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Thiols as markers of redox status in type 1 diabetes mellitus
Introduction: Type 1 diabetes mellitus (T1DM) is associated with inflammation and the production of reactive oxygen species (ROS). Systemically, free thiols (R-SH) can be oxidized by ROS and circulating R-SH concentrations may directly reflect the systemic redox status. In this study the association...
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| creator | van Dijk, Peter R. Pasch, Andreas van Ockenburg-Brunet, Sonja L. Waanders, Femke Eman Abdulle, A. Muis, Marian J. Hillebrands, J. L. Bilo, Henk J. G. van Goor, Harry |
| description | Introduction:
Type 1 diabetes mellitus (T1DM) is associated with inflammation and the production of reactive oxygen species (ROS). Systemically, free thiols (R-SH) can be oxidized by ROS and circulating R-SH concentrations may directly reflect the systemic redox status. In this study the association between R-SH and clinical parameters of T1DM, including glycated haemoglobin A1c (HbA1c), was investigated. This is of particular interest since thiols are amendable to therapeutic intervention.
Methods:
As part of a prospective cohort study, data from 216 patients with a mean age of 45 (12) years, 57% male, diabetes duration 22 (16, 30) years and HbA1c of 60 (11) mmol/mol were examined. Baseline data were collected in 2002 and follow-up data in 2018. Cox proportional hazards regression analysis, with age, sex, HbA1c and R-SH, was used to assess prognostic factors for the development of complications.
Results:
At baseline, the plasma concentration of R-SH was 281.8 ± 34.0 μM. In addition to a lower concentration of NT-proBNP in the highest R-SH quartile (305–379 µM) there were no differences in baseline characteristics between the quartiles of R-SH. The Pearson correlation coefficient for R-SH and NT-proBNP was −0.290 (p |
| doi_str_mv | 10.1177/2042018820903641 |
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| fullrecord | <record><control><sourceid>proquest_doaj_</sourceid><recordid>TN_cdi_doaj_primary_oai_doaj_org_article_811f75a6e92243bb8962b57b784cf985</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sage_id>10.1177_2042018820903641</sage_id><doaj_id>oai_doaj_org_article_811f75a6e92243bb8962b57b784cf985</doaj_id><sourcerecordid>2441512135</sourcerecordid><originalsourceid>FETCH-LOGICAL-c528t-ed411b61c1996bb6e51ef1076a40e6b68350c9d4e3f95acf881f43b0f217e1573</originalsourceid><addsrcrecordid>eNp1kU1v1DAQhiNERau2d04oEhcuAY-_Yh9AQhUflSr1Us6W7Yy3XrLxYieI_nu8bFlopfpia-adZ8bzNs1LIG8B-v4dJZwSUIoSTZjk8Kw52YU6Alo-P7yVOm7OS1mTerhkjMsXzTGrNYJSddK8v7mNaSytLe3G5u-YS5tCm3FIv9oy23kpbZza-W6LLbRDtA5nrFIcx1hzZ81RsGPB8_v7tPn2-dPNxdfu6vrL5cXHq84LquYOBw7gJHjQWjonUQAGIL20nKB0UjFBvB44sqCF9UEpCJw5Eij0CKJnp83lnjskuzbbHOusdybZaP4EUl4Zm-foRzQKIPTCStSUVoZTWlInetcr7oNWorI-7FnbxW1w8DjN2Y4PoA8zU7w1q_TT9ASAMVkBb-4BOf1YsMxmE4uvG7ETpqUYWs0gTDHQVfr6kXSdljzVVRnKOQigwHYTkb3K51RKxnAYBojZWW0eW11LXv3_iUPBX2OroNsLil3hv65PAn8DlbGt3Q</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2441512135</pqid></control><display><type>article</type><title>Thiols as markers of redox status in type 1 diabetes mellitus</title><source>PubMed (Medline)</source><source>Publicly Available Content Database (Proquest) (PQ_SDU_P3)</source><source>SAGE Open Access</source><creator>van Dijk, Peter R. ; Pasch, Andreas ; van Ockenburg-Brunet, Sonja L. ; Waanders, Femke ; Eman Abdulle, A. ; Muis, Marian J. ; Hillebrands, J. L. ; Bilo, Henk J. G. ; van Goor, Harry</creator><creatorcontrib>van Dijk, Peter R. ; Pasch, Andreas ; van Ockenburg-Brunet, Sonja L. ; Waanders, Femke ; Eman Abdulle, A. ; Muis, Marian J. ; Hillebrands, J. L. ; Bilo, Henk J. G. ; van Goor, Harry</creatorcontrib><description>Introduction:
Type 1 diabetes mellitus (T1DM) is associated with inflammation and the production of reactive oxygen species (ROS). Systemically, free thiols (R-SH) can be oxidized by ROS and circulating R-SH concentrations may directly reflect the systemic redox status. In this study the association between R-SH and clinical parameters of T1DM, including glycated haemoglobin A1c (HbA1c), was investigated. This is of particular interest since thiols are amendable to therapeutic intervention.
