Platelet production and destruction in liver cirrhosis
Background & Aims Thrombocytopenia is common in liver cirrhosis (LC) but the mechanisms are not fully understood. The purpose of our work was to evaluate platelet kinetics in LC with different etiologies by examining platelet production and destruction. Methods Ninety-one consecutive LC patients...
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| Veröffentlicht in: | Journal of hepatology 2011-05, Vol.54 (5), p.894-900 |
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| description | Background & Aims Thrombocytopenia is common in liver cirrhosis (LC) but the mechanisms are not fully understood. The purpose of our work was to evaluate platelet kinetics in LC with different etiologies by examining platelet production and destruction. Methods Ninety-one consecutive LC patients (36 HCV, 49 alcoholics, 15 HBV) were enrolled. As controls, 25 subjects with idiopathic thrombocytopenic purpura, 10 subjects with aplastic anemia, and 40 healthy blood donors were studied. Plasma thrombopoietin (TPO) was measured by ELISA. Reticulated platelets (RP) were determined using the Thiazole Orange method. Plasma glycocalicin (GC) was measured using monoclonal antibodies. Platelet associated and serum antiplatelet antibodies were detected by flow cytometry. B-cell monoclonality in PBMC was assessed by immunoglobulin fingerprinting. Results Serum TPO was significantly lower in LC (29.9 ± 18.1 pg/ml) compared to controls (82.3 ± 47.6 pg/ml). The GC levels were higher in LC (any etiology) than in healthy cases. Conversely, the absolute levels of RP were lower in LC (any etiology) than in healthy controls. The platelet-associated and serum anti-platelet antibodies were higher in HCV+ LC compared to healthy subjects ( p |
| doi_str_mv | 10.1016/j.jhep.2010.08.018 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_862600157</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0168827810009190</els_id><sourcerecordid>862600157</sourcerecordid><originalsourceid>FETCH-LOGICAL-c506t-25d032434da1c68dcb792a32d869eefd85108a87d9c183d8211f73725b47833e3</originalsourceid><addsrcrecordid>eNp9kU1rGzEQhkVJqN2kf6CHsJeQ07ojaT9mIRSCST_AkECSs5ClWazteteRdg3-99FiN4UeehISz4zeeYaxLxwWHHjxtVk0G9otBMQHwAVw_MDmvABIocj4GZtHCFMUJc7YpxAaAJBQZR_ZTHCe5Qg4Z8VjqwdqaUh2vrejGVzfJbqziaUw-NPddUnr9uQT47zf9MGFS3Ze6zbQ59N5wV6-3z8vf6arhx-_lner1ORQDKnILUiRycxqbgq0Zl1WQkthsaiIaos5B9RY2spwlBZjrrqUpcjXWYlSkrxgN8e-Md3rGCOprQuG2lZ31I9BYSHivDwvIymOpPF9CJ5qtfNuq_1BcVCTLtWoSZeadClAFXXFoqtT-3G9Jfte8sdPBK5PgA5Gt7XXnXHhL5dBKSVO3O2Royhj78irYBx1hqzzZAZle_f_HN_-KTet61z88TcdKDT96LuoWXEVhAL1NC122iuPK614BfINKX2b9Q</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>862600157</pqid></control><display><type>article</type><title>Platelet production and destruction in liver cirrhosis</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals Complete</source><creator>Pradella, Paola ; Bonetto, Stefania ; Turchetto, Stefano ; Uxa, Laura ; Comar, Consuelo ; Zorat, Francesca ; De Angelis, Vincenzo ; Pozzato, Gabriele</creator><creatorcontrib>Pradella, Paola ; Bonetto, Stefania ; Turchetto, Stefano ; Uxa, Laura ; Comar, Consuelo ; Zorat, Francesca ; De Angelis, Vincenzo ; Pozzato, Gabriele</creatorcontrib><description>Background & Aims Thrombocytopenia is common in liver cirrhosis (LC) but the mechanisms are not fully understood. The purpose of our work was to evaluate platelet kinetics in LC with different etiologies by examining platelet production and destruction. Methods Ninety-one consecutive LC patients (36 HCV, 49 alcoholics, 15 HBV) were enrolled. As controls, 25 subjects with idiopathic thrombocytopenic purpura, 10 subjects with aplastic anemia, and 40 healthy blood donors were studied. Plasma thrombopoietin (TPO) was measured by ELISA. Reticulated platelets (RP) were determined using the Thiazole Orange method. Plasma glycocalicin (GC) was measured using monoclonal antibodies. Platelet associated and serum antiplatelet antibodies were detected by flow cytometry. B-cell monoclonality in PBMC was assessed by immunoglobulin fingerprinting. Results Serum TPO was significantly lower in LC (29.9 ± 18.1 pg/ml) compared to controls (82.3 ± 47.6 pg/ml). The GC levels were higher in LC (any etiology) than in healthy cases. Conversely, the absolute levels of RP were lower in LC (any etiology) than in healthy controls. The platelet-associated and serum anti-platelet antibodies were higher in HCV+ LC compared to healthy subjects ( p <0.0064), alcoholic LC ( p <0.018), and HBV+ LC ( p <0.0001). B-cell monoclonality was found in 27% of the HCV + LC, while it was not found in HBV+ or alcoholic LC. Conclusions Patients with LC present decreased plasma TPO, accelerated platelet turnover, and reduced platelet production. This indicates that LC thrombocytopenia is a multifactorial condition involving both increased platelet clearance and impaired thrombopoiesis.