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Comparison of oxidative stress & leukocyte activation in patients with severe sepsis & burn injury
We evaluated pro- and anti-oxidant disturbances in sepsis and non-sepsis burn patients with systemic inflammatory response syndrome (SIRS). Adhesion molecules and inflammation markers on leukocytes were also analyzed. We hypothesized that oxidative stress and leukocyte activation markers can lead to...
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Published in: | Indian journal of medical research (New Delhi, India : 1994) India : 1994), 2011-07, Vol.134 (1), p.69-78 |
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creator | Mühl, Diana Woth, Gábor Drenkovics, Livia Varga, Adrienn Ghosh, Subhamay Csontos, Csaba Bogár, Lajos Wéber, György Lantos, János |
description | We evaluated pro- and anti-oxidant disturbances in sepsis and non-sepsis burn patients with systemic inflammatory response syndrome (SIRS). Adhesion molecules and inflammation markers on leukocytes were also analyzed. We hypothesized that oxidative stress and leukocyte activation markers can lead to the severity of sepsis.
In 28 severe sepsis and 27 acute burn injury patients blood samples were collected at admission and 4 days consecutively. Oxidative stress markers: production of reactive oxygen species (ROS), myeloperoxidase, malondialdehyde and endogenous antioxidants: plasma protein sulphydryl groups, reduced glutathione, superoxide dismutase and catalase were measured. Flow cytometry was used to determine CD11a, CD14, CD18, CD49d and CD97 adhesion molecules on leukocytes. Procalcitonin, C-reactive protein, fibrinogen, platelet count and lactate were also analyzed.
Pro-oxidant parameters were significantly elevated in sepsis patients at admission, ROS intensity increased in burn patients until the 5th day. Endogenous antioxidant levels except catalase showed increased levels after burn trauma compared to sepsis. Elevated granulocyte activation and suppressed lymphocyte function were found at admission and early activation of granulocytes caused by increasing activation/migration markers in sepsis. Leukocyte adhesion molecule expression confirmed the suppressed lymphocyte and monocyte function in sepsis.
Severe sepsis is accompanied by oxidative stress and pathological leukocyte endothelial cell interactions. The laboratory parameters used for the evaluation of sepsis and several markers of pro- and antioxidant status were different between sepsis and non-sepsis burn patients. The tendency of changes in these parameters may refer to major oxidative stress in sepsis and developing SIRS in burns. |
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In 28 severe sepsis and 27 acute burn injury patients blood samples were collected at admission and 4 days consecutively. Oxidative stress markers: production of reactive oxygen species (ROS), myeloperoxidase, malondialdehyde and endogenous antioxidants: plasma protein sulphydryl groups, reduced glutathione, superoxide dismutase and catalase were measured. Flow cytometry was used to determine CD11a, CD14, CD18, CD49d and CD97 adhesion molecules on leukocytes. Procalcitonin, C-reactive protein, fibrinogen, platelet count and lactate were also analyzed.
Pro-oxidant parameters were significantly elevated in sepsis patients at admission, ROS intensity increased in burn patients until the 5th day. Endogenous antioxidant levels except catalase showed increased levels after burn trauma compared to sepsis. Elevated granulocyte activation and suppressed lymphocyte function were found at admission and early activation of granulocytes caused by increasing activation/migration markers in sepsis. Leukocyte adhesion molecule expression confirmed the suppressed lymphocyte and monocyte function in sepsis.