Methods:
As part of a prospective cohort study, data from 216 patients with a mean age of 45 (12) years, 57% male, diabetes duration 22 (16, 30) years and HbA1c of 60 (11) mmol/mol were examined. Baseline data were collected in 2002 and follow-up data in 2018. Cox proportional hazards regression analysis, with age, sex, HbA1c and R-SH, was used to assess prognostic factors for the development of complications.
Results:
At baseline, the plasma concentration of R-SH was 281.8 ± 34.0 μM. In addition to a lower concentration of NT-proBNP in the highest R-SH quartile (305–379 µM) there were no differences in baseline characteristics between the quartiles of R-SH. The Pearson correlation coefficient for R-SH and NT-proBNP was −0.290 (p < 0.001). No significant correlation between R-SH and baseline HbA1c (r = −0.024, p = 0.726) was present. During follow-up, 42 macrovascular and 92 microvascular complications occurred. In Cox regression, R-SH was not a prognostic factor for the development of microvascular [hazard ratio (HR) 0.999 (95% confidence interval (CI) 0.993, 1.005)] and macrovascular [HR 0.993 (95% CI 0.984, 1.002)] complications.
Conclusions:
In addition to a negative association with NT-proBNP, no relevant relationships between R-SH and parameters of T1DM, including HbA1c, were present in this study.</description><identifier>ISSN: 2042-0188</identifier><identifier>EISSN: 2042-0196</identifier><identifier>DOI: 10.1177/2042018820903641</identifier><identifier>PMID: 32095228</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Complications ; Confidence intervals ; Correlation coefficient ; Correlation coefficients ; Diabetes ; Diabetes mellitus ; Diabetes mellitus (insulin dependent) ; Hemoglobin ; Microvasculature ; Original Research ; Oxidative stress ; Parameters ; Quartiles ; Reactive oxygen species ; Regression analysis ; Statistical analysis ; Thiols</subject><ispartof>Therapeutic advances in endocrinology and metabolism, 2020, Vol.11, p.2042018820903641-2042018820903641</ispartof><rights>The Author(s), 2020</rights><rights>The Author(s), 2020.</rights><rights>The Author(s), 2020. This work is licensed under the Creative Commons Attribution – Non-Commercial License https://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s), 2020 2020 SAGE Publications Ltd unless otherwise noted. Manuscript content on this site is licensed under Creative Commons Licenses</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c528t-ed411b61c1996bb6e51ef1076a40e6b68350c9d4e3f95acf881f43b0f217e1573</citedby><cites>FETCH-LOGICAL-c528t-ed411b61c1996bb6e51ef1076a40e6b68350c9d4e3f95acf881f43b0f217e1573</cites><orcidid>0000-0002-9702-6551</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7011336/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2441512135?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,4024,21966,25753,27853,27923,27924,27925,37012,37013,44590,44945,45333,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32095228$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>van Dijk, Peter R.</creatorcontrib><creatorcontrib>Pasch, Andreas</creatorcontrib><creatorcontrib>van Ockenburg-Brunet, Sonja L.</creatorcontrib><creatorcontrib>Waanders, Femke</creatorcontrib><creatorcontrib>Eman Abdulle, A.</creatorcontrib><creatorcontrib>Muis, Marian J.</creatorcontrib><creatorcontrib>Hillebrands, J. L.</creatorcontrib><creatorcontrib>Bilo, Henk J. G.</creatorcontrib><creatorcontrib>van Goor, Harry</creatorcontrib><title>Thiols as markers of redox status in type 1 diabetes mellitus</title><title>Therapeutic advances in endocrinology and metabolism</title><addtitle>Ther Adv Endocrinol Metab</addtitle><description>Introduction:
Type 1 diabetes mellitus (T1DM) is associated with inflammation and the production of reactive oxygen species (ROS). Systemically, free thiols (R-SH) can be oxidized by ROS and circulating R-SH concentrations may directly reflect the systemic redox status. In this study the association between R-SH and clinical parameters of T1DM, including glycated haemoglobin A1c (HbA1c), was investigated. This is of particular interest since thiols are amendable to therapeutic intervention.
