Does cytokine gene polymorphism affect steroid responses in idiopathic nephrotic syndrome?
Immunological responses may be possibly involved in the pathogenesis of idiopathic nephrotic syndrome (INS). Cytokines act as a potent immunomodulator. Pathogenesis of INS is associated with Th1 and Th2 cytokines imbalance. AIMS, SETTINGS AND DESIGN: We have investigated the association of IL-4, IL-...
Gespeichert in:
| Veröffentlicht in: | Indian journal of medical sciences 2008-10, Vol.62 (10), p.383-391 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 391 |
|---|---|
| container_issue | 10 |
| container_start_page | 383 |
| container_title | Indian journal of medical sciences |
| container_volume | 62 |
| creator | Tripathi, Gaurav Jafar, Tabrez Mandal, Kaushik Mahdi, Abbas A Awasthi, Shally Sharma, Raj K Kumar, Alok Gulati, Sanjeev Agrawal, Suraksha |
| description | Immunological responses may be possibly involved in the pathogenesis of idiopathic nephrotic syndrome (INS). Cytokines act as a potent immunomodulator. Pathogenesis of INS is associated with Th1 and Th2 cytokines imbalance. AIMS, SETTINGS AND DESIGN: We have investigated the association of IL-4, IL-6, and TNF-alpha gene polymorphisms and analyzed the data to evaluate the effect of these polymorphisms on the pathogenesis and clinical course of INS.
One hundred fifty children with INS were selected. Children were analyzed for IL-4, IL-6, and TNF-alpha gene polymorphisms by using polymerase chain reaction and restriction fragment length polymorphism.
Chi-square test was used for different comparisons. The synergistic effects of IL-4, IL-6, and TNF-alpha gene polymorphisms were evaluated by using logistic regression analysis.
We compared the steroid-resistant (SR) and steroid-responsive (SS) groups. Our results showed strong association of IL-6 -G174C, and IL-4 -C590T at genotypic level (P = 0.0121, OR = 14.71, 95% CI = 1.59-136.46; and P = 0.0386, OR = 7.29, 95% CI = 1.26-41.69). TNF-alpha revealed a strong association at genotypic level (P = 0.0121, OR = 14.71, 95% CI = 1.59-136.46), as well as at allelic level (P = 0.0433, OR = 2.251, 95% CI = 1.09-4.66), demonstrating that it may be considered one of the genetic risk factors affecting the steroid response in INS patients. The GG genotype of IL-6 -G174C, TT genotype of IL-4 -C590T, and AA genotype of TNF-alpha -G308A cytokine gene polymorphisms may be causative factors for nonresponsiveness towards steroid therapy among INS children. |
| doi_str_mv | 10.4103/0019-5359.44017 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_69790625</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>69790625</sourcerecordid><originalsourceid>FETCH-LOGICAL-c2787-832c6e5c166764859bd2f1dd3ef4219168f985f513c0946cde38064b1ff6a5f73</originalsourceid><addsrcrecordid>eNpdkD1PwzAQhi0EoqUws6GIgS3U34knhMqnVIkFFhYrdc7UJYmDnQz596S0Aonl7qR73tPpQeic4GtOMJtjTFQqmFDXnGOSHaApUSpPmRT8EE1_txN0EuMGY8qowMdoQhTGuSRkit7vPMTEDJ3_dA0kHzCW1ldD7UO7drFOCmvBdEnsIHhXJgFi65s4ZlyTuNL5tujWziQNtOvgu3GKQ1MGX8PNKTqyRRXhbN9n6O3h_nXxlC5fHp8Xt8vU0CzP0pxRI0EYImUmeS7UqqSWlCUDyylRROZW5cIKwgxWXJoSWI4lXxFrZSFsxmboane3Df6rh9jp2kUDVVU04PuopcoUllSM4OU_cOP70Iy_aaKE4JgLOkLzHWSCjzGA1W1wdREGTbDeOtdbq3prVf84HxMX-7P9qobyj99LZt-mIXv2</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>195540452</pqid></control><display><type>article</type><title>Does cytokine gene polymorphism affect steroid responses in idiopathic nephrotic syndrome?</title><source>MEDLINE</source><source>Bioline International</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Tripathi, Gaurav ; Jafar, Tabrez ; Mandal, Kaushik ; Mahdi, Abbas A ; Awasthi, Shally ; Sharma, Raj K ; Kumar, Alok ; Gulati, Sanjeev ; Agrawal, Suraksha</creator><creatorcontrib>Tripathi, Gaurav ; Jafar, Tabrez ; Mandal, Kaushik ; Mahdi, Abbas A ; Awasthi, Shally ; Sharma, Raj K ; Kumar, Alok ; Gulati, Sanjeev ; Agrawal, Suraksha</creatorcontrib><description>Immunological responses may be possibly involved in the pathogenesis of idiopathic nephrotic syndrome (INS). Cytokines act as a potent immunomodulator. Pathogenesis of INS is associated with Th1 and Th2 cytokines imbalance. AIMS, SETTINGS AND DESIGN: We have investigated the association of IL-4, IL-6, and TNF-alpha gene polymorphisms and analyzed the data to evaluate the effect of these polymorphisms on the pathogenesis and clinical course of INS.