</description><identifier>ISSN: 0168-8278</identifier><identifier>EISSN: 1600-0641</identifier><identifier>DOI: 10.1016/j.jhep.2010.08.018</identifier><identifier>PMID: 21145808</identifier><identifier>CODEN: JOHEEC</identifier><language>eng</language><publisher>Kidlington: Elsevier B.V</publisher><subject>Adolescent ; Adult ; Aged ; Aged, 80 and over ; Anemia, Aplastic - blood ; Anemia, Aplastic - immunology ; Anemia, Aplastic - pathology ; Aplastic anemia ; Autoantibodies - blood ; B-Lymphocytes - immunology ; Biological and medical sciences ; Blood Platelets - immunology ; Blood Platelets - metabolism ; Blood Platelets - pathology ; Child ; Female ; Gastroenterology and Hepatology ; Gastroenterology. Liver. Pancreas. Abdomen ; Glycocalicin ; HBV ; HCV ; Hematologic and hematopoietic diseases ; Humans ; Idiopathic thrombocytopenic purpura ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Liver cirrhosis ; Liver Cirrhosis - blood ; Liver Cirrhosis - immunology ; Liver Cirrhosis - pathology ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Middle Aged ; Other diseases. Semiology ; Platelet diseases and coagulopathies ; Platelet Glycoprotein GPIb-IX Complex - metabolism ; Purpura, Thrombocytopenic, Idiopathic - blood ; Purpura, Thrombocytopenic, Idiopathic - immunology ; Purpura, Thrombocytopenic, Idiopathic - pathology ; Spleen - pathology ; Thrombopoiesis - physiology ; Thrombopoietin ; Thrombopoietin - blood</subject><ispartof>Journal of hepatology, 2011-05, Vol.54 (5), p.894-900</ispartof><rights>European Association for the Study of the Liver</rights><rights>2010 European Association for the Study of the Liver</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2010 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c506t-25d032434da1c68dcb792a32d869eefd85108a87d9c183d8211f73725b47833e3</citedby><cites>FETCH-LOGICAL-c506t-25d032434da1c68dcb792a32d869eefd85108a87d9c183d8211f73725b47833e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0168827810009190$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24073388$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21145808$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pradella, Paola</creatorcontrib><creatorcontrib>Bonetto, Stefania</creatorcontrib><creatorcontrib>Turchetto, Stefano</creatorcontrib><creatorcontrib>Uxa, Laura</creatorcontrib><creatorcontrib>Comar, Consuelo</creatorcontrib><creatorcontrib>Zorat, Francesca</creatorcontrib><creatorcontrib>De Angelis, Vincenzo</creatorcontrib><creatorcontrib>Pozzato, Gabriele</creatorcontrib><title>Platelet production and destruction in liver cirrhosis</title><title>Journal of hepatology</title><addtitle>J Hepatol</addtitle><description>Background & Aims Thrombocytopenia is common in liver cirrhosis (LC) but the mechanisms are not fully understood. The purpose of our work was to evaluate platelet kinetics in LC with different etiologies by examining platelet production and destruction. Methods Ninety-one consecutive LC patients (36 HCV, 49 alcoholics, 15 HBV) were enrolled. As controls, 25 subjects with idiopathic thrombocytopenic purpura, 10 subjects with aplastic anemia, and 40 healthy blood donors were studied. Plasma thrombopoietin (TPO) was measured by ELISA. Reticulated platelets (RP) were determined using the Thiazole Orange method. Plasma glycocalicin (GC) was measured using monoclonal antibodies. Platelet associated and serum antiplatelet antibodies were detected by flow cytometry. B-cell monoclonality in PBMC was assessed by immunoglobulin fingerprinting. Results Serum TPO was significantly lower in LC (29.9 ± 18.1 pg/ml) compared to controls (82.3 ± 47.6 pg/ml). The GC levels were higher in LC (any etiology) than in healthy cases. Conversely, the absolute levels of RP were lower in LC (any etiology) than in healthy controls. The platelet-associated and serum anti-platelet antibodies were higher in HCV+ LC compared to healthy subjects ( p <0.0064), alcoholic LC ( p <0.018), and HBV+ LC ( p <0.0001). B-cell monoclonality was found in 27% of the HCV + LC, while it was not found in HBV+ or alcoholic LC. Conclusions Patients with LC present decreased plasma TPO, accelerated platelet turnover, and reduced platelet production. This indicates that LC thrombocytopenia is a multifactorial condition involving both increased platelet clearance and impaired thrombopoiesis.