Gemfibrozil treatment of hypertriglyceridemia: Improvement on fibrinolysis without change of insulin resistance

The fibrinolytic and metabolic changes associated with gemfibrozil treatment of hypertriglyceridemia were evaluated in 16 patients with type IV hyperlipidemia by criteria of triglyceride levels >250 mg/dl and total cholesterol levels

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Veröffentlicht in:The American heart journal 1997-09, Vol.134 (3), p.565-571
Hauptverfasser: Jeng, Jing-Ren, Jeng, Chii-Yuan, Sheu, Wayne Huey-Herng, Lee, May Meei-Shyuan, Huang, Shyuh-Huei, Shieh, Shyh-Ming
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container_issue 3
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container_title The American heart journal
container_volume 134
creator Jeng, Jing-Ren
Jeng, Chii-Yuan
Sheu, Wayne Huey-Herng
Lee, May Meei-Shyuan
Huang, Shyuh-Huei
Shieh, Shyh-Ming
description The fibrinolytic and metabolic changes associated with gemfibrozil treatment of hypertriglyceridemia were evaluated in 16 patients with type IV hyperlipidemia by criteria of triglyceride levels >250 mg/dl and total cholesterol levels
doi_str_mv 10.1016/S0002-8703(97)70096-6
format Article
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The plasma triglyceride level was significantly lower (323 ± 71 vs 189 ± 57 mg/dl; p = 0.000) and high-density lipoprotein cholesterol level significantly higher (33.5 ± 4.6 vs 38.0 ± 6.7 mg/dl; p = 0.005) after 3 to 4 months of gemfibrozil treatment. However, the glucose and insulin metabolism measured by oral glucose challenge and insulin suppression tests showed no significant changes after gemfibrozil therapy. In contrast, plasma plasminogen activator inhibitor-1 antigen (36.9 ± 12.4 vs 27.3 ± 11.4 ng/ml; p = 0.008) and activity (15.5 ± 5.5 vs 11.8 ± 3.0 IU/ml; p = 0.009) and tissue plasminogen activator antigen (13.2 ± 4.0 vs 10.4 ± 3.7 ng/ml; p = 0.007) were significantly depressed, and tissue plasimogen activator activity (0.57 ± 0.31 vs 0.69 ± 0.38 IU/ml; p = 0.015) was significantly elevated by gemfibrozil. The data indicate that lowering plasma triglyceride and raising high-density lipoprotein cholesterol levels by gemfibrozil treatment also improved the fibrinolytic system without changes of insulin resistance and glucose intolerance in patients with isolated hypertriglyceridemia. (Am Heart J 1997;134:565-71.)</description><identifier>ISSN: 0002-8703</identifier><identifier>EISSN: 1097-6744</identifier><identifier>DOI: 10.1016/S0002-8703(97)70096-6</identifier><identifier>PMID: 9327717</identifier><identifier>CODEN: AHJOA2</identifier><language>eng</language><publisher>New York, NY: Mosby, Inc</publisher><subject>Adult ; Aged ; Biological and medical sciences ; Cholesterol, HDL - blood ; Female ; Fibrinolysis - drug effects ; Gemfibrozil - pharmacology ; Gemfibrozil - therapeutic use ; General and cellular metabolism. Vitamins ; Humans ; Hypertriglyceridemia - blood ; Hypertriglyceridemia - drug therapy ; Hypertriglyceridemia - physiopathology ; Hypolipidemic Agents - pharmacology ; Hypolipidemic Agents - therapeutic use ; Insulin Resistance ; Male ; Medical sciences ; Middle Aged ; Pharmacology. 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The plasma triglyceride level was significantly lower (323 ± 71 vs 189 ± 57 mg/dl; p = 0.000) and high-density lipoprotein cholesterol level significantly higher (33.5 ± 4.6 vs 38.0 ± 6.7 mg/dl; p = 0.005) after 3 to 4 months of gemfibrozil treatment. However, the glucose and insulin metabolism measured by oral glucose challenge and insulin suppression tests showed no significant changes after gemfibrozil therapy. In contrast, plasma plasminogen activator inhibitor-1 antigen (36.9 ± 12.4 vs 27.3 ± 11.4 ng/ml; p = 0.008) and activity (15.5 ± 5.5 vs 11.8 ± 3.0 IU/ml; p = 0.009) and tissue plasminogen activator antigen (13.2 ± 4.0 vs 10.4 ± 3.7 ng/ml; p = 0.007) were significantly depressed, and tissue plasimogen activator activity (0.57 ± 0.31 vs 0.69 ± 0.38 IU/ml; p = 0.015) was significantly elevated by gemfibrozil. The data indicate that lowering plasma triglyceride and raising high-density lipoprotein cholesterol levels by gemfibrozil treatment also improved the fibrinolytic system without changes of insulin resistance and glucose intolerance in patients with isolated hypertriglyceridemia. (Am Heart J 1997;134:565-71.)