Macrophage migration inhibitory factor polymorphisms do not predict therapeutic response to glucocorticoids or to tumour necrosis factor α-neutralising treatments in rheumatoid arthritis
Background:Macrophage migration inhibitory factor (MIF) is an inflammatory mediator associated with RA severity. In various diseases, MIF polymorphisms are associated with clinical response glucocorticoid (GC) treatment. It is unclear whether MIF polymorphisms determine GC response in rheumatoid art...
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| Veröffentlicht in: | Annals of the rheumatic diseases 2007-11, Vol.66 (11), p.1525-1530 |
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| container_title | Annals of the rheumatic diseases |
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| creator | Radstake, Timothy R D J Fransen, Jaap Toonen, Erik J M Coenen, Marieke J H Eijsbouts, Agnes E Donn, Rachelle van den Hoogen, Frank H J van Riel, Piet L C M |
| description | Background:Macrophage migration inhibitory factor (MIF) is an inflammatory mediator associated with RA severity. In various diseases, MIF polymorphisms are associated with clinical response glucocorticoid (GC) treatment. It is unclear whether MIF polymorphisms determine GC response in rheumatoid arthritis (RA) and to other RA treatments. Therefore, the question of whether two functional variants in MIF are associated with the response to tumour necrosis factor (TNF)α-neutralising and GC treatments in RA was investigated.Methods:Data from two cohorts of an RA registry were used. For patients who started with TNFα-neutralising (infliximab) or GC treatment, courses with a duration of at least 3 months were included and response to TNFα blockers or GC was calculated according to the European League Against Rheumatism response criteria. MIF −173G→C genotyping was achieved using an assay-on-demand allelic discrimination assay, and alleles of the CATT repeat element were identified using a fluorescently labelled PCR primer and capillary electrophoresis. Logistic-regression modelling was used for the statistical analysis.Results:In total, 192 courses of oral prednisone or methylprednisolone injections in 98 patients with RA and 90 patients with RA who were on TNFα-neutralising treatments were documented. In all, 27% of the patients with RA were found to be heterozygous for seven CATT repeats (CATT7) and 31% were heterozygous for −173C. Respectively, 4% and 6% of the patients with RA were homozygous for the MIF CATT7 repeat or the MIF −173C allele. Carrier status and homozygosity for CATT7 repeat and the MIF −173C allele were not associated with response to GC (odds ratios (ORs) close to 1) or to TNFα-neutralising treatment (ORs close to 2).Conclusion:The MIF-CATT7 repeat and the MIF−173G→C functional variant are not strongly associated with a decreased clinical response to TNFα-neutralising or GC treatment in RA. |
| doi_str_mv | 10.1136/ard.2006.064394 |
| format | Article |
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In various diseases, MIF polymorphisms are associated with clinical response glucocorticoid (GC) treatment. It is unclear whether MIF polymorphisms determine GC response in rheumatoid arthritis (RA) and to other RA treatments. Therefore, the question of whether two functional variants in MIF are associated with the response to tumour necrosis factor (TNF)α-neutralising and GC treatments in RA was investigated.Methods:Data from two cohorts of an RA registry were used. For patients who started with TNFα-neutralising (infliximab) or GC treatment, courses with a duration of at least 3 months were included and response to TNFα blockers or GC was calculated according to the European League Against Rheumatism response criteria. MIF −173G→C genotyping was achieved using an assay-on-demand allelic discrimination assay, and alleles of the CATT repeat element were identified using a fluorescently labelled PCR primer and capillary electrophoresis. Logistic-regression modelling was used for the statistical analysis.Results:In total, 192 courses of oral prednisone or methylprednisolone injections in 98 patients with RA and 90 patients with RA who were on TNFα-neutralising treatments