Severe sepsis is accompanied by oxidative stress and pathological leukocyte endothelial cell interactions. The laboratory parameters used for the evaluation of sepsis and several markers of pro- and antioxidant status were different between sepsis and non-sepsis burn patients. The tendency of changes in these parameters may refer to major oxidative stress in sepsis and developing SIRS in burns.</description><identifier>ISSN: 0971-5916</identifier><identifier>PMID: 21808137</identifier><language>eng</language><publisher>India: Medknow Publications and Media Pvt. Ltd</publisher><subject>Aged ; Analysis ; Blood ; Burns ; Burns - physiopathology ; Burns and scalds ; Catalase - blood ; Cell Adhesion Molecules - blood ; Consent ; Failure ; Female ; Free radicals ; Glutathione - blood ; Granulocytes ; Granulocytes - metabolism ; Granulocytes - pathology ; Hematology ; Humans ; Inflammation ; Intensive care ; Laboratories ; Leukocytes - metabolism ; Leukocytes - pathology ; Lymphocyte transformation ; Lymphocytes ; Male ; Malondialdehyde - blood ; Middle Aged ; Mortality ; Original ; Oxidative Stress ; Peroxidase - blood ; Reactive oxygen species ; Reactive Oxygen Species - blood ; Sepsis ; Sepsis - physiopathology ; Superoxide Dismutase - blood ; Systemic Inflammatory Response Syndrome - physiopathology ; Trauma</subject><ispartof>Indian journal of medical research (New Delhi, India : 1994), 2011-07, Vol.134 (1), p.69-78</ispartof><rights>COPYRIGHT 2011 Medknow Publications and Media Pvt. Ltd.</rights><rights>2011. This work is published under https://creativecommons.org/licenses/by-nc-sa/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>Copyright: © The Indian Journal of Medical Research 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3171920/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2258255881?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,37012,37013,44590,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21808137$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mühl, Diana</creatorcontrib><creatorcontrib>Woth, Gábor</creatorcontrib><creatorcontrib>Drenkovics, Livia</creatorcontrib><creatorcontrib>Varga, Adrienn</creatorcontrib><creatorcontrib>Ghosh, Subhamay</creatorcontrib><creatorcontrib>Csontos, Csaba</creatorcontrib><creatorcontrib>Bogár, Lajos</creatorcontrib><creatorcontrib>Wéber, György</creatorcontrib><creatorcontrib>Lantos, János</creatorcontrib><title>Comparison of oxidative stress & leukocyte activation in patients with severe sepsis & burn injury</title><title>Indian journal of medical research (New Delhi, India : 1994)</title><addtitle>Indian J Med Res</addtitle><description>We evaluated pro- and anti-oxidant disturbances in sepsis and non-sepsis burn patients with systemic inflammatory response syndrome (SIRS). Adhesion molecules and inflammation markers on leukocytes were also analyzed. We hypothesized that oxidative stress and leukocyte activation markers can lead to the severity of sepsis.
In 28 severe sepsis and 27 acute burn injury patients blood samples were collected at admission and 4 days consecutively. Oxidative stress markers: production of reactive oxygen species (ROS), myeloperoxidase, malondialdehyde and endogenous antioxidants: plasma protein sulphydryl groups, reduced glutathione, superoxide dismutase and catalase were measured. Flow cytometry was used to determine CD11a, CD14, CD18, CD49d and CD97 adhesion molecules on leukocytes. Procalcitonin, C-reactive protein, fibrinogen, platelet count and lactate were also analyzed.
Pro-oxidant parameters were significantly elevated in sepsis patients at admission, ROS intensity increased in burn patients until the 5th day. Endogenous antioxidant levels except catalase showed increased levels after burn trauma compared to sepsis. Elevated granulocyte activation and suppressed lymphocyte function were found at admission and early activation of granulocytes caused by increasing activation/migration markers in sepsis. Leukocyte adhesion molecule expression confirmed the suppressed lymphocyte and monocyte function in sepsis.
