The pathogenesis of accelerated fibrinolysis in hepatosplenic schistosomiasis
Seventy patients with different stages of hepatosplenic schistosomiasis and 18 non-bilharzial normal controls were studied. Plasminogen, plasminogen activators (PA), tissue-type plasminogen activator (t-PA), urokinase-type plasminogen activator (u-PA), α2-antiplasmin (α2-AP), plasminogen activator i...
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| Veröffentlicht in: | Blood coagulation & fibrinolysis 1992-12, Vol.3 (6), p.819-822 |
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| container_title | Blood coagulation & fibrinolysis |
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| creator | Omran, S A Madkour, B A Essawy, F M Toima, S M El Kaliouby, A H Shams El Din, A A |
| description | Seventy patients with different stages of hepatosplenic schistosomiasis and 18 non-bilharzial normal controls were studied. Plasminogen, plasminogen activators (PA), tissue-type plasminogen activator (t-PA), urokinase-type plasminogen activator (u-PA), α2-antiplasmin (α2-AP), plasminogen activator inhibitor (PAI), fibrinogen/fibrin degradation products (FDP) and D-dimer were determined to elucidate the role of plasminogen activators and inhibitors in the pathogenesis of accelerated fibrinolysis in schistosomiasis. There was a progressive increase in the levels of PA, t-PA, u-PA, FDP and D-dimer indicating enhanced fibrinolytic activity with advancing disease. In addition, there was progressive decrease of plasminogen, α2-AP and PAI levels which might be due to decreased hepatic synthesis and/or increased peripheral consumption. These findings suggest that the pathogenesis of accelerated fibrinolysis in schistosomiasis is multifactorial, but may be due to the progressive increase in the levels of plasminogen activators. In addition, the increase of FDP and D-dimer levels are evidence of secondary fibrinolysis following thrombin generation. |
| doi_str_mv | 10.1097/00001721-199212000-00038 |
| format | Article |
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Plasminogen, plasminogen activators (PA), tissue-type plasminogen activator (t-PA), urokinase-type plasminogen activator (u-PA), α2-antiplasmin (α2-AP), plasminogen activator inhibitor (PAI), fibrinogen/fibrin degradation products (FDP) and D-dimer were determined to elucidate the role of plasminogen activators and inhibitors in the pathogenesis of accelerated fibrinolysis in schistosomiasis. There was a progressive increase in the levels of PA, t-PA, u-PA, FDP and D-dimer indicating enhanced fibrinolytic activity with advancing disease. In addition, there was progressive decrease of plasminogen, α2-AP and PAI levels which might be due to decreased hepatic synthesis and/or increased peripheral consumption. These findings suggest that the pathogenesis of accelerated fibrinolysis in schistosomiasis is multifactorial, but may be due to the progressive increase in the levels of plasminogen activators. In addition, the increase of FDP and D-dimer levels are evidence of secondary fibrinolysis following thrombin generation.</description><identifier>ISSN: 0957-5235</identifier><identifier>EISSN: 1473-5733</identifier><identifier>DOI: 10.1097/00001721-199212000-00038</identifier><identifier>PMID: 1489902</identifier><language>eng</language><publisher>Philadelphia, PA: Lippincott-Raven Publishers</publisher><subject>alpha-2-Antiplasmin - analysis ; Biological and medical sciences ; Diseases caused by trematodes ; Female ; Fibrin Fibrinogen Degradation Products - analysis ; Fibrinolysis ; Helminthic diseases ; Hepatomegaly - blood ; Hepatomegaly - etiology ; Humans ; Infectious diseases ; Male ; Medical sciences ; Parasitic diseases ; Plasminogen - analysis ; Plasminogen Activator Inhibitor 1 - analysis ; Plasminogen Activators - analysis ; Schistosomiases ; Schistosomiasis mansoni - blood ; Schistosomiasis mansoni - complications ; Splenomegaly - blood ; Splenomegaly - etiology</subject><ispartof>Blood coagulation & fibrinolysis, 1992-12, Vol.3 (6), p.819-822</ispartof><rights>Lippincott-Raven Publishers.