Analysis of thrombophilic genetic mutations in patients with Sheehan`s syndrome: is thrombophilia responsible for the pathogenesis of Sheehan`s syndrome?
The gene mutations of Factor V R506Q (FV-Leiden), prothrombin (FII G20210A), methylene tetrahydrofolate reductase (MTHFR) C677T and A1298C and PAI-1 4G/5G are well-established risk factors for thrombosis. We aimed to investigate the prevalence of these gene mutations and their possible impact on the...
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| Veröffentlicht in: | Pituitary 2011-06, Vol.14 (2), p.168-173 |
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| creator | Gokalp, Deniz Tuzcu, Alpaslan Bahceci, Mithat Ayyildiz, Orhan Yurt, Murat Celik, Yusuf Alpagat, Gulistan |
| description | The gene mutations of Factor V R506Q (FV-Leiden), prothrombin (FII G20210A), methylene tetrahydrofolate reductase (MTHFR) C677T and A1298C and PAI-1 4G/5G are well-established risk factors for thrombosis. We aimed to investigate the prevalence of these gene mutations and their possible impact on the development of pathogenesis in patients with Sheehan’s syndrome (SS). 40 female patients with SS compared to a control group of 45 healthy women. The presence of FV-Leiden, FII G20210A, MTHFR C677T, MTHFR A1298C and PAI-1 4G/5G gene mutations were assessed by polymerase chain reaction analysis with a light cycler analyzer. An odds ratio of greater than one is considered to increase the risk of SS disease as found in Factor V Leiden, FII G20210A, MTHFR C677T, MTHFR A1298C and PAI-1 4G/5G polymorphism, as follows respectively: 1.13, 1.85, 6.00, 8.14 and 1.45. MTHFR C677T and MTHFR A1298C polymorphism were found significantly higher in SS patients than the control group (
P
0.05). The level of plasma total homocysteine (tHcy) was significantly higher in patients with SS than in the control group (
P
|
| doi_str_mv | 10.1007/s11102-010-0276-x |
| format | Article |
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P
< 0.001), however FV-Leiden, FII G20210A and PAI-1 4G/5G polymorphism showed no significant difference (
P
> 0.05). The level of plasma total homocysteine (tHcy) was significantly higher in patients with SS than in the control group (
P
< 0.001). We suggest that the genetic mutations of FV-Leiden, FII G20210A, MTHFR C677T, MTHFR A1298C and PAI-1 4G/5G increase the risk of SS. Also, high plasma tHcy levels may be a risk factor for the development of SS.</description><identifier>ISSN: 1386-341X</identifier><identifier>EISSN: 1573-7403</identifier><identifier>DOI: 10.1007/s11102-010-0276-x</identifier><identifier>PMID: 21107737</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Adult ; Case-Control Studies ; DNA Mutational Analysis ; Endocrinology ; Factor V - genetics ; Female ; Genetic Predisposition to Disease ; Human Physiology ; Humans ; Hypopituitarism - etiology ; Hypopituitarism - genetics ; Medicine ; Medicine & Public Health ; Methylenetetrahydrofolate Reductase (NADPH2) - genetics ; Middle Aged ; Mutation - physiology ; Plasminogen Activator Inhibitor 1 - genetics ; Polymorphism, Single Nucleotide ; Prothrombin - genetics ; Thrombophilia - complications ; Thrombophilia - genetics</subject><ispartof>Pituitary, 2011-06, Vol.14 (2), p.168-173</ispartof><rights>Springer Science+Business Media, LLC 2010</rights><rights>Springer Science+Business Media, LLC 2011</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c402t-3bbf28897be08acef36fb7e72aa301b11fc072084bee257850f427cda4ae69fd3</citedby><cites>FETCH-LOGICAL-c402t-3bbf28897be08acef36fb7e72aa301b11fc072084bee257850f427cda4ae69fd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11102-010-0276-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11102-010-0276-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27922,27923,41486,42555,51317</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21107737$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gokalp, Deniz</creatorcontrib><creatorcontrib>Tuzcu, Alpaslan</creatorcontrib><creatorcontrib>Bahceci, Mithat</creatorcontrib><creatorcontrib>Ayyildiz, Orhan</creatorcontrib><creatorcontrib>Yurt, Murat</creatorcontrib><creatorcontrib>Celik, Yusuf</creatorcontrib><creatorcontrib>Alpagat, Gulistan</creatorcontrib><title>Analysis of thrombophilic genetic mutations in patients with Sheehan`s syndrome: is thrombophilia responsible for the pathogenesis of Sheehan`s syndrome?