Severe sepsis is accompanied by oxidative stress and pathological leukocyte endothelial cell interactions. The laboratory parameters used for the evaluation of sepsis and several markers of pro- and antioxidant status were different between sepsis and non-sepsis burn patients. The tendency of changes in these parameters may refer to major oxidative stress in sepsis and developing SIRS in burns.</description><subject>Aged</subject><subject>Analysis</subject><subject>Blood</subject><subject>Burns</subject><subject>Burns - physiopathology</subject><subject>Burns and scalds</subject><subject>Catalase - blood</subject><subject>Cell Adhesion Molecules - blood</subject><subject>Consent</subject><subject>Failure</subject><subject>Female</subject><subject>Free radicals</subject><subject>Glutathione - blood</subject><subject>Granulocytes</subject><subject>Granulocytes - metabolism</subject><subject>Granulocytes - pathology</subject><subject>Hematology</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Intensive care</subject><subject>Laboratories</subject><subject>Leukocytes - metabolism</subject><subject>Leukocytes - pathology</subject><subject>Lymphocyte transformation</subject><subject>Lymphocytes</subject><subject>Male</subject><subject>Malondialdehyde - blood</subject><subject>Middle Aged</subject><subject>Mortality</subject><subject>Original</subject><subject>Oxidative Stress</subject><subject>Peroxidase - blood</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - blood</subject><subject>Sepsis</subject><subject>Sepsis - physiopathology</subject><subject>Superoxide Dismutase - blood</subject><subject>Systemic Inflammatory Response Syndrome - physiopathology</subject><subject>Trauma</subject><issn>0971-5916</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNptkUtLxDAUhbtQdHz8BQkIuhrJo0mTjSCDLxDc6Dqk7c1MxrapSTs6_94MjqIiWSTkfPfcnJudbIJVQaZcEbGfHcS4xJgoWqi9bJ8SiSVhxSQrZ77tTXDRd8hb5N9dbQa3AhSHADGiM9TA-OKr9QDIVElJakJdh_p0gm6I6M0NCxRhBSFVQR_dpqocw4ZajmF9lO1a00Q43u6H2fPN9dPsbvrweHs_u3qYzqnCw9RanpcF4bKmpSFClDXLqcFFpUjNMOHclowZI6QwtSytZETkUDBpuTQ5JYodZpefvv1YtlBX6XHBNLoPrjVhrb1x-rfSuYWe-5VmpEiDwcngfGsQ_OsIcdCtixU0jenAj1FLiZUSeb5pdfqHXPoUOKXTlHJJOZdpvN_U3DSgXWd9alttPPUVFSmqIIIm6uIfKq0aWlf5DqxL978KTn7m_A749ansA_sonJo</recordid><startdate>20110701</startdate><enddate>20110701</enddate><creator>Mühl, Diana</creator><creator>Woth, Gábor</creator><creator>Drenkovics, Livia</creator><creator>Varga, Adrienn</creator><creator>Ghosh, Subhamay</creator><creator>Csontos, Csaba</creator><creator>Bogár, Lajos</creator><creator>Wéber, György</creator><creator>Lantos, János</creator><general>Medknow Publications and Media Pvt. Ltd</general><general>Scientific Scholar</general><general>Medknow Publications</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</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>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20110701</creationdate><title>Comparison of oxidative stress & leukocyte activation in patients with severe sepsis & burn injury</title><author>Mühl, Diana ; Woth, Gábor ; Drenkovics, Livia ; Varga, Adrienn ; Ghosh, Subhamay ; Csontos, Csaba ; Bogár, Lajos ; Wéber, György ; Lantos, János</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-g290t-ff54b7158d2ba166bd342a07c91d30155fb33aa686ad8bf83164e738f58a42193</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Aged</topic><topic>Analysis</topic><topic>Blood</topic><topic>Burns</topic><topic>Burns - physiopathology</topic><topic>Burns and scalds</topic><topic>Catalase - blood</topic><topic>Cell Adhesion Molecules - blood</topic><topic>Consent</topic><topic>Failure</topic><topic>Female</topic><topic>Free radicals</topic><topic>Glutathione - blood</topic><topic>Granulocytes</topic><topic>Granulocytes - metabolism</topic><topic>Granulocytes - pathology</topic><topic>Hematology</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Intensive care</topic><topic>Laboratories</topic><topic>Leukocytes - metabolism</topic><topic>Leukocytes - pathology</topic><topic>Lymphocyte transformation</topic><topic>Lymphocytes</topic><topic>Male</topic><topic>Malondialdehyde - blood</topic><topic>Middle Aged</topic><topic>Mortality</topic><topic>Original</topic><topic>Oxidative Stress</topic><topic>Peroxidase - blood</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - blood</topic><topic>Sepsis</topic><topic>Sepsis - physiopathology</topic><topic>Superoxide Dismutase - blood</topic><topic>Systemic