</rights><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4798-6d517c0f690842fe22ea05b427794784eb7e2bff2a0e4ed62aab825a7f39e5ef3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>309,310,314,780,784,789,790,23930,23931,25140,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4546973$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1489902$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Omran, S A</creatorcontrib><creatorcontrib>Madkour, B A</creatorcontrib><creatorcontrib>Essawy, F M</creatorcontrib><creatorcontrib>Toima, S M</creatorcontrib><creatorcontrib>El Kaliouby, A H</creatorcontrib><creatorcontrib>Shams El Din, A A</creatorcontrib><title>The pathogenesis of accelerated fibrinolysis in hepatosplenic schistosomiasis</title><title>Blood coagulation & fibrinolysis</title><addtitle>Blood Coagul Fibrinolysis</addtitle><description>Seventy patients with different stages of hepatosplenic schistosomiasis and 18 non-bilharzial normal controls were studied. Plasminogen, plasminogen activators (PA), tissue-type plasminogen activator (t-PA), urokinase-type plasminogen activator (u-PA), α2-antiplasmin (α2-AP), plasminogen activator inhibitor (PAI), fibrinogen/fibrin degradation products (FDP) and D-dimer were determined to elucidate the role of plasminogen activators and inhibitors in the pathogenesis of accelerated fibrinolysis in schistosomiasis. There was a progressive increase in the levels of PA, t-PA, u-PA, FDP and D-dimer indicating enhanced fibrinolytic activity with advancing disease. In addition, there was progressive decrease of plasminogen, α2-AP and PAI levels which might be due to decreased hepatic synthesis and/or increased peripheral consumption. These findings suggest that the pathogenesis of accelerated fibrinolysis in schistosomiasis is multifactorial, but may be due to the progressive increase in the levels of plasminogen activators. In addition, the increase of FDP and D-dimer levels are evidence of secondary fibrinolysis following thrombin generation.</description><subject>alpha-2-Antiplasmin - analysis</subject><subject>Biological and medical sciences</subject><subject>Diseases caused by trematodes</subject><subject>Female</subject><subject>Fibrin Fibrinogen Degradation Products - analysis</subject><subject>Fibrinolysis</subject><subject>Helminthic diseases</subject><subject>Hepatomegaly - blood</subject><subject>Hepatomegaly - etiology</subject><subject>Humans</subject><subject>Infectious diseases</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Parasitic diseases</subject><subject>Plasminogen - analysis</subject><subject>Plasminogen Activator Inhibitor 1 - analysis</subject><subject>Plasminogen Activators - analysis</subject><subject>Schistosomiases</subject><subject>Schistosomiasis mansoni - blood</subject><subject>Schistosomiasis mansoni - complications</subject><subject>Splenomegaly - blood</subject><subject>Splenomegaly - etiology</subject><issn>0957-5235</issn><issn>1473-5733</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1992</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kctOAyEUhonRaK0-gsksjLtRrmVYmsZbUuOmrglDDw5KhwrTGN9eaquuJCHk5P8OkO8gVBF8SbCSV7gsIimpiVKU0FLVZbNmD40Il6wWkrF9NMJKyFpQJo7Qcc6vG4Q38hAdEt4ohekIPc47qFZm6OIL9JB9rqKrjLUQIJkBFpXzbfJ9DJ-bzPdVB4WOeRWg97bKtvO5lHHpTQFO0IEzIcPp7hyj59ub-fS-nj3dPUyvZ7XlUjX1ZCGItNhNFG44dUApGCxaTqVUXDYcWgm0dY4aDBwWE2pM21BhpGMKBDg2Rhfbe1cpvq8hD3rpc_lzMD3EddaSCYIl5QVstqBNMecETq-SX5r0qQnWG5P6x6T-Nam_TZbWs90b63YJi7_GrbqSn-9yk60JLpne-vyLccEnqkxhjPgW-4hhgJTfwvoDku7AhKHT_82RfQGQXovi</recordid><startdate>199212</startdate><enddate>199212</enddate><creator>Omran, S A</creator><creator>Madkour, B A</creator><creator>Essawy, F M</creator><creator>Toima, S M</creator><creator>El Kaliouby, A H</creator><creator>Shams El Din, A A</creator><general>Lippincott-Raven Publishers</general><general>The Scientist</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>199212</creationdate><title>The pathogenesis of accelerated fibrinolysis in hepatosplenic schistosomiasis</title><author>Omran, S A ; Madkour, B A ; Essawy, F M ; Toima, S M ; El