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Anemia, Aplastic - blood</subject><subject>Anemia, Aplastic - immunology</subject><subject>Anemia, Aplastic - pathology</subject><subject>Aplastic anemia</subject><subject>Autoantibodies - blood</subject><subject>B-Lymphocytes - immunology</subject><subject>Biological and medical sciences</subject><subject>Blood Platelets - immunology</subject><subject>Blood Platelets - metabolism</subject><subject>Blood Platelets - pathology</subject><subject>Child</subject><subject>Female</subject><subject>Gastroenterology and Hepatology</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Glycocalicin</subject><subject>HBV</subject><subject>HCV</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Idiopathic thrombocytopenic purpura</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Liver cirrhosis</subject><subject>Liver Cirrhosis - blood</subject><subject>Liver Cirrhosis - immunology</subject><subject>Liver Cirrhosis - pathology</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Other diseases. Semiology</subject><subject>Platelet diseases and coagulopathies</subject><subject>Platelet Glycoprotein GPIb-IX Complex - metabolism</subject><subject>Purpura, Thrombocytopenic, Idiopathic - blood</subject><subject>Purpura, Thrombocytopenic, Idiopathic - immunology</subject><subject>Purpura, Thrombocytopenic, Idiopathic - pathology</subject><subject>Spleen - pathology</subject><subject>Thrombopoiesis - physiology</subject><subject>Thrombopoietin</subject><subject>Thrombopoietin - blood</subject><issn>0168-8278</issn><issn>1600-0641</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1rGzEQhkVJqN2kf6CHsJeQ07ojaT9mIRSCST_AkECSs5ClWazteteRdg3-99FiN4UeehISz4zeeYaxLxwWHHjxtVk0G9otBMQHwAVw_MDmvABIocj4GZtHCFMUJc7YpxAaAJBQZR_ZTHCe5Qg4Z8VjqwdqaUh2vrejGVzfJbqziaUw-NPddUnr9uQT47zf9MGFS3Ze6zbQ59N5wV6-3z8vf6arhx-_lner1ORQDKnILUiRycxqbgq0Zl1WQkthsaiIaos5B9RY2spwlBZjrrqUpcjXWYlSkrxgN8e-Md3rGCOprQuG2lZ31I9BYSHivDwvIymOpPF9CJ5qtfNuq_1BcVCTLtWoSZeadClAFXXFoqtT-3G9Jfte8sdPBK5PgA5Gt7XXnXHhL5dBKSVO3O2Royhj78irYBx1hqzzZAZle_f_HN_-KTet61z88TcdKDT96LuoWXEVhAL1NC122iuPK614BfINKX2b9Q</recordid><startdate>20110501</startdate><enddate>20110501</enddate><creator>Pradella, Paola</creator><creator>Bonetto, Stefania</creator><creator>Turchetto, Stefano</creator><creator>Uxa, Laura</creator><creator>Comar, Consuelo</creator><creator>Zorat, Francesca</creator><creator>De Angelis, Vincenzo</creator><creator>Pozzato, Gabriele</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><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>7X8</scope></search><sort><creationdate>20110501</creationdate><title>Platelet production and destruction in liver cirrhosis</title><author>Pradella, Paola ; Bonetto, Stefania ; Turchetto, Stefano ; Uxa, Laura ; Comar, Consuelo ; Zorat, Francesca ; De Angelis, Vincenzo ; Pozzato, Gabriele</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c506t-25d032434da1c68dcb792a32d869eefd85108a87d9c183d8211f73725b47833e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Anemia, Aplastic - blood</topic><topic>Anemia, Aplastic - immunology</topic><topic>Anemia, Aplastic - pathology</topic><topic>Aplastic anemia</topic><topic>Autoantibodies - blood</topic><topic>B-Lymphocytes - immunology</topic><topic>Biological and medical sciences</topic><topic>Blood Platelets - immunology</topic><topic>Blood Platelets - metabolism</topic><topic>Blood Platelets - pathology</topic><topic>Child</topic><topic>Female</topic><topic>Gastroenterology and Hepatology</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Glycocalicin</topic><topic>HBV</topic><topic>HCV</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Idiopathic thrombocytopenic purpura</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Liver cirrhosis</topic><topic>Liver Cirrhosis - blood</topic><topic>Liver Cirrhosis - immunology</topic><topic>Liver Cirrhosis - pathology</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Other diseases. Semiology</topic><topic>Platelet diseases and coagulopathies</topic><topic>Platelet Glycoprotein GPIb-IX Complex - metabolism</topic><topic>Purpura, Thrombocytopenic, Idiopathic - blood</topic><topic>Purpura, Thrombocytopenic, Idiopathic - immunology</topic><topic>Purpura, Thrombocytopenic, Idiopathic - pathology</topic><topic>Spleen - pathology</topic><topic>Thrombopoiesis - physiology</topic><topic>Thrombopoietin</topic><topic>Thrombopoietin - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pradella, Paola</creatorcontrib><creatorcontrib>Bonetto, Stefania</creatorcontrib><creatorcontrib>Turchetto, Stefano</creatorcontrib><creatorcontrib>Uxa, Laura</creatorcontrib><creatorcontrib>Comar, Consuelo</creatorcontrib><creatorcontrib>Zorat, Francesca</creatorcontrib><creatorcontrib>De Angelis, Vincenzo</creatorcontrib><creatorcontrib>Pozzato, Gabriele</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of hepatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pradella, Paola</au><au>Bonetto, Stefania</au><au>Turchetto, Stefano</au><au>Uxa, Laura</au><au>Comar, Consuelo</au><au>Zorat, Francesca</au><au>De Angelis, Vincenzo</au><au>Pozzato, Gabriele</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Platelet production and destruction in liver cirrhosis</atitle><jtitle>Journal of hepatology</jtitle><addtitle>J Hepatol</addtitle><date>2011-05-01</date><risdate>2011</risdate><volume>54</volume><issue>5</issue><spage>894</spage><epage>900</epage><pages>894-900</pages><issn>0168-8278</issn><eissn>1600-0641</eissn><coden>JOHEEC</coden><abstract>Background & Aims Thrombocytopenia is common in liver cirrhosis (LC) but the mechanisms are not fully understood. The purpose of our work was to evaluate platelet kinetics in LC with different etiologies by examining platelet production and destruction. Methods Ninety-one consecutive LC patients (36 HCV, 49 alcoholics, 15 HBV) were enrolled. As controls, 25 subjects with idiopathic thrombocytopenic purpura, 10 subjects with aplastic anemia, and 40 healthy blood donors were studied. Plasma thrombopoietin (TPO) was measured by ELISA. Reticulated platelets (RP) were determined using the Thiazole Orange method. Plasma glycocalicin (GC) was measured using monoclonal antibodies. Platelet associated and serum antiplatelet antibodies were detected by flow cytometry. B-cell monoclonality in PBMC was assessed by immunoglobulin fingerprinting. Results Serum TPO was significantly lower in LC (29.9 ± 18.1 pg/ml) compared to controls (82.3 ± 47.6 pg/ml). The GC levels were higher in LC (any etiology) than in healthy cases. Conversely, the absolute levels of RP were lower in LC (any etiology) than in healthy controls. The platelet-associated and serum anti-platelet antibodies were higher in HCV+ LC compared to healthy subjects ( p <0.0064), alcoholic LC ( p <0.018), and HBV+ LC ( p <0.0001). B-cell monoclonality was found in 27% of the HCV + LC, while it was not found in HBV+ or alcoholic LC. Conclusions Patients with LC present decreased plasma TPO, accelerated platelet turnover, and reduced platelet production. This indicates that LC thrombocytopenia is a multifactorial condition involving both increased platelet clearance and impaired thrombopoiesis.</abstract><cop>Kidlington</cop><pub>Elsevier B.V</pub><pmid>21145808</pmid><doi>10.1016/j.jhep.2010.08.018</doi><tpages>7</tpages></addata></record> |
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| subjects | Adolescent Adult Aged Aged, 80 and over Anemia, Aplastic - blood Anemia, Aplastic - immunology Anemia, Aplastic - pathology Aplastic anemia Autoantibodies - blood B-Lymphocytes - immunology Biological and medical sciences Blood Platelets - immunology Blood Platelets - metabolism Blood Platelets - pathology Child Female Gastroenterology and Hepatology Gastroenterology. Liver. Pancreas. Abdomen Glycocalicin HBV HCV Hematologic and hematopoietic diseases Humans Idiopathic thrombocytopenic purpura Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Liver cirrhosis Liver Cirrhosis - blood Liver Cirrhosis - immunology Liver Cirrhosis - pathology Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Middle Aged Other diseases. Semiology Platelet diseases and coagulopathies Platelet Glycoprotein GPIb-IX Complex - metabolism Purpura, Thrombocytopenic, Idiopathic - blood Purpura, Thrombocytopenic, Idiopathic - immunology Purpura, Thrombocytopenic, Idiopathic - pathology Spleen - pathology Thrombopoiesis - physiology Thrombopoietin Thrombopoietin - blood |
| title | Platelet production and destruction in liver cirrhosis |
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