Source:http://linkedlifedata.com/resource/pubmed/id/17087362
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
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pubmed:dateCreated |
2006-11-7
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pubmed:abstractText |
Recent experimental and epidemiological findings suggest that infectious agents may play a role in the development and progression of atherosclerosis. We previously reported that Chlamydia pneumoniae (C. pneumoniae) infection reduces the effectiveness of lipid-lowering therapy for carotid atherosclerosis and that this micro-organism may play a role in the progression of atherosclerosis. In this study, we investigated the possible association between hepatitis C virus (HCV) infection and carotid arteriosclerosis. A total of 165 asymptomatic hypercholesterolemic patients were randomized to receive probucol (500 mg/day, n=82) or pravastatin (10 mg/day, n=83) and were followed for 2 years. The 2-year change of the maximum common carotid artery intima-media thickness (Max-IMT) was the primary endpoint, while the Max-IMT and the incidence of major cardiovascular events were secondary endpoint. All serum samples were tested for antibody to HCV (anti-HCV) by enzyme-linked immunosorbent assay (ELISA), and all anti-HCV-positive samples were assayed for HCV RNA. Patients without HCV infection (n=25) showed a significant reduction of Max-IMT (-10.9%) (p<0.0001), while a small decrease of Max-IMT was noted in the patients with HCV infection (n=25) (-0. 3%). Significant differences in the reduction of serum total cholesterol and LDL cholesterol were found between patients with and without HCV infection (both p<0.0001). No significant difference in therapeutic effect was noted between the probucol and the pravastatin groups. After adjustment for confounding risk factors, both C. pneumoniae infection and anti-HCV positivity were associated with a greater risk of an increase in Max-IMT (8.5635 [1.3738-15.7532], p<0.05, 9.5040 [0.2886-18.7194], p<0.05, respectively). These findings suggest that both chronic HCV infection and C. pneumoniae infection can reduce the effectiveness of lipid-lowering therapy for carotid atherosclerosis, and that the HCV may play a role in the progression of atherosclerosis in HCV infected patients.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0016-254X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
97
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
245-55
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pubmed:meshHeading |
pubmed-meshheading:17087362-Adult,
pubmed-meshheading:17087362-Aged,
pubmed-meshheading:17087362-Aged, 80 and over,
pubmed-meshheading:17087362-Anticholesteremic Agents,
pubmed-meshheading:17087362-Carotid Artery Diseases,
pubmed-meshheading:17087362-Chlamydophila Infections,
pubmed-meshheading:17087362-Chlamydophila pneumoniae,
pubmed-meshheading:17087362-Disease Progression,
pubmed-meshheading:17087362-Female,
pubmed-meshheading:17087362-Hepatitis C,
pubmed-meshheading:17087362-Humans,
pubmed-meshheading:17087362-Male,
pubmed-meshheading:17087362-Middle Aged,
pubmed-meshheading:17087362-Pravastatin,
pubmed-meshheading:17087362-Probucol
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pubmed:year |
2006
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pubmed:articleTitle |
Both hepatitis C virus and Chlamydia pneumoniae infection are related to the progression of carotid atherosclerosis in patients undergoing lipid lowering therapy.
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pubmed:affiliation |
Department of General Medicine, Kyushu University Hospital.
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pubmed:publicationType |
Journal Article,
Randomized Controlled Trial,
Research Support, Non-U.S. Gov't
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