Methods:
As part of a prospective cohort study, data from 216 patients with a mean age of 45 (12) years, 57% male, diabetes duration 22 (16, 30) years and HbA1c of 60 (11) mmol/mol were examined. Baseline data were collected in 2002 and follow-up data in 2018. Cox proportional hazards regression analysis, with age, sex, HbA1c and R-SH, was used to assess prognostic factors for the development of complications.
Results:
At baseline, the plasma concentration of R-SH was 281.8 ± 34.0 μM. In addition to a lower concentration of NT-proBNP in the highest R-SH quartile (305–379 µM) there were no differences in baseline characteristics between the quartiles of R-SH. The Pearson correlation coefficient for R-SH and NT-proBNP was −0.290 (p < 0.001). No significant correlation between R-SH and baseline HbA1c (r = −0.024, p = 0.726) was present. During follow-up, 42 macrovascular and 92 microvascular complications occurred. In Cox regression, R-SH was not a prognostic factor for the development of microvascular [hazard ratio (HR) 0.999 (95% confidence interval (CI) 0.993, 1.005)] and macrovascular [HR 0.993 (95% CI 0.984, 1.002)] complications.
Conclusions:
In addition to a negative association with NT-proBNP, no relevant relationships between R-SH and parameters of T1DM, including HbA1c, were present in this study.</description><subject>Complications</subject><subject>Confidence intervals</subject><subject>Correlation coefficient</subject><subject>Correlation coefficients</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes mellitus (insulin dependent)</subject><subject>Hemoglobin</subject><subject>Microvasculature</subject><subject>Original Research</subject><subject>Oxidative stress</subject><subject>Parameters</subject><subject>Quartiles</subject><subject>Reactive oxygen species</subject><subject>Regression analysis</subject><subject>Statistical analysis</subject><subject>Thiols</subject><issn>2042-0188</issn><issn>2042-0196</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>AFRWT</sourceid><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNp1kU1v1DAQhiNERau2d04oEhcuAY-_Yh9AQhUflSr1Us6W7Yy3XrLxYieI_nu8bFlopfpia-adZ8bzNs1LIG8B-v4dJZwSUIoSTZjk8Kw52YU6Alo-P7yVOm7OS1mTerhkjMsXzTGrNYJSddK8v7mNaSytLe3G5u-YS5tCm3FIv9oy23kpbZza-W6LLbRDtA5nrFIcx1hzZ81RsGPB8_v7tPn2-dPNxdfu6vrL5cXHq84LquYOBw7gJHjQWjonUQAGIL20nKB0UjFBvB44sqCF9UEpCJw5Eij0CKJnp83lnjskuzbbHOusdybZaP4EUl4Zm-foRzQKIPTCStSUVoZTWlInetcr7oNWorI-7FnbxW1w8DjN2Y4PoA8zU7w1q_TT9ASAMVkBb-4BOf1YsMxmE4uvG7ETpqUYWs0gTDHQVfr6kXSdljzVVRnKOQigwHYTkb3K51RKxnAYBojZWW0eW11LXv3_iUPBX2OroNsLil3hv65PAn8DlbGt3Q</recordid><startdate>2020</startdate><enddate>2020</enddate><creator>van Dijk, Peter R.</creator><creator>Pasch, Andreas</creator><creator>van Ockenburg-Brunet, Sonja L.</creator><creator>Waanders, Femke</creator><creator>Eman Abdulle, A.</creator><creator>Muis, Marian J.</creator><creator>Hillebrands, J. L.</creator><creator>Bilo, Henk J. G.</creator><creator>van Goor, Harry</creator><general>SAGE Publications</general><general>Sage Publications Ltd</general><general>SAGE Publishing</general><scope>AFRWT</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>NAPCQ</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-9702-6551</orcidid></search><sort><creationdate>2020</creationdate><title>Thiols as markers of redox status in type 1 diabetes mellitus</title><author>van Dijk, Peter R. ; Pasch, Andreas ; van Ockenburg-Brunet, Sonja L. ; Waanders, Femke ; Eman Abdulle, A. ; Muis, Marian J. ; Hillebrands, J. L. ; Bilo, Henk J. G. ; van Goor, Harry</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c528t-ed411b61c1996bb6e51ef1076a40e6b68350c9d4e3f95acf881f43b0f217e1573</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Complications</topic><topic>Confidence intervals</topic><topic>Correlation coefficient</topic><topic>Correlation coefficients</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes mellitus (insulin dependent)</topic><topic>Hemoglobin</topic><topic>Microvasculature</topic><topic>Original Research</topic><topic>Oxidative stress</topic><topic>Parameters</topic><topic>Quartiles</topic><topic>Reactive oxygen species</topic><topic>Regression analysis</topic><topic>Statistical analysis</topic><topic>Thiols</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>van Dijk, Peter R.