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Drugs affecting plasma fibrinogen levels
Current knowledge indicates that high plasma levels of fibrinogen help predict stroke and myocardial infarction. It is known that plasma fibrinogen is synthesized in the liver, that interleukin-6 (IL-6) affects this synthesis, and that, when exposed to appropriate stimuli, monocytes generate a varie...
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Published in: | Cardiovascular drugs and therapy 1992-02, Vol.6 (1), p.25-27 |
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container_title | Cardiovascular drugs and therapy |
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creator | DI MINNO, G MANCINI, M |
description | Current knowledge indicates that high plasma levels of fibrinogen help predict stroke and myocardial infarction. It is known that plasma fibrinogen is synthesized in the liver, that interleukin-6 (IL-6) affects this synthesis, and that, when exposed to appropriate stimuli, monocytes generate a variety of monokines, including IL-6. It is also known that prolonged administration of N-3 fatty acids, ticlopidine, fibrates, pentoxifylline, or alcohol lower plasma fibrinogen levels. The mechanism(s) involved in this effect are poorly understood. However, in view of the role of IL-6 and monocytes in the regulation of plasma fibrinogen levels, it is conceivable that the lowering effect of these drugs involves effects on some steps of the regulatory machinery. In addition to fibrinogen, IL-6 regulates the synthesis of other acute-phase proteins. This raises the question of whether high plasma fibrinogen levels do reflect the response of an acute-phase reactant to the severity of the atherosclerotic vascular damage taking place. Current evidence is inconclusive with respect to this possibility. On the other hand, the epidemiological data available indicate that measurements of plasma fibrinogen should be included in the cardiovascular risk-factor profile. In view of this, we believe that information emerging from population-based studies in which plasma fibrinogen is measured is important to identify appropriate directions to be followed to address unsolved issues in the area. |
doi_str_mv | 10.1007/BF00050913 |
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It is known that plasma fibrinogen is synthesized in the liver, that interleukin-6 (IL-6) affects this synthesis, and that, when exposed to appropriate stimuli, monocytes generate a variety of monokines, including IL-6. It is also known that prolonged administration of N-3 fatty acids, ticlopidine, fibrates, pentoxifylline, or alcohol lower plasma fibrinogen levels. The mechanism(s) involved in this effect are poorly understood. However, in view of the role of IL-6 and monocytes in the regulation of plasma fibrinogen levels, it is conceivable that the lowering effect of these drugs involves effects on some steps of the regulatory machinery. In addition to fibrinogen, IL-6 regulates the synthesis of other acute-phase proteins. This raises the question of whether high plasma fibrinogen levels do reflect the response of an acute-phase reactant to the severity of the atherosclerotic vascular damage taking place. Current evidence is inconclusive with respect to this possibility. On the other hand, the epidemiological data available indicate that measurements of plasma fibrinogen should be included in the cardiovascular risk-factor profile. In view of this, we believe that information emerging from population-based studies in which plasma fibrinogen is measured is important to identify appropriate directions to be followed to address unsolved issues in the area.</description><identifier>ISSN: 0920-3206</identifier><identifier>EISSN: 1573-7241</identifier><identifier>DOI: 10.1007/BF00050913</identifier><identifier>PMID: 1576094</identifier><identifier>CODEN: CDTHET</identifier><language>eng</language><publisher>Dordrecht: Springer</publisher><subject>Biological and medical sciences ; Blood. Blood coagulation. Reticuloendothelial system ; Fibrinogen - analysis ; Humans ; Interleukin-6 - pharmacology ; Medical sciences ; Pharmacology. 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It is known that plasma fibrinogen is synthesized in the liver, that interleukin-6 (IL-6) affects this synthesis, and that, when exposed to appropriate stimuli, monocytes generate a variety of monokines, including IL-6. It is also known that prolonged administration of N-3 fatty acids, ticlopidine, fibrates, pentoxifylline, or alcohol lower plasma fibrinogen levels. The mechanism(s) involved in this effect are poorly understood. However, in view of the role of IL-6 and monocytes in the regulation of plasma fibrinogen levels, it is conceivable that the lowering effect of these drugs involves effects on some steps of the regulatory machinery. In addition to fibrinogen, IL-6 regulates the synthesis of other acute-phase proteins. This raises the question of whether high plasma fibrinogen levels do reflect the response of an acute-phase reactant to the severity of the atherosclerotic vascular damage taking place. Current evidence is inconclusive with respect to this possibility. On the other hand, the epidemiological data available indicate that measurements of plasma fibrinogen should be included in the cardiovascular risk-factor profile. In view of this, we believe that information emerging from population-based studies in which plasma fibrinogen is measured is important to identify appropriate directions to be followed to address unsolved issues in the area.</description><subject>Biological and medical sciences</subject><subject>Blood. Blood coagulation. Reticuloendothelial system</subject><subject>Fibrinogen - analysis</subject><subject>Humans</subject><subject>Interleukin-6 - pharmacology</subject><subject>Medical sciences</subject><subject>Pharmacology. 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Blood coagulation. Reticuloendothelial system</topic><topic>Fibrinogen - analysis</topic><topic>Humans</topic><topic>Interleukin-6 - pharmacology</topic><topic>Medical sciences</topic><topic>Pharmacology. Drug treatments</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>DI MINNO, G</creatorcontrib><creatorcontrib>MANCINI, M</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>Cardiovascular drugs and therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>DI MINNO, G</au><au>MANCINI, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Drugs affecting plasma fibrinogen levels</atitle><jtitle>Cardiovascular drugs and therapy</jtitle><addtitle>Cardiovasc Drugs Ther</addtitle><date>1992-02-01</date><risdate>1992</risdate><volume>6</volume><issue>1</issue><spage>25</spage><epage>27</epage><pages>25-27</pages><issn>0920-3206</issn><eissn>1573-7241</eissn><coden>CDTHET</coden><abstract>Current knowledge indicates that high plasma levels of fibrinogen help predict stroke and myocardial infarction. It is known that plasma fibrinogen is synthesized in the liver, that interleukin-6 (IL-6) affects this synthesis, and that, when exposed to appropriate stimuli, monocytes generate a variety of monokines, including IL-6. It is also known that prolonged administration of N-3 fatty acids, ticlopidine, fibrates, pentoxifylline, or alcohol lower plasma fibrinogen levels. The mechanism(s) involved in this effect are poorly understood. However, in view of the role of IL-6 and monocytes in the regulation of plasma fibrinogen levels, it is conceivable that the lowering effect of these drugs involves effects on some steps of the regulatory machinery. In addition to fibrinogen, IL-6 regulates the synthesis of other acute-phase proteins. This raises the question of whether high plasma fibrinogen levels do reflect the response of an acute-phase reactant to the severity of the atherosclerotic vascular damage taking place. Current evidence is inconclusive with respect to this possibility. On the other hand, the epidemiological data available indicate that measurements of plasma fibrinogen should be included in the cardiovascular risk-factor profile. In view of this, we believe that information emerging from population-based studies in which plasma fibrinogen is measured is important to identify appropriate directions to be followed to address unsolved issues in the area.</abstract><cop>Dordrecht</cop><pub>Springer</pub><pmid>1576094</pmid><doi>10.1007/BF00050913</doi><tpages>3</tpages></addata></record> |
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subjects | Biological and medical sciences Blood. Blood coagulation. Reticuloendothelial system Fibrinogen - analysis Humans Interleukin-6 - pharmacology Medical sciences Pharmacology. Drug treatments |
title | Drugs affecting plasma fibrinogen levels |
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