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Islet cell and insulin autoantibodies in subjects at high risk for development of type 1 (insulin-dependent) diabetes mellitus: the Lyon family study
Genetic determination as well as prospective analysis of islet cell autoantibodies and autoantibodies to insulin were conducted in a population of 479 first degree relatives of 174 Type 1 (insulin-dependent) diabetic patients. Analysis of HLA haplotypes within families illustrated the high frequency...
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| Published in: | Diabetologia 1988-10, Vol.31 (10), p.741-746 |
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| Main Authors: | , , , , , , |
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| cites | cdi_FETCH-LOGICAL-c378t-23927c854195c648540766249e6339596512cb9c82c92306a9a40b2d34a2ebac3 |
| container_end_page | 746 |
| container_issue | 10 |
| container_start_page | 741 |
| container_title | Diabetologia |
| container_volume | 31 |
| creator | THIVOLET, C BEAUFRERE, B BETUEL, H CHATELAIN, P DURAND, A TOURNIAIRE, J FRANCOIS, R |
| description | Genetic determination as well as prospective analysis of islet cell autoantibodies and autoantibodies to insulin were conducted in a population of 479 first degree relatives of 174 Type 1 (insulin-dependent) diabetic patients. Analysis of HLA haplotypes within families illustrated the high frequency of DR3 and DR4 alleles with preferential transmission from parent to both affected and unaffected offspring. DR4 was preferentially associated with DQw3.2 (TA10-) in 60/73 (82.2%) patients and 101/127 (79.5%) relatives. Relatives have been followed for a period of 800 subject-years. Twenty-two out of 430 relatives (5.1%) were found islet cell antibodies (ICA-IgG) positive. Seven sera with low titres became negative 6 months later at two different determinations. Fifteen sera ICA-IgG and ICA-protein A positive with high titres remained positive thereafter. Half of the ICA positive relatives were also found insulin autoantibodies (IAA) positive. All but 3 ICA negative relatives did not have IAA in their sera. Analysis of IAA specificity with competition experiments indicated that most antibodies recognised epitopes shared between human and pork insulins while four were specific for human insulin determinants. Analysis of class I and class II HLA antigen distribution indicated no particular allelic restriction in antibody positive individuals. Metabolic status of antibody positive relatives was determined with oral and intravenous charge of glucose. Two haplo-identical DR3-DQw2 brothers became diabetic during the study. One child and one mother both with DR4-DQw3.2 became intolerant to glucose. Each of these relatives had high titre ICA prior to metabolic deterioration. |
| doi_str_mv | 10.1007/BF00274776 |
| format | article |
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Analysis of HLA haplotypes within families illustrated the high frequency of DR3 and DR4 alleles with preferential transmission from parent to both affected and unaffected offspring. DR4 was preferentially associated with DQw3.2 (TA10-) in 60/73 (82.2%) patients and 101/127 (79.5%) relatives. Relatives have been followed for a period of 800 subject-years. Twenty-two out of 430 relatives (5.1%) were found islet cell antibodies (ICA-IgG) positive. Seven sera with low titres became negative 6 months later at two different determinations. Fifteen sera ICA-IgG and ICA-protein A positive with high titres remained positive thereafter. Half of the ICA positive relatives were also found insulin autoantibodies (IAA) positive. All but 3 ICA negative relatives did not have IAA in their sera. Analysis of IAA specificity with competition experiments indicated that most antibodies recognised epitopes shared between human and pork insulins while four were specific for human insulin determinants. Analysis of class I and class II HLA antigen distribution indicated no particular allelic restriction in antibody positive individuals. Metabolic status of antibody positive relatives was determined with oral and intravenous charge of glucose. Two haplo-identical DR3-DQw2 brothers became diabetic during the study. One child and one mother both with DR4-DQw3.2 became intolerant to glucose. Each of these relatives had high titre ICA prior to metabolic deterioration.