One hundred fifty children with INS were selected. Children were analyzed for IL-4, IL-6, and TNF-alpha gene polymorphisms by using polymerase chain reaction and restriction fragment length polymorphism.
Chi-square test was used for different comparisons. The synergistic effects of IL-4, IL-6, and TNF-alpha gene polymorphisms were evaluated by using logistic regression analysis.
We compared the steroid-resistant (SR) and steroid-responsive (SS) groups. Our results showed strong association of IL-6 -G174C, and IL-4 -C590T at genotypic level (P = 0.0121, OR = 14.71, 95% CI = 1.59-136.46; and P = 0.0386, OR = 7.29, 95% CI = 1.26-41.69). TNF-alpha revealed a strong association at genotypic level (P = 0.0121, OR = 14.71, 95% CI = 1.59-136.46), as well as at allelic level (P = 0.0433, OR = 2.251, 95% CI = 1.09-4.66), demonstrating that it may be considered one of the genetic risk factors affecting the steroid response in INS patients. The GG genotype of IL-6 -G174C, TT genotype of IL-4 -C590T, and AA genotype of TNF-alpha -G308A cytokine gene polymorphisms may be causative factors for nonresponsiveness towards steroid therapy among INS children.</description><identifier>ISSN: 0019-5359</identifier><identifier>EISSN: 1998-3654</identifier><identifier>DOI: 10.4103/0019-5359.44017</identifier><identifier>PMID: 19008611</identifier><language>eng</language><publisher>India: Medip Academy</publisher><subject>Adolescent ; Celiac disease ; Cells ; Child ; Child, Preschool ; Confidence intervals ; Cytokines ; Cytokines - genetics ; Drug Resistance - genetics ; Female ; Gene expression ; Gene Frequency ; Genotype ; Genotype & phenotype ; Glucocorticoids - therapeutic use ; Humans ; Infant ; Interleukin-4 - genetics ; Interleukin-6 - genetics ; Male ; Nephrotic Syndrome - drug therapy ; Nephrotic Syndrome - genetics ; Physical examinations ; Polymorphism, Genetic ; Proteins ; Regression analysis ; Sample size ; Studies ; Tumor Necrosis Factor-alpha - genetics</subject><ispartof>Indian journal of medical sciences, 2008-10, Vol.62 (10), p.383-391</ispartof><rights>Copyright Medknow Publications Oct 2008</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2787-832c6e5c166764859bd2f1dd3ef4219168f985f513c0946cde38064b1ff6a5f73</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19008611$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tripathi, Gaurav</creatorcontrib><creatorcontrib>Jafar, Tabrez</creatorcontrib><creatorcontrib>Mandal, Kaushik</creatorcontrib><creatorcontrib>Mahdi, Abbas A</creatorcontrib><creatorcontrib>Awasthi, Shally</creatorcontrib><creatorcontrib>Sharma, Raj K</creatorcontrib><creatorcontrib>Kumar, Alok</creatorcontrib><creatorcontrib>Gulati, Sanjeev</creatorcontrib><creatorcontrib>Agrawal, Suraksha</creatorcontrib><title>Does cytokine gene polymorphism affect steroid responses in idiopathic nephrotic syndrome?</title><title>Indian journal of medical sciences</title><addtitle>Indian J Med Sci</addtitle><description>Immunological responses may be possibly involved in the pathogenesis of idiopathic nephrotic syndrome (INS). Cytokines act as a potent immunomodulator. Pathogenesis of INS is associated with Th1 and Th2 cytokines imbalance. AIMS, SETTINGS AND DESIGN: We have investigated the association of IL-4, IL-6, and TNF-alpha gene polymorphisms and analyzed the data to evaluate the effect of these polymorphisms on the pathogenesis and clinical course of INS.
One hundred fifty children with INS were selected. Children were analyzed for IL-4, IL-6, and TNF-alpha gene polymorphisms by using polymerase chain reaction and restriction fragment length polymorphism.
Chi-square test was used for different comparisons. The synergistic effects of IL-4, IL-6, and TNF-alpha gene polymorphisms were evaluated by using logistic regression analysis.