Inflammatory Response Syndrome - physiopathology</topic><topic>Trauma</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mühl, Diana</creatorcontrib><creatorcontrib>Woth, Gábor</creatorcontrib><creatorcontrib>Drenkovics, Livia</creatorcontrib><creatorcontrib>Varga, Adrienn</creatorcontrib><creatorcontrib>Ghosh, Subhamay</creatorcontrib><creatorcontrib>Csontos, Csaba</creatorcontrib><creatorcontrib>Bogár, Lajos</creatorcontrib><creatorcontrib>Wéber, György</creatorcontrib><creatorcontrib>Lantos, János</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</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>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library (ProQuest Database)</collection><collection>Science Database</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content 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>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Indian journal of medical research (New Delhi, India : 1994)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mühl, Diana</au><au>Woth, Gábor</au><au>Drenkovics, Livia</au><au>Varga, Adrienn</au><au>Ghosh, Subhamay</au><au>Csontos, Csaba</au><au>Bogár, Lajos</au><au>Wéber, György</au><au>Lantos, János</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Comparison of oxidative stress & leukocyte activation in patients with severe sepsis & burn injury</atitle><jtitle>Indian journal of medical research (New Delhi, India : 1994)</jtitle><addtitle>Indian J Med Res</addtitle><date>2011-07-01</date><risdate>2011</risdate><volume>134</volume><issue>1</issue><spage>69</spage><epage>78</epage><pages>69-78</pages><issn>0971-5916</issn><abstract>We evaluated pro- and anti-oxidant disturbances in sepsis and non-sepsis burn patients with systemic inflammatory response syndrome (SIRS). Adhesion molecules and inflammation markers on leukocytes were also analyzed. We hypothesized that oxidative stress and leukocyte activation markers can lead to the severity of sepsis.
In 28 severe sepsis and 27 acute burn injury patients blood samples were collected at admission and 4 days consecutively. Oxidative stress markers: production of reactive oxygen species (ROS), myeloperoxidase, malondialdehyde and endogenous antioxidants: plasma protein sulphydryl groups, reduced glutathione, superoxide dismutase and catalase were measured. Flow cytometry was used to determine CD11a, CD14, CD18, CD49d and CD97 adhesion molecules on leukocytes. Procalcitonin, C-reactive protein, fibrinogen, platelet count and lactate were also analyzed.
Pro-oxidant parameters were significantly elevated in sepsis patients at admission, ROS intensity increased in burn patients until the 5th day. Endogenous antioxidant levels except catalase showed increased levels after burn trauma compared to sepsis. Elevated granulocyte activation and suppressed lymphocyte function were found at admission and early activation of granulocytes caused by increasing activation/migration markers in sepsis. Leukocyte adhesion molecule expression confirmed the suppressed lymphocyte and monocyte function in sepsis.
Severe sepsis is accompanied by oxidative stress and pathological leukocyte endothelial cell interactions. The laboratory parameters used for the evaluation of sepsis and several markers of pro- and antioxidant status were different between sepsis and non-sepsis burn patients. The tendency of changes in these parameters may refer to major oxidative stress in sepsis and developing SIRS in burns.</abstract><cop>India</cop><pub>Medknow Publications and Media Pvt. Ltd</pub><pmid>21808137</pmid><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aged Analysis Blood Burns Burns - physiopathology Burns and scalds Catalase - blood Cell Adhesion Molecules - blood Consent Failure Female Free radicals Glutathione - blood Granulocytes Granulocytes - metabolism Granulocytes - pathology Hematology Humans Inflammation Intensive care Laboratories Leukocytes - metabolism Leukocytes - pathology Lymphocyte transformation Lymphocytes Male Malondialdehyde - blood Middle Aged Mortality Original Oxidative Stress Peroxidase - blood Reactive oxygen species Reactive Oxygen Species - blood Sepsis Sepsis - physiopathology Superoxide Dismutase - blood Systemic Inflammatory Response Syndrome - physiopathology Trauma |
title | Comparison of oxidative stress & leukocyte activation in patients with severe sepsis & burn injury |
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