</title><title>Pituitary</title><addtitle>Pituitary</addtitle><addtitle>Pituitary</addtitle><description>The gene mutations of Factor V R506Q (FV-Leiden), prothrombin (FII G20210A), methylene tetrahydrofolate reductase (MTHFR) C677T and A1298C and PAI-1 4G/5G are well-established risk factors for thrombosis. We aimed to investigate the prevalence of these gene mutations and their possible impact on the development of pathogenesis in patients with Sheehan’s syndrome (SS). 40 female patients with SS compared to a control group of 45 healthy women. The presence of FV-Leiden, FII G20210A, MTHFR C677T, MTHFR A1298C and PAI-1 4G/5G gene mutations were assessed by polymerase chain reaction analysis with a light cycler analyzer. An odds ratio of greater than one is considered to increase the risk of SS disease as found in Factor V Leiden, FII G20210A, MTHFR C677T, MTHFR A1298C and PAI-1 4G/5G polymorphism, as follows respectively: 1.13, 1.85, 6.00, 8.14 and 1.45. MTHFR C677T and MTHFR A1298C polymorphism were found significantly higher in SS patients than the control group (
P
< 0.001), however FV-Leiden, FII G20210A and PAI-1 4G/5G polymorphism showed no significant difference (
P
> 0.05). The level of plasma total homocysteine (tHcy) was significantly higher in patients with SS than in the control group (
P
< 0.001). We suggest that the genetic mutations of FV-Leiden, FII G20210A, MTHFR C677T, MTHFR A1298C and PAI-1 4G/5G increase the risk of SS. Also, high plasma tHcy levels may be a risk factor for the development of SS.</description><subject>Adult</subject><subject>Case-Control Studies</subject><subject>DNA Mutational Analysis</subject><subject>Endocrinology</subject><subject>Factor V - genetics</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>Human Physiology</subject><subject>Humans</subject><subject>Hypopituitarism - etiology</subject><subject>Hypopituitarism - genetics</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Methylenetetrahydrofolate Reductase (NADPH2) - genetics</subject><subject>Middle Aged</subject><subject>Mutation - physiology</subject><subject>Plasminogen Activator Inhibitor 1 - genetics</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Prothrombin - genetics</subject><subject>Thrombophilia - complications</subject><subject>Thrombophilia - genetics</subject><issn>1386-341X</issn><issn>1573-7403</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkU1rFTEUhkNR2lr9Ad2U4MbV1JOPO5nrRkrRtlBwoYK7mMw96aTMJGMyg70_xX9rhnv9QBFX50Ce9zmQl5BTBucMQL3MjDHgFTCogKu6ejggx2ylRKUkiEdlF01dCck-HZEnOd9DAUHIQ3LES04poY7Jt4tg-m32mUZHpy7Fwcax871v6R0GnMoc5slMPoZMfaBjWTFMmX71U0ffd4idCZ8zzduwKWF8RYvqd4-hCfNY0t72SF1M5RUXTReXA_vLf4tePyWPnekzPtvPE_Lx7ZsPl9fV7burm8uL26qVwKdKWOt406yVRWhMi07UzipU3BgBzDLmWlAcGmkR-Uo1K3CSq3ZjpMF67TbihLzYeccUv8yYJz343GLfm4BxzrpRNS8muf4_WSvBV2INhXz-B3kf51R-eoFqCZJJVSC2g9oUc07o9Jj8YNJWM9BLv3rXry616aVf_VAyZ3vxbAfc_Ez8KLQAfAfk8hTuMP26_G_rdwR8tLk</recordid><startdate>20110601</startdate><enddate>20110601</enddate><creator>Gokalp, Deniz</creator><creator>Tuzcu, Alpaslan</creator><creator>Bahceci, Mithat</creator><creator>Ayyildiz, Orhan</creator><creator>Yurt, Murat</creator><creator>Celik, Yusuf</creator><creator>Alpagat, Gulistan</creator><general>Springer US</general><general>Springer Nature B.V</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>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>20110601</creationdate><title>Analysis of thrombophilic genetic mutations in patients with Sheehan`s syndrome: is thrombophilia responsible for the pathogenesis of Sheehan`s syndrome?