were documented. In all, 27% of the patients with RA were found to be heterozygous for seven CATT repeats (CATT7) and 31% were heterozygous for −173C. Respectively, 4% and 6% of the patients with RA were homozygous for the MIF CATT7 repeat or the MIF −173C allele. Carrier status and homozygosity for CATT7 repeat and the MIF −173C allele were not associated with response to GC (odds ratios (ORs) close to 1) or to TNFα-neutralising treatment (ORs close to 2).Conclusion:The MIF-CATT7 repeat and the MIF−173G→C functional variant are not strongly associated with a decreased clinical response to TNFα-neutralising or GC treatment in RA.</description><identifier>ISSN: 0003-4967</identifier><identifier>EISSN: 1468-2060</identifier><identifier>DOI: 10.1136/ard.2006.064394</identifier><identifier>PMID: 17456524</identifier><language>eng</language><publisher>England: BMJ Publishing Group Ltd and European League Against Rheumatism</publisher><subject>Adult ; Aged ; Antibodies, Monoclonal - therapeutic use ; Antirheumatic Agents - therapeutic use ; Arthritis, Rheumatoid - drug therapy ; Arthritis, Rheumatoid - genetics ; Cohort Studies ; Extended Report ; Female ; glucocorticoids ; Glucocorticoids - therapeutic use ; Humans ; Infliximab ; macrophage inhibitory factor ; Macrophage Migration-Inhibitory Factors - genetics ; Male ; Middle Aged ; Phenotype ; Polymorphism, Genetic ; Prognosis ; Registries ; rheumatoid arthritis ; Severity of Illness Index ; Treatment Outcome ; Tumor Necrosis Factor-alpha - antagonists & inhibitors</subject><ispartof>Annals of the rheumatic diseases, 2007-11, Vol.66 (11), p.1525-1530</ispartof><rights>2007 BMJ Publishing Group Ltd and European League Against Rheumatism</rights><rights>Copyright © 2007 BMJ Publishing Group and European League Against Rheumatism</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttp://ard.bmj.com/content/66/11/1525.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttp://ard.bmj.com/content/66/11/1525.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,230,314,727,780,784,885,23570,27923,27924,53790,53792,77471,77502</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17456524$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Radstake, Timothy R D J</creatorcontrib><creatorcontrib>Fransen, Jaap</creatorcontrib><creatorcontrib>Toonen, Erik J M</creatorcontrib><creatorcontrib>Coenen, Marieke J H</creatorcontrib><creatorcontrib>Eijsbouts, Agnes E</creatorcontrib><creatorcontrib>Donn, Rachelle</creatorcontrib><creatorcontrib>van den Hoogen, Frank H J</creatorcontrib><creatorcontrib>van Riel, Piet L C M</creatorcontrib><title>Macrophage migration inhibitory factor polymorphisms do not predict therapeutic response to glucocorticoids or to tumour necrosis factor α-neutralising treatments in rheumatoid arthritis</title><title>Annals of the rheumatic diseases</title><addtitle>Ann Rheum Dis</addtitle><description>Background:Macrophage migration inhibitory factor (MIF) is an inflammatory mediator associated with RA severity. In various diseases, MIF polymorphisms are associated with clinical response glucocorticoid (GC) treatment. It is unclear whether MIF polymorphisms determine GC response in rheumatoid arthritis (RA) and to other RA treatments. Therefore, the question of whether two functional variants in MIF are associated with the response to tumour necrosis factor (TNF)α-neutralising and GC treatments in RA was investigated.Methods:Data from two cohorts of an RA registry were used. For patients who started with TNFα-neutralising (infliximab) or GC treatment, courses with a duration of at least 3 months were included and response to TNFα blockers or GC was calculated according to the European League Against Rheumatism response criteria. MIF −173G→C genotyping was achieved using an assay-on-demand allelic discrimination assay, and alleles of the CATT repeat element were identified using a fluorescently labelled PCR primer and capillary electrophoresis. Logistic-regression modelling was used for the statistical analysis.Results:In total, 192 courses of oral prednisone or methylprednisolone injections in 98 patients with RA and 90 patients with RA who were on TNFα-neutralising treatments were