We compared the steroid-resistant (SR) and steroid-responsive (SS) groups. Our results showed strong association of IL-6 -G174C, and IL-4 -C590T at genotypic level (P = 0.0121, OR = 14.71, 95% CI = 1.59-136.46; and P = 0.0386, OR = 7.29, 95% CI = 1.26-41.69). TNF-alpha revealed a strong association at genotypic level (P = 0.0121, OR = 14.71, 95% CI = 1.59-136.46), as well as at allelic level (P = 0.0433, OR = 2.251, 95% CI = 1.09-4.66), demonstrating that it may be considered one of the genetic risk factors affecting the steroid response in INS patients. The GG genotype of IL-6 -G174C, TT genotype of IL-4 -C590T, and AA genotype of TNF-alpha -G308A cytokine gene polymorphisms may be causative factors for nonresponsiveness towards steroid therapy among INS children.</description><subject>Adolescent</subject><subject>Celiac disease</subject><subject>Cells</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Confidence intervals</subject><subject>Cytokines</subject><subject>Cytokines - genetics</subject><subject>Drug Resistance - genetics</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Frequency</subject><subject>Genotype</subject><subject>Genotype & phenotype</subject><subject>Glucocorticoids - therapeutic use</subject><subject>Humans</subject><subject>Infant</subject><subject>Interleukin-4 - genetics</subject><subject>Interleukin-6 - genetics</subject><subject>Male</subject><subject>Nephrotic Syndrome - drug therapy</subject><subject>Nephrotic Syndrome - genetics</subject><subject>Physical examinations</subject><subject>Polymorphism, Genetic</subject><subject>Proteins</subject><subject>Regression analysis</subject><subject>Sample size</subject><subject>Studies</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><issn>0019-5359</issn><issn>1998-3654</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkD1PwzAQhi0EoqUws6GIgS3U34knhMqnVIkFFhYrdc7UJYmDnQz596S0Aonl7qR73tPpQeic4GtOMJtjTFQqmFDXnGOSHaApUSpPmRT8EE1_txN0EuMGY8qowMdoQhTGuSRkit7vPMTEDJ3_dA0kHzCW1ldD7UO7drFOCmvBdEnsIHhXJgFi65s4ZlyTuNL5tujWziQNtOvgu3GKQ1MGX8PNKTqyRRXhbN9n6O3h_nXxlC5fHp8Xt8vU0CzP0pxRI0EYImUmeS7UqqSWlCUDyylRROZW5cIKwgxWXJoSWI4lXxFrZSFsxmboane3Df6rh9jp2kUDVVU04PuopcoUllSM4OU_cOP70Iy_aaKE4JgLOkLzHWSCjzGA1W1wdREGTbDeOtdbq3prVf84HxMX-7P9qobyj99LZt-mIXv2</recordid><startdate>20081001</startdate><enddate>20081001</enddate><creator>Tripathi, Gaurav</creator><creator>Jafar, Tabrez</creator><creator>Mandal, Kaushik</creator><creator>Mahdi, Abbas A</creator><creator>Awasthi, Shally</creator><creator>Sharma, Raj K</creator><creator>Kumar, Alok</creator><creator>Gulati, Sanjeev</creator><creator>Agrawal, Suraksha</creator><general>Medip Academy</general><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20081001</creationdate><title>Does cytokine gene polymorphism affect steroid responses in idiopathic nephrotic syndrome?</title><author>Tripathi, Gaurav ; Jafar, Tabrez ; Mandal, Kaushik ; Mahdi, Abbas A ; Awasthi, Shally ; Sharma, Raj K ; Kumar, Alok ; Gulati, Sanjeev ; Agrawal, Suraksha</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2787-832c6e5c166764859bd2f1dd3ef4219168f985f513c0946cde38064b1ff6a5f73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adolescent</topic><topic>Celiac disease</topic><topic>Cells</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Confidence intervals</topic><topic>Cytokines</topic><topic>Cytokines - genetics</topic><topic>Drug Resistance - genetics</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Frequency</topic><topic>Genotype</topic><topic>Genotype & phenotype</topic><topic>Glucocorticoids - therapeutic use</topic><topic>Humans</topic><topic>Infant</topic><topic>Interleukin-4 - genetics</topic><topic>Interleukin-6 - genetics</topic><topic>Male</topic><topic>Nephrotic Syndrome - drug therapy</topic><topic>Nephrotic Syndrome - genetics</topic><topic>Physical examinations</topic><topic>Polymorphism, Genetic</topic><topic>Proteins</topic><topic>Regression analysis</topic><topic>Sample size</topic><topic>Studies</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><toplevel>online_resources</toplevel><creatorcontrib>Tripathi, Gaurav</creatorcontrib><creatorcontrib>Jafar, Tabrez</creatorcontrib><creatorcontrib>Mandal, Kaushik</creatorcontrib><creatorcontrib>Mahdi, Abbas A</creatorcontrib><creatorcontrib>Awasthi, Shally</creatorcontrib><creatorcontrib>Sharma, Raj