</title><author>Gokalp, Deniz ; Tuzcu, Alpaslan ; Bahceci, Mithat ; Ayyildiz, Orhan ; Yurt, Murat ; Celik, Yusuf ; Alpagat, Gulistan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c402t-3bbf28897be08acef36fb7e72aa301b11fc072084bee257850f427cda4ae69fd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adult</topic><topic>Case-Control Studies</topic><topic>DNA Mutational Analysis</topic><topic>Endocrinology</topic><topic>Factor V - genetics</topic><topic>Female</topic><topic>Genetic Predisposition to Disease</topic><topic>Human Physiology</topic><topic>Humans</topic><topic>Hypopituitarism - etiology</topic><topic>Hypopituitarism - genetics</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Methylenetetrahydrofolate Reductase (NADPH2) - genetics</topic><topic>Middle Aged</topic><topic>Mutation - physiology</topic><topic>Plasminogen Activator Inhibitor 1 - genetics</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Prothrombin - genetics</topic><topic>Thrombophilia - complications</topic><topic>Thrombophilia - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gokalp, Deniz</creatorcontrib><creatorcontrib>Tuzcu, Alpaslan</creatorcontrib><creatorcontrib>Bahceci, Mithat</creatorcontrib><creatorcontrib>Ayyildiz, Orhan</creatorcontrib><creatorcontrib>Yurt, Murat</creatorcontrib><creatorcontrib>Celik, Yusuf</creatorcontrib><creatorcontrib>Alpagat, Gulistan</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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Pituitary</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gokalp, Deniz</au><au>Tuzcu, Alpaslan</au><au>Bahceci, Mithat</au><au>Ayyildiz, Orhan</au><au>Yurt, Murat</au><au>Celik, Yusuf</au><au>Alpagat, Gulistan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Analysis of thrombophilic genetic mutations in patients with Sheehan`s syndrome: is thrombophilia responsible for the pathogenesis of Sheehan`s syndrome?</atitle><jtitle>Pituitary</jtitle><stitle>Pituitary</stitle><addtitle>Pituitary</addtitle><date>2011-06-01</date><risdate>2011</risdate><volume>14</volume><issue>2</issue><spage>168</spage><epage>173</epage><pages>168-173</pages><issn>1386-341X</issn><eissn>1573-7403</eissn><abstract>The gene mutations of Factor V R506Q (FV-Leiden), prothrombin (FII G20210A), methylene tetrahydrofolate reductase (MTHFR) C677T and A1298C and PAI-1 4G/5G are well-established risk factors for thrombosis. We aimed to investigate the prevalence of these gene mutations and their possible impact on the development of pathogenesis in patients with Sheehan’s syndrome (SS). 40 female patients with SS compared to a control group of 45 healthy women. The presence of FV-Leiden, FII G20210A, MTHFR C677T, MTHFR A1298C and PAI-1 4G/5G gene mutations were assessed by polymerase chain reaction analysis with a light cycler analyzer. An odds ratio of greater than one is considered to increase the risk of SS disease as found in Factor V Leiden, FII G20210A, MTHFR C677T, MTHFR A1298C and PAI-1 4G/5G polymorphism, as follows respectively: 1.13, 1.85, 6.00, 8.14 and 1.45. MTHFR C677T and MTHFR A1298C polymorphism were found significantly higher in SS patients than the control group (
P
< 0.001), however FV-Leiden, FII G20210A and PAI-1 4G/5G polymorphism showed no significant difference (
P
> 0.05). The level of plasma total homocysteine (tHcy) was significantly higher in patients with SS than in the control group (
P
< 0.001). We suggest that the genetic mutations of FV-Leiden, FII G20210A, MTHFR C677T, MTHFR A1298C and PAI-1 4G/5G increase the risk of SS. Also, high plasma tHcy levels may be a risk factor for the development of SS.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>21107737</pmid><doi>10.1007/s11102-010-0276-x</doi><tpages>6</tpages></addata></record> |
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| ispartof | Pituitary, 2011-06, Vol.14 (2), p.168-173 |
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| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Adult Case-Control Studies DNA Mutational Analysis Endocrinology Factor V - genetics Female Genetic Predisposition to Disease Human Physiology Humans Hypopituitarism - etiology Hypopituitarism - genetics Medicine Medicine & Public Health Methylenetetrahydrofolate Reductase (NADPH2) - genetics Middle Aged Mutation - physiology Plasminogen Activator Inhibitor 1 - genetics Polymorphism, Single Nucleotide Prothrombin - genetics Thrombophilia - complications Thrombophilia - genetics |
| title | Analysis of thrombophilic genetic mutations in patients with Sheehan`s syndrome: is thrombophilia responsible for the pathogenesis of Sheehan`s syndrome? |
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