documented. In all, 27% of the patients with RA were found to be heterozygous for seven CATT repeats (CATT7) and 31% were heterozygous for −173C. Respectively, 4% and 6% of the patients with RA were homozygous for the MIF CATT7 repeat or the MIF −173C allele. Carrier status and homozygosity for CATT7 repeat and the MIF −173C allele were not associated with response to GC (odds ratios (ORs) close to 1) or to TNFα-neutralising treatment (ORs close to 2).Conclusion:The MIF-CATT7 repeat and the MIF−173G→C functional variant are not strongly associated with a decreased clinical response to TNFα-neutralising or GC treatment in RA.</description><subject>Adult</subject><subject>Aged</subject><subject>Antibodies, Monoclonal - therapeutic use</subject><subject>Antirheumatic Agents - therapeutic use</subject><subject>Arthritis, Rheumatoid - drug therapy</subject><subject>Arthritis, Rheumatoid - genetics</subject><subject>Cohort Studies</subject><subject>Extended Report</subject><subject>Female</subject><subject>glucocorticoids</subject><subject>Glucocorticoids - therapeutic use</subject><subject>Humans</subject><subject>Infliximab</subject><subject>macrophage inhibitory factor</subject><subject>Macrophage Migration-Inhibitory Factors - genetics</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Phenotype</subject><subject>Polymorphism, Genetic</subject><subject>Prognosis</subject><subject>Registries</subject><subject>rheumatoid arthritis</subject><subject>Severity of Illness Index</subject><subject>Treatment Outcome</subject><subject>Tumor Necrosis Factor-alpha - antagonists & inhibitors</subject><issn>0003-4967</issn><issn>1468-2060</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVks1u1DAUhS0EokNhzQ55xQIpgx3_JRskNOJPFJCgIHaW49yZuMRxajuIeSzWvAPPhEfTFlhd-d7j7xzZF6GHlKwpZfKpif26JkSuieSs5bfQinLZVDWR5DZaEUJYxVupTtC9lC7KkTS0uYtOqOJCipqv0K93xsYwD2YH2LtdNNmFCbtpcJ3LIe7x1thS8RzGvQ9xHlzyCfcBTyHjOULvbMZ5gGhmWLKzOEKaw5QA54B342KDDbH0g-sTLpzSzYsPS8QTFOPk0rXD75_VVBDRjC65aYdzBJM9TDmVODgOsHiTCwabmIfoskv30Z2tGRM8uKqn6PPLF-eb19XZh1dvNs_Pqo4xlStGlOi2ygjTckaNqBuutn3XEVLbw3tQ4A3pRSs7ABCdVZbKpiGstYoCkcBO0bMjd146D70tmUpKPUfnTdzrYJz-fzK5Qe_Cd11TSmUtCuDxFSCGywVS1t4lC-NoJghL0rJhrZCtKsJH_zrdWFz_VxFUR4FLGX7czE38pqViSuj3Xzaa86_849vzRn8q-idHfecv_tKIPixPudXrw_Lo4_KwP4ZgvR0</recordid><startdate>20071101</startdate><enddate>20071101</enddate><creator>Radstake, Timothy R D J</creator><creator>Fransen, Jaap</creator><creator>Toonen, Erik J M</creator><creator>Coenen, Marieke J H</creator><creator>Eijsbouts, Agnes E</creator><creator>Donn, Rachelle</creator><creator>van den Hoogen, Frank H J</creator><creator>van Riel, Piet L C M</creator><general>BMJ Publishing Group Ltd and European League Against Rheumatism</general><general>BMJ Group</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20071101</creationdate><title>Macrophage migration inhibitory factor polymorphisms do not predict therapeutic response to glucocorticoids or to tumour necrosis factor α-neutralising treatments in rheumatoid arthritis</title><author>Radstake, Timothy R D J ; Fransen, Jaap ; Toonen, Erik J M ; Coenen, Marieke J H ; Eijsbouts, Agnes E ; Donn, Rachelle ; van den Hoogen, Frank H J ; van Riel, Piet L C M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b337t-3075bf7a5a9431a52847fdbb002c08181e480d596beee5bc7c1688039c71e06e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Antibodies, Monoclonal - therapeutic use</topic><topic>Antirheumatic Agents - therapeutic use</topic><topic>Arthritis, Rheumatoid - drug therapy</topic><topic>Arthritis, Rheumatoid - genetics</topic><topic>Cohort Studies</topic><topic>Extended Report</topic><topic>Female</topic><topic>glucocorticoids</topic><topic>Glucocorticoids - therapeutic use</topic><topic>Humans</topic><topic>Infliximab</topic><topic>macrophage inhibitory factor</topic><topic>Macrophage Migration-Inhibitory Factors - genetics</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Phenotype</topic><topic>Polymorphism, Genetic</topic><topic>Prognosis</topic><topic>Registries</topic><topic>rheumatoid arthritis</topic><topic>Severity of Illness Index</topic><topic>Treatment Outcome</topic><topic>Tumor Necrosis Factor-alpha - antagonists & inhibitors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Radstake, Timothy R D J</creatorcontrib><creatorcontrib>Fransen, Jaap</creatorcontrib><creatorcontrib>Toonen, Erik J M</creatorcontrib><creatorcontrib>Coenen, Marieke J H</creatorcontrib><creatorcontrib>Eijsbouts, Agnes E</creatorcontrib><creatorcontrib>Donn, Rachelle</creatorcontrib><creatorcontrib>van den Hoogen, Frank H J</creatorcontrib><creatorcontrib>van Riel, Piet L C M</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Annals of the rheumatic diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Radstake, Timothy R D J</au><au>Fransen, Jaap</au><au>Toonen, Erik J M</au><au>Coenen, Marieke J H</au><au>Eijsbouts, Agnes E</au><au>Donn, Rachelle</au><au>van den Hoogen, Frank H J</au><au>van Riel, Piet L C M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Macrophage migration inhibitory factor polymorphisms do not predict therapeutic response to glucocorticoids or to tumour necrosis factor α-neutralising treatments in rheumatoid arthritis</atitle><jtitle>Annals of the rheumatic diseases</jtitle><addtitle>Ann Rheum Dis</addtitle><date>2007-11-01</date><risdate>2007</risdate><volume>66</volume><issue>11</issue><spage>1525</spage><epage>1530</epage><pages>1525-1530</pages><issn>0003-4967</issn><eissn>1468-2060</eissn><abstract>Background:Macrophage migration inhibitory factor (MIF) is an inflammatory mediator associated with RA severity. In various diseases, MIF polymorphisms are associated with clinical response glucocorticoid (GC) treatment. It is unclear whether MIF polymorphisms determine GC response in rheumatoid arthritis (RA) and to other RA treatments. Therefore, the question of whether two functional variants in MIF are associated with the response to tumour necrosis factor (TNF)α-neutralising and GC treatments in RA was investigated.Methods:Data from two cohorts of an RA registry were used. For patients who started with TNFα-neutralising (infliximab) or GC treatment, courses with a duration of at least 3 months were included and response to TNFα blockers or GC was calculated according to the European League Against Rheumatism response criteria. MIF −173G→C genotyping was achieved using an assay-on-demand allelic discrimination assay, and alleles of the CATT repeat element were identified using a fluorescently labelled PCR primer and capillary electrophoresis. Logistic-regression modelling was used for the statistical analysis.Results:In total, 192 courses of oral prednisone or methylprednisolone injections in 98 patients with RA and 90 patients with RA who were on TNFα-neutralising treatments were documented. In all, 27% of the patients with RA were found to be heterozygous for seven CATT repeats (CATT7) and 31% were heterozygous for −173C. Respectively, 4% and 6% of the patients with RA were homozygous for the MIF CATT7 repeat or the MIF −173C allele. Carrier status and homozygosity for CATT7 repeat and the MIF −173C allele were not associated with response to GC (odds ratios (ORs) close to 1) or to TNFα-neutralising treatment (ORs close to 2).Conclusion:The MIF-CATT7 repeat and the MIF−173G→C functional variant are not strongly associated with a decreased clinical response to TNFα-neutralising or GC treatment in RA.</abstract><cop>England</cop><pub>BMJ Publishing Group Ltd and European League Against Rheumatism</pub><pmid>17456524</pmid><doi>10.1136/ard.2006.064394</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Antibodies, Monoclonal - therapeutic use Antirheumatic Agents - therapeutic use Arthritis, Rheumatoid - drug therapy Arthritis, Rheumatoid - genetics Cohort Studies Extended Report Female glucocorticoids Glucocorticoids - therapeutic use Humans Infliximab macrophage inhibitory factor Macrophage Migration-Inhibitory Factors - genetics Male Middle Aged Phenotype Polymorphism, Genetic Prognosis Registries rheumatoid arthritis Severity of Illness Index Treatment Outcome Tumor Necrosis Factor-alpha - antagonists & inhibitors |
| title | Macrophage migration inhibitory factor polymorphisms do not predict therapeutic response to glucocorticoids or to tumour necrosis factor α-neutralising treatments in rheumatoid arthritis |
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