Impaired Platelet Aggregation and Rebalanced Hemostasis in Patients with Chronic Hepatitis C Virus Infection

Increased risk of both cardiovascular disease (CVD) and bleeding has been found in patients with chronic hepatitis C (CHC) infection, and a re-balanced hemostasis has been proposed. The aim of this study was to investigate functional whole blood coagulation and platelet function in CHC infection. Th...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:International journal of molecular sciences 2017-05, Vol.18 (5), p.1016
Hauptverfasser: Nielsen, Nick S, Jespersen, Sofie, Gaardbo, Julie C, Arnbjerg, Caroline J, Clausen, Mette R, Kjær, Mette, Gerstoft, Jan, Ballegaard, Vibe, Ostrowski, Sisse R, Nielsen, Susanne D
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page
container_issue 5
container_start_page 1016
container_title International journal of molecular sciences
container_volume 18
creator Nielsen, Nick S
Jespersen, Sofie
Gaardbo, Julie C
Arnbjerg, Caroline J
Clausen, Mette R
Kjær, Mette
Gerstoft, Jan
Ballegaard, Vibe
Ostrowski, Sisse R
Nielsen, Susanne D
description Increased risk of both cardiovascular disease (CVD) and bleeding has been found in patients with chronic hepatitis C (CHC) infection, and a re-balanced hemostasis has been proposed. The aim of this study was to investigate functional whole blood coagulation and platelet function in CHC infection. The prospective study included 82 patients with CHC infection (39 with advanced liver fibrosis and 43 with no or mild liver fibrosis) and 39 healthy controls. A total of 33 patients were treated for CHC infection and achieved sustained virological response (SVR). Baseline and post-treatment blood samples were collected. Hemostasis was assessed by both standard coagulation tests and functional whole blood hemostatic assays (thromboelastograhy (TEG), and platelet aggregation (Multiplate). Patients with CHC and advanced fibrosis had impaired platelet aggregation both compared to patients with no or mild fibrosis and to healthy controls. Patients with CHC and advanced fibrosis also had lower antithrombin, platelet count, and coagulation factors II-VII-X compared to healthy controls. In contrast, TEG did not differ between groups. In treated patients achieving SVR, post-treatment platelet count was higher than pre-treatment counts ( = 0.033) and ADPtest, ASPItest, and RISTOhightest all increased post treatment (all < 0.05). All Multiplate tests values, however, remained below those in the healthy controls. CHC-infected patients displayed evidence of rebalanced hemostasis with only partly hemostatic normalization in patients achieving SVR. The implications of rebalanced hemostasis and especially the impact on risk of CVD and bleeding warrants further studies.
doi_str_mv 10.3390/ijms18051016
format Article
fullrecord <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5454929</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1896415028</sourcerecordid><originalsourceid>FETCH-LOGICAL-c412t-4e9f5d5f1f78b022f34079069c19fbd6284d77f1688659c145b37b05fa4dd2173</originalsourceid><addsrcrecordid>eNpdkUFrGzEQhUVoiZ00t5yDoJcc4lajlXZXl4IxSWwI1JQ2V6HdlWyZXcmVtAn991WIE9yeZpj5eLyZh9AlkC9FIchXuxsi1IQDgfIETYFROiOkrD4c9RN0FuOOEFpQLk7RhNashtxPUb8a9soG3eF1r5LudcLzzSbojUrWO6xch3_oRvXKtZlZ6sHHpKKN2Dq8zox2KeJnm7Z4sQ3e2TYz-zxPGVngRxvGiFfO6PZF7hP6aFQf9cWhnqNfd7c_F8vZw_f71WL-MGsZ0DRjWhjecQOmqhtCqSkYqQQpRQvCNF2Z3XdVZaCs65LnIeNNUTWEG8W6jkJVnKNvr7r7sRl012aTQfVyH-ygwh_plZX_bpzdyo1_kpxxJqjIAtcHgeB_jzomOdjY6j6_QfsxSqhFyYATWmf083_ozo_B5fMkCCBcCGAkUzevVBt8jEGbdzNA5EuM8jjGjF8dH_AOv-VW_AX8uJlc</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1910599140</pqid></control><display><type>article</type><title>Impaired