</description><identifier>ISSN: 0012-186X</identifier><identifier>EISSN: 1432-0428</identifier><identifier>DOI: 10.1007/BF00274776</identifier><identifier>PMID: 3071483</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>Adolescent ; Adult ; Autoantibodies - analysis ; Biological and medical sciences ; Child ; Diabetes Mellitus, Type 1 - genetics ; Diabetes Mellitus, Type 1 - immunology ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Female ; France ; Haplotypes ; HLA Antigens - analysis ; Humans ; Insulin Antibodies - analysis ; Islets of Langerhans - immunology ; Male ; Medical sciences ; Risk Factors</subject><ispartof>Diabetologia, 1988-10, Vol.31 (10), p.741-746</ispartof><rights>1989 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c378t-23927c854195c648540766249e6339596512cb9c82c92306a9a40b2d34a2ebac3</citedby><cites>FETCH-LOGICAL-c378t-23927c854195c648540766249e6339596512cb9c82c92306a9a40b2d34a2ebac3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,783,787,27936,27937</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=7263797$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/3071483$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>THIVOLET, C</creatorcontrib><creatorcontrib>BEAUFRERE, B</creatorcontrib><creatorcontrib>BETUEL, H</creatorcontrib><creatorcontrib>CHATELAIN, P</creatorcontrib><creatorcontrib>DURAND, A</creatorcontrib><creatorcontrib>TOURNIAIRE, J</creatorcontrib><creatorcontrib>FRANCOIS, R</creatorcontrib><title>Islet cell and insulin autoantibodies in subjects at high risk for development of type 1 (insulin-dependent) diabetes mellitus: the Lyon family study</title><title>Diabetologia</title><addtitle>Diabetologia</addtitle><description>Genetic determination as well as prospective analysis of islet cell autoantibodies and autoantibodies to insulin were conducted in a population of 479 first degree relatives of 174 Type 1 (insulin-dependent) diabetic patients. Analysis of HLA haplotypes within families illustrated the high frequency of DR3 and DR4 alleles with preferential transmission from parent to both affected and unaffected offspring. DR4 was preferentially associated with DQw3.2 (TA10-) in 60/73 (82.2%) patients and 101/127 (79.5%) relatives. Relatives have been followed for a period of 800 subject-years. Twenty-two out of 430 relatives (5.1%) were found islet cell antibodies (ICA-IgG) positive. Seven sera with low titres became negative 6 months later at two different determinations. Fifteen sera ICA-IgG and ICA-protein A positive with high titres remained positive thereafter. Half of the ICA positive relatives were also found insulin autoantibodies (IAA) positive. All but 3 ICA negative relatives did not have IAA in their sera. Analysis of IAA specificity with competition experiments indicated that most antibodies recognised epitopes shared between human and pork insulins while four were specific for human insulin determinants. Analysis of class I and class II HLA antigen distribution indicated no particular allelic restriction in antibody positive individuals. Metabolic status of antibody positive relatives was determined with oral and intravenous charge of glucose. Two haplo-identical DR3-DQw2 brothers became diabetic during the study. One child and one mother both with DR4-DQw3.2 became intolerant to glucose. Each of these relatives had high titre ICA prior to metabolic deterioration.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Autoantibodies - analysis</subject><subject>Biological and medical sciences</subject><subject>Child</subject><subject>Diabetes Mellitus, Type 1 - genetics</subject><subject>Diabetes Mellitus, Type 1 - immunology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Female</subject><subject>France</subject><subject>Haplotypes</subject><subject>HLA Antigens - analysis</subject><subject>Humans</subject><subject>Insulin Antibodies - analysis</subject><subject>Islets of Langerhans - immunology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Risk Factors</subject><issn>0012-186X</issn><issn>1432-0428</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1988</creationdate><recordtype>article</recordtype><recordid>eNqFkU2L1TAUhoMo43V04144CxEVqvlq0rjTwdGBC24U3JU0OfVmbJPapEJ_iP_XDlPGpasc8j48B85LyFNG3zBK9dsPl5RyLbVW98iBScErKnlznxwoZbxijfr-kDzK-ZpSKmqpzsiZoJrJRhzIn6s8YAGHwwA2eggxL0OIYJeSbCyhSz5g3r4hL901upLBFjiFHyeYQ_4JfZrB428c0jRiLJB6KOuEwODlrqo8Thj9Fr4CH2yHZfON275QlvwOygnhuKYIvR3DsEIui18fkwe9HTI-2d9z8u3y49eLz9Xxy6eri_fHygndlIoLw7VraslM7ZTcBqqV4tKgEsLURtWMu864hjvDBVXWWEk77oW0HDvrxDl5ceud5vRrwVzaMeSbW9iIacmtbrSgwrD_gqyWnNOm3sDXt6CbU84z9u00h9HOa8toe1NW-6-sDX62W5duRH-H7u1s-fM9t9nZoZ9tdCHfYZoroY0WfwGaPZvL</recordid><startdate>19881001</startdate><enddate>19881001</enddate><creator>THIVOLET, C</creator><creator>BEAUFRERE, B</creator><creator>BETUEL, H</creator><creator>CHATELAIN, P</creator><creator>DURAND, A</creator><creator>TOURNIAIRE, J</creator><creator>FRANCOIS, R</creator><general>Springer</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>19881001</creationdate><title>Islet