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Article: Atorvastatin lowers C-reactive protein and improves endothelium-dependent vasodilation in type 2 diabetes mellitus
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TitleAtorvastatin lowers C-reactive protein and improves endothelium-dependent vasodilation in type 2 diabetes mellitus
 
AuthorsTan, KCB1 2
Chow, WS2
Tam, SCF2
Ai, VHG1
Lam, CHL2
Lam, KSL1
 
Issue Date2002
 
PublisherThe Endocrine Society. The Journal's web site is located at http://jcem.endojournals.org
 
CitationJournal Of Clinical Endocrinology And Metabolism, 2002, v. 87 n. 2, p. 563-568 [How to Cite?]
DOI: http://dx.doi.org/10.1210/jc.87.2.563
 
AbstractEndothelial dysfunction is frequently found in diabetic subjects. This study was performed to investigate whether atorvastatin therapy was able to reverse endothelial dysfunction in type 2 diabetes and, if so, whether the effect was due to its antiinflammatory action. Eighty patients (baseline low density lipoprotein, 4.37 ± 0.71 mmol/liter) were randomized to atorvastatin (10 mg daily for 3 months, followed by 20 mg daily for 3 months) or placebo in a double blind study. Endothelial function was assessed by high resolution vascular ultrasound, and high sensitivity C-reactive protein (CRP) was assessed by immunoturbidimetric assay. Diabetic patients had higher CRP (P < 0.01) than matched nondiabetic controls, and both endothelium-dependent and independent vasodilation were impaired (P < 0.01). Atorvastatin (10 and 20 rog) lowered plasma cholesterol by 32.9% and 38.0%, triglyceride by 15.4% and 23.1%, and low density lipoprotein by 43.4% and 50.1%, respectively. At 6 months, plasma CRP decreased in the atorvastatin group compared with baseline (P < 0.05). Endothelium-dependent vasodilation improved in the atorvastatin group compared with the placebo group (P < 0.05). The percent change in endothelium-dependent vasodilation at 6 months correlated with the percent change in CRP (r = -0.44; P < 0.05), but not with changes in plasma lipids. In conclusion, treatment with atorvastatin in type 2 diabetes led to a significant improvement in endothelium-dependent vasodilation, which might be partly related to its anti-inflammatory effect.
 
ISSN0021-972X
2012 Impact Factor: 6.43
2012 SCImago Journal Rankings: 2.555
 
DOIhttp://dx.doi.org/10.1210/jc.87.2.563
 
ISI Accession Number IDWOS:000174351500021
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorTan, KCB
 
dc.contributor.authorChow, WS
 
dc.contributor.authorTam, SCF
 
dc.contributor.authorAi, VHG
 
dc.contributor.authorLam, CHL
 
dc.contributor.authorLam, KSL
 
dc.date.accessioned2010-09-06T07:38:22Z
 
dc.date.available2010-09-06T07:38:22Z
 
dc.date.issued2002
 
dc.description.abstractEndothelial dysfunction is frequently found in diabetic subjects. This study was performed to investigate whether atorvastatin therapy was able to reverse endothelial dysfunction in type 2 diabetes and, if so, whether the effect was due to its antiinflammatory action. Eighty patients (baseline low density lipoprotein, 4.37 ± 0.71 mmol/liter) were randomized to atorvastatin (10 mg daily for 3 months, followed by 20 mg daily for 3 months) or placebo in a double blind study. Endothelial function was assessed by high resolution vascular ultrasound, and high sensitivity C-reactive protein (CRP) was assessed by immunoturbidimetric assay. Diabetic patients had higher CRP (P < 0.01) than matched nondiabetic controls, and both endothelium-dependent and independent vasodilation were impaired (P < 0.01). Atorvastatin (10 and 20 rog) lowered plasma cholesterol by 32.9% and 38.0%, triglyceride by 15.4% and 23.1%, and low density lipoprotein by 43.4% and 50.1%, respectively. At 6 months, plasma CRP decreased in the atorvastatin group compared with baseline (P < 0.05). Endothelium-dependent vasodilation improved in the atorvastatin group compared with the placebo group (P < 0.05). The percent change in endothelium-dependent vasodilation at 6 months correlated with the percent change in CRP (r = -0.44; P < 0.05), but not with changes in plasma lipids. In conclusion, treatment with atorvastatin in type 2 diabetes led to a significant improvement in endothelium-dependent vasodilation, which might be partly related to its anti-inflammatory effect.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationJournal Of Clinical Endocrinology And Metabolism, 2002, v. 87 n. 2, p. 563-568 [How to Cite?]
DOI: http://dx.doi.org/10.1210/jc.87.2.563
 