Platelet Aggregation and Rebalanced Hemostasis in Patients with Chronic Hepatitis C Virus Infection</title><source>MDPI - Multidisciplinary Digital Publishing Institute</source><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><creator>Nielsen, Nick S ; Jespersen, Sofie ; Gaardbo, Julie C ; Arnbjerg, Caroline J ; Clausen, Mette R ; Kjær, Mette ; Gerstoft, Jan ; Ballegaard, Vibe ; Ostrowski, Sisse R ; Nielsen, Susanne D</creator><creatorcontrib>Nielsen, Nick S ; Jespersen, Sofie ; Gaardbo, Julie C ; Arnbjerg, Caroline J ; Clausen, Mette R ; Kjær, Mette ; Gerstoft, Jan ; Ballegaard, Vibe ; Ostrowski, Sisse R ; Nielsen, Susanne D</creatorcontrib><description>Increased risk of both cardiovascular disease (CVD) and bleeding has been found in patients with chronic hepatitis C (CHC) infection, and a re-balanced hemostasis has been proposed. The aim of this study was to investigate functional whole blood coagulation and platelet function in CHC infection. The prospective study included 82 patients with CHC infection (39 with advanced liver fibrosis and 43 with no or mild liver fibrosis) and 39 healthy controls. A total of 33 patients were treated for CHC infection and achieved sustained virological response (SVR). Baseline and post-treatment blood samples were collected. Hemostasis was assessed by both standard coagulation tests and functional whole blood hemostatic assays (thromboelastograhy (TEG), and platelet aggregation (Multiplate). Patients with CHC and advanced fibrosis had impaired platelet aggregation both compared to patients with no or mild fibrosis and to healthy controls. Patients with CHC and advanced fibrosis also had lower antithrombin, platelet count, and coagulation factors II-VII-X compared to healthy controls. In contrast, TEG did not differ between groups. In treated patients achieving SVR, post-treatment platelet count was higher than pre-treatment counts ( = 0.033) and ADPtest, ASPItest, and RISTOhightest all increased post treatment (all &lt; 0.05). All Multiplate tests values, however, remained below those in the healthy controls. CHC-infected patients displayed evidence of rebalanced hemostasis with only partly hemostatic normalization in patients achieving SVR. The implications of rebalanced hemostasis and especially the impact on risk of CVD and bleeding warrants further studies.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms18051016</identifier><identifier>PMID: 28481325</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Adult ; Antithrombin ; Assaying ; Bleeding ; Blood coagulation ; Blood Coagulation Factors - metabolism ; Blood platelets ; Cardiovascular diseases ; Case-Control Studies ; Chronic infection ; Coagulation ; Coagulation factors ; Female ; Fibrosis ; Functional anatomy ; Hemostasis ; Hemostatics ; Hepatitis ; Hepatitis C ; Hepatitis C, Chronic - blood ; Hepatitis C, Chronic - drug therapy ; Hepatitis C, Chronic - pathology ; Humans ; Infections ; Interferon ; Liver ; Male ; Middle Aged ; Patients ; Platelet Aggregation ; Pretreatment ; Risk ; Sustained Virologic Response</subject><ispartof>International journal of molecular sciences, 2017-05, Vol.18 (5), p.1016</ispartof><rights>Copyright MDPI AG 2017</rights><rights>2017 by the authors. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-4e9f5d5f1f78b022f34079069c19fbd6284d77f1688659c145b37b05fa4dd2173</citedby><cites>FETCH-LOGICAL-c412t-4e9f5d5f1f78b022f34079069c19fbd6284d77f1688659c145b37b05fa4dd2173</cites><orcidid>0000-0002-3083-3914</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/PMC5454929/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5454929/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28481325$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nielsen, Nick S</creatorcontrib><creatorcontrib>Jespersen, Sofie</creatorcontrib><creatorcontrib>Gaardbo, Julie C</creatorcontrib><creatorcontrib>Arnbjerg, Caroline J</creatorcontrib><creatorcontrib>Clausen, Mette R</creatorcontrib><creatorcontrib>Kjær, Mette</creatorcontrib><creatorcontrib>Gerstoft, Jan</creatorcontrib><creatorcontrib>Ballegaard, Vibe</creatorcontrib><creatorcontrib>Ostrowski, Sisse R</creatorcontrib><creatorcontrib>Nielsen, Susanne D</creatorcontrib><title>Impaired Platelet Aggregation and Rebalanced Hemostasis in Patients with Chronic Hepatitis C Virus Infection</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Increased risk of both cardiovascular disease (CVD) and bleeding has been found in patients with chronic hepatitis C (CHC) infection, and a re-balanced hemostasis has been proposed. The aim of this study was to investigate functional whole blood coagulation and platelet function in CHC infection. The prospective study included 82 patients with CHC infection (39 with advanced liver fibrosis and 43 with no or mild liver fibrosis) and 39 healthy controls. A total of 33 patients were treated for CHC infection and achieved sustained virological response (SVR). Baseline and post-treatment blood samples were collected. Hemostasis was assessed by both standard coagulation tests and functional whole blood hemostatic assays (thromboelastograhy (TEG), and platelet aggregation (Multiplate). Patients with CHC and advanced fibrosis had impaired platelet aggregation both compared to patients with no or mild fibrosis and to healthy controls. Patients with CHC and advanced fibrosis also had lower antithrombin, platelet count, and coagulation factors II-VII-X compared to healthy controls. In contrast, TEG did not differ between groups. In treated patients achieving SVR, post-treatment platelet count was higher than pre-treatment counts ( = 0.033) and ADPtest, ASPItest, and RISTOhightest all increased post treatment (all &lt; 0.05). All Multiplate tests values, however, remained below those in the healthy controls. CHC-infected patients displayed evidence of rebalanced hemostasis with only partly hemostatic normalization in patients achieving SVR. The implications of rebalanced hemostasis and especially the impact on risk of CVD and bleeding warrants further studies.</description><subject>Adult</subject><subject>Antithrombin</subject><subject>Assaying</subject><subject>Bleeding</subject><subject>Blood coagulation</subject><subject>Blood Coagulation Factors - metabolism</subject><subject>Blood platelets</subject><subject>Cardiovascular diseases</subject><subject>Case-Control Studies</subject><subject>Chronic infection</subject><subject>Coagulation</subject><subject>Coagulation factors</subject><subject>Female</subject><subject>Fibrosis</subject><subject>Functional anatomy</subject><subject>Hemostasis</subject><subject>Hemostatics</subject><subject>Hepatitis</subject><subject>Hepatitis C</subject><subject>Hepatitis C, Chronic - blood</subject><subject>Hepatitis C, Chronic - drug therapy</subject><subject>Hepatitis C, Chronic - pathology</subject><subject>Humans</subject><subject>Infections</subject><subject>Interferon</subject><subject>Liver</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Patients</subject><subject>Platelet Aggregation</subject><subject>Pretreatment</subject><subject>Risk</subject><subject>Sustained Virologic