Kaliouby, A H ; Shams El Din, A A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4798-6d517c0f690842fe22ea05b427794784eb7e2bff2a0e4ed62aab825a7f39e5ef3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1992</creationdate><topic>alpha-2-Antiplasmin - analysis</topic><topic>Biological and medical sciences</topic><topic>Diseases caused by trematodes</topic><topic>Female</topic><topic>Fibrin Fibrinogen Degradation Products - analysis</topic><topic>Fibrinolysis</topic><topic>Helminthic diseases</topic><topic>Hepatomegaly - blood</topic><topic>Hepatomegaly - etiology</topic><topic>Humans</topic><topic>Infectious diseases</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Parasitic diseases</topic><topic>Plasminogen - analysis</topic><topic>Plasminogen Activator Inhibitor 1 - analysis</topic><topic>Plasminogen Activators - analysis</topic><topic>Schistosomiases</topic><topic>Schistosomiasis mansoni - blood</topic><topic>Schistosomiasis mansoni - complications</topic><topic>Splenomegaly - blood</topic><topic>Splenomegaly - etiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Omran, S A</creatorcontrib><creatorcontrib>Madkour, B A</creatorcontrib><creatorcontrib>Essawy, F M</creatorcontrib><creatorcontrib>Toima, S M</creatorcontrib><creatorcontrib>El Kaliouby, A H</creatorcontrib><creatorcontrib>Shams El Din, A A</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>Blood coagulation & fibrinolysis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Omran, S A</au><au>Madkour, B A</au><au>Essawy, F M</au><au>Toima, S M</au><au>El Kaliouby, A H</au><au>Shams El Din, A A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The pathogenesis of accelerated fibrinolysis in hepatosplenic schistosomiasis</atitle><jtitle>Blood coagulation & fibrinolysis</jtitle><addtitle>Blood Coagul Fibrinolysis</addtitle><date>1992-12</date><risdate>1992</risdate><volume>3</volume><issue>6</issue><spage>819</spage><epage>822</epage><pages>819-822</pages><issn>0957-5235</issn><eissn>1473-5733</eissn><abstract>Seventy patients with different stages of hepatosplenic schistosomiasis and 18 non-bilharzial normal controls were studied. Plasminogen, plasminogen activators (PA), tissue-type plasminogen activator (t-PA), urokinase-type plasminogen activator (u-PA), α2-antiplasmin (α2-AP), plasminogen activator inhibitor (PAI), fibrinogen/fibrin degradation products (FDP) and D-dimer were determined to elucidate the role of plasminogen activators and inhibitors in the pathogenesis of accelerated fibrinolysis in schistosomiasis. There was a progressive increase in the levels of PA, t-PA, u-PA, FDP and D-dimer indicating enhanced fibrinolytic activity with advancing disease. In addition, there was progressive decrease of plasminogen, α2-AP and PAI levels which might be due to decreased hepatic synthesis and/or increased peripheral consumption. These findings suggest that the pathogenesis of accelerated fibrinolysis in schistosomiasis is multifactorial, but may be due to the progressive increase in the levels of plasminogen activators. In addition, the increase of FDP and D-dimer levels are evidence of secondary fibrinolysis following thrombin generation.</abstract><cop>Philadelphia, PA</cop><pub>Lippincott-Raven Publishers</pub><pmid>1489902</pmid><doi>10.1097/00001721-199212000-00038</doi><tpages>4</tpages></addata></record> |
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| subjects | alpha-2-Antiplasmin - analysis Biological and medical sciences Diseases caused by trematodes Female Fibrin Fibrinogen Degradation Products - analysis Fibrinolysis Helminthic diseases Hepatomegaly - blood Hepatomegaly - etiology Humans Infectious diseases Male Medical sciences Parasitic diseases Plasminogen - analysis Plasminogen Activator Inhibitor 1 - analysis Plasminogen Activators - analysis Schistosomiases Schistosomiasis mansoni - blood Schistosomiasis mansoni - complications Splenomegaly - blood Splenomegaly - etiology |
| title | The pathogenesis of accelerated fibrinolysis in hepatosplenic schistosomiasis |
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