cell and insulin autoantibodies in subjects at high risk for development of type 1 (insulin-dependent) diabetes mellitus: the Lyon family study</title><author>THIVOLET, C ; BEAUFRERE, B ; BETUEL, H ; CHATELAIN, P ; DURAND, A ; TOURNIAIRE, J ; FRANCOIS, R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c378t-23927c854195c648540766249e6339596512cb9c82c92306a9a40b2d34a2ebac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1988</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Autoantibodies - analysis</topic><topic>Biological and medical sciences</topic><topic>Child</topic><topic>Diabetes Mellitus, Type 1 - genetics</topic><topic>Diabetes Mellitus, Type 1 - immunology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Female</topic><topic>France</topic><topic>Haplotypes</topic><topic>HLA Antigens - analysis</topic><topic>Humans</topic><topic>Insulin Antibodies - analysis</topic><topic>Islets of Langerhans - immunology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>THIVOLET, C</creatorcontrib><creatorcontrib>BEAUFRERE, B</creatorcontrib><creatorcontrib>BETUEL, H</creatorcontrib><creatorcontrib>CHATELAIN, P</creatorcontrib><creatorcontrib>DURAND, A</creatorcontrib><creatorcontrib>TOURNIAIRE, J</creatorcontrib><creatorcontrib>FRANCOIS, R</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Diabetologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>THIVOLET, C</au><au>BEAUFRERE, B</au><au>BETUEL, H</au><au>CHATELAIN, P</au><au>DURAND, A</au><au>TOURNIAIRE, J</au><au>FRANCOIS, R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Islet cell and insulin autoantibodies in subjects at high risk for development of type 1 (insulin-dependent) diabetes mellitus: the Lyon family study</atitle><jtitle>Diabetologia</jtitle><addtitle>Diabetologia</addtitle><date>1988-10-01</date><risdate>1988</risdate><volume>31</volume><issue>10</issue><spage>741</spage><epage>746</epage><pages>741-746</pages><issn>0012-186X</issn><eissn>1432-0428</eissn><abstract>Genetic determination as well as prospective analysis of islet cell autoantibodies and autoantibodies to insulin were conducted in a population of 479 first degree relatives of 174 Type 1 (insulin-dependent) diabetic patients. Analysis of HLA haplotypes within families illustrated the high frequency of DR3 and DR4 alleles with preferential transmission from parent to both affected and unaffected offspring. DR4 was preferentially associated with DQw3.2 (TA10-) in 60/73 (82.2%) patients and 101/127 (79.5%) relatives. Relatives have been followed for a period of 800 subject-years. Twenty-two out of 430 relatives (5.1%) were found islet cell antibodies (ICA-IgG) positive. Seven sera with low titres became negative 6 months later at two different determinations. Fifteen sera ICA-IgG and ICA-protein A positive with high titres remained positive thereafter. Half of the ICA positive relatives were also found insulin autoantibodies (IAA) positive. All but 3 ICA negative relatives did not have IAA in their sera. Analysis of IAA specificity with competition experiments indicated that most antibodies recognised epitopes shared between human and pork insulins while four were specific for human insulin determinants. Analysis of class I and class II HLA antigen distribution indicated no particular allelic restriction in antibody positive individuals. Metabolic status of antibody positive relatives was determined with oral and intravenous charge of glucose. Two haplo-identical DR3-DQw2 brothers became diabetic during the study. One child and one mother both with DR4-DQw3.2 became intolerant to glucose. Each of these relatives had high titre ICA prior to metabolic deterioration.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>3071483</pmid><doi>10.1007/BF00274776</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Diabetologia, 1988-10, Vol.31 (10), p.741-746 |
| issn | 0012-186X 1432-0428 |
| language | eng |
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| source | Springer LINK Archives |
| subjects | Adolescent Adult Autoantibodies - analysis Biological and medical sciences Child Diabetes Mellitus, Type 1 - genetics Diabetes Mellitus, Type 1 - immunology Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Female France Haplotypes HLA Antigens - analysis Humans Insulin Antibodies - analysis Islets of Langerhans - immunology Male Medical sciences Risk Factors |
| title | Islet cell and insulin autoantibodies in subjects at high risk for development of type 1 (insulin-dependent) diabetes mellitus: the Lyon family study |
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