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Article: Atorvastatin lowers C-reactive protein and improves endothelium-dependent vasodilation in type 2 diabetes mellitus

TitleAtorvastatin lowers C-reactive protein and improves endothelium-dependent vasodilation in type 2 diabetes mellitus
Authors
Issue Date2002
PublisherThe Endocrine Society. The Journal's web site is located at http://jcem.endojournals.org
Citation
Journal Of Clinical Endocrinology And Metabolism, 2002, v. 87 n. 2, p. 563-568 How to Cite?
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 ± 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.
Persistent Identifierhttp://hdl.handle.net/10722/78028
ISSN
2013 Impact Factor: 6.310
2013 SCImago Journal Rankings: 3.169
ISI Accession Number ID
References

 

Author Affiliations
  1. The University of Hong Kong
  2. Queen Mary Hospital Hong Kong
DC FieldValueLanguage
dc.contributor.authorTan, KCBen_HK
dc.contributor.authorChow, WSen_HK
dc.contributor.authorTam, SCFen_HK
dc.contributor.authorAi, VHGen_HK
dc.contributor.authorLam, CHLen_HK
dc.contributor.authorLam, KSLen_HK
dc.date.accessioned2010-09-06T07:38:22Z-
dc.date.available2010-09-06T07:38:22Z-
dc.date.issued2002en_HK
dc.identifier.citationJournal Of Clinical Endocrinology And Metabolism, 2002, v. 87 n. 2, p. 563-568en_HK
dc.identifier.issn0021-972Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/78028-
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.en_HK
dc.languageengen_HK
dc.publisherThe Endocrine Society. The Journal's web site is located at http://jcem.endojournals.orgen_HK
dc.relation.ispartofJournal of Clinical Endocrinology and Metabolismen_HK
dc.rightsJournal of Clinical Endocrinology and Metabolism. Copyright © The Endocrine Society.en_HK
dc.subject.meshAnti-Inflammatory Agents - therapeutic useen_HK
dc.subject.meshAnticholesteremic Agents - therapeutic useen_HK
dc.subject.meshC-Reactive Protein - analysis - antagonists & inhibitorsen_HK
dc.subject.meshCholesterol - blooden_HK
dc.subject.meshDiabetes Mellitus, Type 2 - drug therapy - physiopathology - ultrasonographyen_HK
dc.subject.meshDouble-Blind Methoden_HK
dc.subject.meshEndothelium, Vascular - drug effects - physiopathology - ultrasonographyen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHeptanoic Acids - therapeutic useen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshPyrroles - therapeutic useen_HK
dc.subject.meshReference Valuesen_HK
dc.subject.meshTriglycerides - antagonists & inhibitors - blooden_HK
dc.subject.meshVasodilation - drug effectsen_HK
dc.titleAtorvastatin lowers C-reactive protein and improves endothelium-dependent vasodilation in type 2 diabetes mellitusen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-972X&volume=87&spage=563&epage=568&date=2002&atitle=Atorvastatin+lowers+C-reactive+protein+and+improves+endothelium-dependent+vasodilation+in+type+2+diabetes+mellitusen_HK
dc.identifier.emailTan, KCB:kcbtan@hku.hken_HK
dc.identifier.emailLam, KSL:ksllam@hku.hken_HK
dc.identifier.authorityTan, KCB=rp00402en_HK
dc.identifier.authorityLam, KSL=rp00343en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1210/jc.87.2.563en_HK
dc.identifier.pmid11836286en_HK
dc.identifier.scopuseid_2-s2.0-0036172495en_HK
dc.identifier.hkuros66537en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036172495&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume87en_HK
dc.identifier.issue2en_HK
dc.identifier.spage563en_HK
dc.identifier.epage568en_HK
dc.identifier.isiWOS:000174351500021-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTan, KCB=8082703100en_HK
dc.identifier.scopusauthoridChow, WS=7402281153en_HK
dc.identifier.scopusauthoridTam, SCF=7202037323en_HK
dc.identifier.scopusauthoridAi, VHG=6603342063en_HK
dc.identifier.scopusauthoridLam, CHL=14119182300en_HK
dc.identifier.scopusauthoridLam, KSL=8082870600en_HK

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