Response</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkUFrGzEQhUVoiZ00t5yDoJcc4lajlXZXl4IxSWwI1JQ2V6HdlWyZXcmVtAn991WIE9yeZpj5eLyZh9AlkC9FIchXuxsi1IQDgfIETYFROiOkrD4c9RN0FuOOEFpQLk7RhNashtxPUb8a9soG3eF1r5LudcLzzSbojUrWO6xch3_oRvXKtZlZ6sHHpKKN2Dq8zox2KeJnm7Z4sQ3e2TYz-zxPGVngRxvGiFfO6PZF7hP6aFQf9cWhnqNfd7c_F8vZw_f71WL-MGsZ0DRjWhjecQOmqhtCqSkYqQQpRQvCNF2Z3XdVZaCs65LnIeNNUTWEG8W6jkJVnKNvr7r7sRl012aTQfVyH-ygwh_plZX_bpzdyo1_kpxxJqjIAtcHgeB_jzomOdjY6j6_QfsxSqhFyYATWmf083_ozo_B5fMkCCBcCGAkUzevVBt8jEGbdzNA5EuM8jjGjF8dH_AOv-VW_AX8uJlc</recordid><startdate>20170508</startdate><enddate>20170508</enddate><creator>Nielsen, Nick S</creator><creator>Jespersen, Sofie</creator><creator>Gaardbo, Julie C</creator><creator>Arnbjerg, Caroline J</creator><creator>Clausen, Mette R</creator><creator>Kjær, Mette</creator><creator>Gerstoft, Jan</creator><creator>Ballegaard, Vibe</creator><creator>Ostrowski, Sisse R</creator><creator>Nielsen, Susanne D</creator><general>MDPI AG</general><general>MDPI</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>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-3083-3914</orcidid></search><sort><creationdate>20170508</creationdate><title>Impaired Platelet Aggregation and Rebalanced Hemostasis in Patients with Chronic Hepatitis C Virus Infection</title><author>Nielsen, Nick S ; Jespersen, Sofie ; Gaardbo, Julie C ; Arnbjerg, Caroline J ; Clausen, Mette R ; Kjær, Mette ; Gerstoft, Jan ; Ballegaard, Vibe ; Ostrowski, Sisse R ; Nielsen, Susanne D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c412t-4e9f5d5f1f78b022f34079069c19fbd6284d77f1688659c145b37b05fa4dd2173</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adult</topic><topic>Antithrombin</topic><topic>Assaying</topic><topic>Bleeding</topic><topic>Blood coagulation</topic><topic>Blood Coagulation Factors - metabolism</topic><topic>Blood platelets</topic><topic>Cardiovascular diseases</topic><topic>Case-Control Studies</topic><topic>Chronic infection</topic><topic>Coagulation</topic><topic>Coagulation factors</topic><topic>Female</topic><topic>Fibrosis</topic><topic>Functional anatomy</topic><topic>Hemostasis</topic><topic>Hemostatics</topic><topic>Hepatitis</topic><topic>Hepatitis C</topic><topic>Hepatitis C, Chronic - blood</topic><topic>Hepatitis C, Chronic - drug therapy</topic><topic>Hepatitis C, Chronic - pathology</topic><topic>Humans</topic><topic>Infections</topic><topic>Interferon</topic><topic>Liver</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Patients</topic><topic>Platelet Aggregation</topic><topic>Pretreatment</topic><topic>Risk</topic><topic>Sustained Virologic Response</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nielsen, Nick S</creatorcontrib><creatorcontrib>Jespersen, Sofie</creatorcontrib><creatorcontrib>Gaardbo, Julie C</creatorcontrib><creatorcontrib>Arnbjerg, Caroline J</creatorcontrib><creatorcontrib>Clausen, Mette R</creatorcontrib><creatorcontrib>Kjær, Mette</creatorcontrib><creatorcontrib>Gerstoft, Jan</creatorcontrib><creatorcontrib>Ballegaard, Vibe</creatorcontrib><creatorcontrib>Ostrowski, Sisse R</creatorcontrib><creatorcontrib>Nielsen, Susanne D</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 &amp; 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 &amp; Medical Complete (Alumni)</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nielsen, Nick S</au><au>Jespersen, Sofie</au><au>Gaardbo, Julie C</au><au>Arnbjerg, Caroline J</au><au>Clausen, Mette R</au><au>Kjær, Mette</au><au>Gerstoft, Jan</au><au>Ballegaard, Vibe</au><au>Ostrowski, Sisse R</au><au>Nielsen, Susanne D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impaired Platelet Aggregation and Rebalanced Hemostasis in Patients with Chronic Hepatitis C Virus