</description><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Cholesterol, HDL - blood</subject><subject>Female</subject><subject>Fibrinolysis - drug effects</subject><subject>Gemfibrozil - pharmacology</subject><subject>Gemfibrozil - therapeutic use</subject><subject>General and cellular metabolism. Vitamins</subject><subject>Humans</subject><subject>Hypertriglyceridemia - blood</subject><subject>Hypertriglyceridemia - drug therapy</subject><subject>Hypertriglyceridemia - physiopathology</subject><subject>Hypolipidemic Agents - pharmacology</subject><subject>Hypolipidemic Agents - therapeutic use</subject><subject>Insulin Resistance</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Pharmacology. 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Vitamins</topic><topic>Humans</topic><topic>Hypertriglyceridemia - blood</topic><topic>Hypertriglyceridemia - drug therapy</topic><topic>Hypertriglyceridemia - physiopathology</topic><topic>Hypolipidemic Agents - pharmacology</topic><topic>Hypolipidemic Agents - therapeutic use</topic><topic>Insulin Resistance</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Pharmacology. Drug treatments</topic><topic>Triglycerides - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jeng, Jing-Ren</creatorcontrib><creatorcontrib>Jeng, Chii-Yuan</creatorcontrib><creatorcontrib>Sheu, Wayne Huey-Herng</creatorcontrib><creatorcontrib>Lee, May Meei-Shyuan</creatorcontrib><creatorcontrib>Huang, Shyuh-Huei</creatorcontrib><creatorcontrib>Shieh, Shyh-Ming</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>The American heart journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jeng, Jing-Ren</au><au>Jeng, Chii-Yuan</au><au>Sheu, Wayne Huey-Herng</au><au>Lee, May Meei-Shyuan</au><au>Huang, Shyuh-Huei</au><au>Shieh, Shyh-Ming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gemfibrozil treatment of hypertriglyceridemia: Improvement on fibrinolysis without change of insulin resistance</atitle><jtitle>The American heart journal</jtitle><addtitle>Am Heart J</addtitle><date>1997-09-01</date><risdate>1997</risdate><volume>134</volume><issue>3</issue><spage>565</spage><epage>571</epage><pages>565-571</pages><issn>0002-8703</issn><eissn>1097-6744</eissn><coden>AHJOA2</coden><abstract>The fibrinolytic and metabolic changes associated with gemfibrozil treatment of hypertriglyceridemia were evaluated in 16 patients with type IV hyperlipidemia by criteria of triglyceride levels &gt;250 mg/dl and total cholesterol levels &lt;220 mg/dl. The plasma triglyceride level was significantly lower (323 ± 71 vs 189 ± 57 mg/dl; p = 0.000) and high-density lipoprotein cholesterol level significantly higher (33.5 ± 4.6 vs 38.0 ± 6.7 mg/dl; p = 0.005) after 3 to 4 months of gemfibrozil treatment. However, the glucose and insulin metabolism measured by oral glucose challenge and insulin suppression tests showed no significant changes after gemfibrozil therapy. In contrast, plasma plasminogen activator inhibitor-1 antigen (36.9 ± 12.4 vs 27.3 ± 11.4 ng/ml; p = 0.008) and activity (15.5 ± 5.5 vs 11.8 ± 3.0 IU/ml; p = 0.009) and tissue plasminogen activator antigen (13.2 ± 4.0 vs 10.4 ± 3.7 ng/ml; p = 0.007) were significantly depressed, and tissue plasimogen activator activity (0.57 ± 0.31 vs 0.69 ± 0.38 IU/ml; p = 0.015) was significantly elevated by gemfibrozil. The data indicate that lowering plasma triglyceride and raising high-density lipoprotein cholesterol levels by gemfibrozil treatment also improved the fibrinolytic system without changes of insulin resistance and glucose intolerance in patients with isolated hypertriglyceridemia. (Am Heart J 1997;134:565-71.)</abstract><cop>New York, NY</cop><pub>Mosby, Inc</pub><pmid>9327717</pmid><doi>10.1016/S0002-8703(97)70096-6</doi><tpages>7</tpages></addata></record>
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subjects Adult
Aged
Biological and medical sciences
Cholesterol, HDL - blood
Female
Fibrinolysis - drug effects
Gemfibrozil - pharmacology
Gemfibrozil - therapeutic use
General and cellular metabolism. Vitamins
Humans
Hypertriglyceridemia - blood
Hypertriglyceridemia - drug therapy
Hypertriglyceridemia - physiopathology
Hypolipidemic Agents - pharmacology
Hypolipidemic Agents - therapeutic use
Insulin Resistance
Male
Medical sciences
Middle Aged
Pharmacology. Drug treatments
Triglycerides - blood
title Gemfibrozil treatment of hypertriglyceridemia: Improvement on fibrinolysis without change of insulin resistance
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