dc.identifier.doihttp://dx.doi.org/10.1210/jc.87.2.563
 
dc.identifier.epage568
 
dc.identifier.hkuros66537
 
dc.identifier.isiWOS:000174351500021
 
dc.identifier.issn0021-972X
2012 Impact Factor: 6.43
2012 SCImago Journal Rankings: 2.555
 
dc.identifier.issue2
 
dc.identifier.openurl
 
dc.identifier.pmid11836286
 
dc.identifier.scopuseid_2-s2.0-0036172495
 
dc.identifier.spage563
 
dc.identifier.urihttp://hdl.handle.net/10722/78028
 
dc.identifier.volume87
 
dc.languageeng
 
dc.publisherThe Endocrine Society. The Journal's web site is located at http://jcem.endojournals.org
 
dc.publisher.placeUnited States
 
dc.relation.ispartofJournal of Clinical Endocrinology and Metabolism
 
dc.relation.referencesReferences in Scopus
 
dc.rightsJournal of Clinical Endocrinology and Metabolism. Copyright © The Endocrine Society.
 
dc.subject.meshAnti-Inflammatory Agents - therapeutic use
 
dc.subject.meshAnticholesteremic Agents - therapeutic use
 
dc.subject.meshC-Reactive Protein - analysis - antagonists & inhibitors
 
dc.subject.meshCholesterol - blood
 
dc.subject.meshDiabetes Mellitus, Type 2 - drug therapy - physiopathology - ultrasonography
 
dc.subject.meshDouble-Blind Method
 
dc.subject.meshEndothelium, Vascular - drug effects - physiopathology - ultrasonography
 
dc.subject.meshFemale
 
dc.subject.meshHeptanoic Acids - therapeutic use
 
dc.subject.meshHumans
 
dc.subject.meshMale
 
dc.subject.meshMiddle Aged
 
dc.subject.meshPyrroles - therapeutic use
 
dc.subject.meshReference Values
 
dc.subject.meshTriglycerides - antagonists & inhibitors - blood
 
dc.subject.meshVasodilation - drug effects
 
dc.titleAtorvastatin lowers C-reactive protein and improves endothelium-dependent vasodilation in type 2 diabetes mellitus
 
dc.typeArticle
 
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<contributor.author>Lam, KSL</contributor.author>
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<description.abstract>Endothelial dysfunction is frequently found in diabetic subjects. This study was performed to investigate whether atorvastatin therapy was able to reverse endothelial dysfunction in type 2 diabetes and, if so, whether the effect was due to its antiinflammatory action. Eighty patients (baseline low density lipoprotein, 4.37 &#177; 0.71 mmol/liter) were randomized to atorvastatin (10 mg daily for 3 months, followed by 20 mg daily for 3 months) or placebo in a double blind study. Endothelial function was assessed by high resolution vascular ultrasound, and high sensitivity C-reactive protein (CRP) was assessed by immunoturbidimetric assay. Diabetic patients had higher CRP (P &lt; 0.01) than matched nondiabetic controls, and both endothelium-dependent and independent vasodilation were impaired (P &lt; 0.01). Atorvastatin (10 and 20 rog) lowered plasma cholesterol by 32.9% and 38.0%, triglyceride by 15.4% and 23.1%, and low density lipoprotein by 43.4% and 50.1%, respectively. At 6 months, plasma CRP decreased in the atorvastatin group compared with baseline (P &lt; 0.05). Endothelium-dependent vasodilation improved in the atorvastatin group compared with the placebo group (P &lt; 0.05). The percent change in endothelium-dependent vasodilation at 6 months correlated with the percent change in CRP (r = -0.44; P &lt; 0.05), but not with changes in plasma lipids. In conclusion, treatment with atorvastatin in type 2 diabetes led to a significant improvement in endothelium-dependent vasodilation, which might be partly related to its anti-inflammatory effect.</description.abstract>
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<subject.mesh>Female</subject.mesh>
<subject.mesh>Heptanoic Acids - therapeutic use</subject.mesh>
<subject.mesh>Humans</subject.mesh>
<subject.mesh>Male</subject.mesh>
<subject.mesh>Middle Aged</subject.mesh>
<subject.mesh>Pyrroles - therapeutic use</subject.mesh>
<subject.mesh>Reference Values</subject.mesh>
<subject.mesh>Triglycerides - antagonists &amp; inhibitors - blood</subject.mesh>
<subject.mesh>Vasodilation - drug effects</subject.mesh>
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Author Affiliations
  1. The University of Hong Kong
  2. Queen Mary Hospital Hong Kong