Infection</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2017-05-08</date><risdate>2017</risdate><volume>18</volume><issue>5</issue><spage>1016</spage><pages>1016-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Increased risk of both cardiovascular disease (CVD) and bleeding has been found in patients with chronic hepatitis C (CHC) infection, and a re-balanced hemostasis has been proposed. The aim of this study was to investigate functional whole blood coagulation and platelet function in CHC infection. The prospective study included 82 patients with CHC infection (39 with advanced liver fibrosis and 43 with no or mild liver fibrosis) and 39 healthy controls. A total of 33 patients were treated for CHC infection and achieved sustained virological response (SVR). Baseline and post-treatment blood samples were collected. Hemostasis was assessed by both standard coagulation tests and functional whole blood hemostatic assays (thromboelastograhy (TEG), and platelet aggregation (Multiplate). Patients with CHC and advanced fibrosis had impaired platelet aggregation both compared to patients with no or mild fibrosis and to healthy controls. Patients with CHC and advanced fibrosis also had lower antithrombin, platelet count, and coagulation factors II-VII-X compared to healthy controls. In contrast, TEG did not differ between groups. In treated patients achieving SVR, post-treatment platelet count was higher than pre-treatment counts ( = 0.033) and ADPtest, ASPItest, and RISTOhightest all increased post treatment (all &lt; 0.05). All Multiplate tests values, however, remained below those in the healthy controls. CHC-infected patients displayed evidence of rebalanced hemostasis with only partly hemostatic normalization in patients achieving SVR. The implications of rebalanced hemostasis and especially the impact on risk of CVD and bleeding warrants further studies.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>28481325</pmid><doi>10.3390/ijms18051016</doi><orcidid>https://orcid.org/0000-0002-3083-3914</orcidid><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 1422-0067
ispartof International journal of molecular sciences, 2017-05, Vol.18 (5), p.1016
issn 1422-0067
1661-6596
1422-0067
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5454929
source MDPI - Multidisciplinary Digital Publishing Institute; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central
subjects Adult
Antithrombin
Assaying
Bleeding
Blood coagulation
Blood Coagulation Factors - metabolism
Blood platelets
Cardiovascular diseases
Case-Control Studies
Chronic infection
Coagulation
Coagulation factors
Female
Fibrosis
Functional anatomy
Hemostasis
Hemostatics
Hepatitis
Hepatitis C
Hepatitis C, Chronic - blood
Hepatitis C, Chronic - drug therapy
Hepatitis C, Chronic - pathology
Humans
Infections
Interferon
Liver
Male
Middle Aged
Patients
Platelet Aggregation
Pretreatment
Risk
Sustained Virologic Response
title Impaired Platelet Aggregation and Rebalanced Hemostasis in Patients with Chronic Hepatitis C Virus Infection
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-08T04%3A57%3A47IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Impaired%20Platelet%20Aggregation%20and%20Rebalanced%20Hemostasis%20in%20Patients%20with%20Chronic%20Hepatitis%20C%20Virus%20Infection&rft.jtitle=International%20journal%20of%20molecular%20sciences&rft.au=Nielsen,%20Nick%20S&rft.date=2017-05-08&rft.volume=18&rft.issue=5&rft.spage=1016&rft.pages=1016-&rft.issn=1422-0067&rft.eissn=1422-0067&rft_id=info:doi/10.3390/ijms18051016&rft_dat=%3Cproquest_pubme%3E1896415028%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1910599140&rft_id=info:pmid/28481325&rfr_iscdi=true