</creatorcontrib><creatorcontrib>Pasch, Andreas</creatorcontrib><creatorcontrib>van Ockenburg-Brunet, Sonja L.</creatorcontrib><creatorcontrib>Waanders, Femke</creatorcontrib><creatorcontrib>Eman Abdulle, A.</creatorcontrib><creatorcontrib>Muis, Marian J.</creatorcontrib><creatorcontrib>Hillebrands, J. L.</creatorcontrib><creatorcontrib>Bilo, Henk J. G.</creatorcontrib><creatorcontrib>van Goor, Harry</creatorcontrib><collection>SAGE Open Access</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</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 Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Nursing & Allied Health Premium</collection><collection>Publicly Available Content Database (Proquest) (PQ_SDU_P3)</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Therapeutic advances in endocrinology and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>van Dijk, Peter R.</au><au>Pasch, Andreas</au><au>van Ockenburg-Brunet, Sonja L.</au><au>Waanders, Femke</au><au>Eman Abdulle, A.</au><au>Muis, Marian J.</au><au>Hillebrands, J. L.</au><au>Bilo, Henk J. G.</au><au>van Goor, Harry</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Thiols as markers of redox status in type 1 diabetes mellitus</atitle><jtitle>Therapeutic advances in endocrinology and metabolism</jtitle><addtitle>Ther Adv Endocrinol Metab</addtitle><date>2020</date><risdate>2020</risdate><volume>11</volume><spage>2042018820903641</spage><epage>2042018820903641</epage><pages>2042018820903641-2042018820903641</pages><issn>2042-0188</issn><eissn>2042-0196</eissn><abstract>Introduction:
Type 1 diabetes mellitus (T1DM) is associated with inflammation and the production of reactive oxygen species (ROS). Systemically, free thiols (R-SH) can be oxidized by ROS and circulating R-SH concentrations may directly reflect the systemic redox status. In this study the association between R-SH and clinical parameters of T1DM, including glycated haemoglobin A1c (HbA1c), was investigated. This is of particular interest since thiols are amendable to therapeutic intervention.
Methods:
As part of a prospective cohort study, data from 216 patients with a mean age of 45 (12) years, 57% male, diabetes duration 22 (16, 30) years and HbA1c of 60 (11) mmol/mol were examined. Baseline data were collected in 2002 and follow-up data in 2018. Cox proportional hazards regression analysis, with age, sex, HbA1c and R-SH, was used to assess prognostic factors for the development of complications.
Results:
At baseline, the plasma concentration of R-SH was 281.8 ± 34.0 μM. In addition to a lower concentration of NT-proBNP in the highest R-SH quartile (305–379 µM) there were no differences in baseline characteristics between the quartiles of R-SH. The Pearson correlation coefficient for R-SH and NT-proBNP was −0.290 (p < 0.001). No significant correlation between R-SH and baseline HbA1c (r = −0.024, p = 0.726) was present. During follow-up, 42 macrovascular and 92 microvascular complications occurred. In Cox regression, R-SH was not a prognostic factor for the development of microvascular [hazard ratio (HR) 0.999 (95% confidence interval (CI) 0.993, 1.005)] and macrovascular [HR 0.993 (95% CI 0.984, 1.002)] complications.
Conclusions:
In addition to a negative association with NT-proBNP, no relevant relationships between R-SH and parameters of T1DM, including HbA1c, were present in this study.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>32095228</pmid><doi>10.1177/2042018820903641</doi><orcidid>https://orcid.org/0000-0002-9702-6551</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Complications Confidence intervals Correlation coefficient Correlation coefficients Diabetes Diabetes mellitus Diabetes mellitus (insulin dependent) Hemoglobin Microvasculature Original Research Oxidative stress Parameters Quartiles Reactive oxygen species Regression analysis Statistical analysis Thiols |
| title | Thiols as markers of redox status in type 1 diabetes mellitus |
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