K</creatorcontrib><creatorcontrib>Kumar, Alok</creatorcontrib><creatorcontrib>Gulati, Sanjeev</creatorcontrib><creatorcontrib>Agrawal, Suraksha</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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>ProQuest Central Essentials</collection><collection>ProQuest Central</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</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>MEDLINE - Academic</collection><jtitle>Indian journal of medical sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tripathi, Gaurav</au><au>Jafar, Tabrez</au><au>Mandal, Kaushik</au><au>Mahdi, Abbas A</au><au>Awasthi, Shally</au><au>Sharma, Raj K</au><au>Kumar, Alok</au><au>Gulati, Sanjeev</au><au>Agrawal, Suraksha</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Does cytokine gene polymorphism affect steroid responses in idiopathic nephrotic syndrome?</atitle><jtitle>Indian journal of medical sciences</jtitle><addtitle>Indian J Med Sci</addtitle><date>2008-10-01</date><risdate>2008</risdate><volume>62</volume><issue>10</issue><spage>383</spage><epage>391</epage><pages>383-391</pages><issn>0019-5359</issn><eissn>1998-3654</eissn><abstract>Immunological responses may be possibly involved in the pathogenesis of idiopathic nephrotic syndrome (INS). Cytokines act as a potent immunomodulator. Pathogenesis of INS is associated with Th1 and Th2 cytokines imbalance. AIMS, SETTINGS AND DESIGN: We have investigated the association of IL-4, IL-6, and TNF-alpha gene polymorphisms and analyzed the data to evaluate the effect of these polymorphisms on the pathogenesis and clinical course of INS.
One hundred fifty children with INS were selected. Children were analyzed for IL-4, IL-6, and TNF-alpha gene polymorphisms by using polymerase chain reaction and restriction fragment length polymorphism.
Chi-square test was used for different comparisons. The synergistic effects of IL-4, IL-6, and TNF-alpha gene polymorphisms were evaluated by using logistic regression analysis.
We compared the steroid-resistant (SR) and steroid-responsive (SS) groups. Our results showed strong association of IL-6 -G174C, and IL-4 -C590T at genotypic level (P = 0.0121, OR = 14.71, 95% CI = 1.59-136.46; and P = 0.0386, OR = 7.29, 95% CI = 1.26-41.69). TNF-alpha revealed a strong association at genotypic level (P = 0.0121, OR = 14.71, 95% CI = 1.59-136.46), as well as at allelic level (P = 0.0433, OR = 2.251, 95% CI = 1.09-4.66), demonstrating that it may be considered one of the genetic risk factors affecting the steroid response in INS patients. The GG genotype of IL-6 -G174C, TT genotype of IL-4 -C590T, and AA genotype of TNF-alpha -G308A cytokine gene polymorphisms may be causative factors for nonresponsiveness towards steroid therapy among INS children.</abstract><cop>India</cop><pub>Medip Academy</pub><pmid>19008611</pmid><doi>10.4103/0019-5359.44017</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0019-5359 |
| ispartof | Indian journal of medical sciences, 2008-10, Vol.62 (10), p.383-391 |
| issn | 0019-5359 1998-3654 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_69790625 |
| source | MEDLINE; Bioline International; EZB-FREE-00999 freely available EZB journals |
| subjects | Adolescent Celiac disease Cells Child Child, Preschool Confidence intervals Cytokines Cytokines - genetics Drug Resistance - genetics Female Gene expression Gene Frequency Genotype Genotype & phenotype Glucocorticoids - therapeutic use Humans Infant Interleukin-4 - genetics Interleukin-6 - genetics Male Nephrotic Syndrome - drug therapy Nephrotic Syndrome - genetics Physical examinations Polymorphism, Genetic Proteins Regression analysis Sample size Studies Tumor Necrosis Factor-alpha - genetics |
| title | Does cytokine gene polymorphism affect steroid responses in idiopathic nephrotic syndrome? |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-01T22%3A39%3A37IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Does%20cytokine%20gene%20polymorphism%20affect%20steroid%20responses%20in%20idiopathic%20nephrotic%20syndrome?&rft.jtitle=Indian%20journal%20of%20medical%20sciences&rft.au=Tripathi,%20Gaurav&rft.date=2008-10-01&rft.volume=62&rft.issue=10&rft.spage=383&rft.epage=391&rft.pages=383-391&rft.issn=0019-5359&rft.eissn=1998-3654&rft_id=info:doi/10.4103/0019-5359.44017&rft_dat=%3Cproquest_cross%3E69790625%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=195540452&rft_id=info:pmid/19008611&rfr_iscdi=true |