-DQ2). The expression of thyroid autoantibodies was related to 21-OHAb but not to TTGAb. The presence of autoantibodies was associated with and predictive of disease.
In this large cohort of individuals with type 1 diabetes, the expression of organ-specific autoantibodies was very high. The grouping of autoantibody expression suggests common factors contributing to the clustering.</abstract><cop>United States</cop><pub>American Diabetes Association</pub><pmid>15793184</pmid><doi>10.2337/diacare.28.4.850</doi><tpages>6</tpages></addata></record> |
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| subjects | Adolescent Antibody Specificity Autoantibodies Autoantibodies - blood Autoimmune Diseases - epidemiology Autoimmune Diseases - immunology Causes of Celiac Disease - blood Celiac Disease - immunology Child Child, Preschool Diabetes Diabetes Mellitus, Type 1 - blood Diabetes Mellitus, Type 1 - immunology Evaluation Female HLA Antigens - immunology Humans Iodide Peroxidase - immunology Lymphatic system Male Medical disorders Organ Specificity Prevalence Risk Factors Thyroglobulin - immunology Thyroiditis, Autoimmune Type 1 diabetes |
| title | Autoantibody "subspecificity" in type 1 diabetes: risk for organ-specific autoimmunity clusters in distinct groups |
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