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
2011 Impact Factor: 5.967
2011 SCImago Journal Rankings: 0.579
DOIhttp://dx.doi.org/10.1210/jc.87.2.563
ISI Accession Number IDWOS:000174351500021
ReferencesReferences in Scopus
DC Field
Value
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
2011 Impact Factor: 5.967
2011 SCImago Journal Rankings: 0.579
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
Author Affiliations
  1. The University of Hong Kong
  2. Queen Mary Hospital Hong Kong