pubmed-article:17087362 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17087362 | lifeskim:mentions | umls-concept:C0220847 | lld:lifeskim |
pubmed-article:17087362 | lifeskim:mentions | umls-concept:C0021311 | lld:lifeskim |
pubmed-article:17087362 | lifeskim:mentions | umls-concept:C0030705 | lld:lifeskim |
pubmed-article:17087362 | lifeskim:mentions | umls-concept:C0087111 | lld:lifeskim |
pubmed-article:17087362 | lifeskim:mentions | umls-concept:C0085504 | lld:lifeskim |
pubmed-article:17087362 | lifeskim:mentions | umls-concept:C0439849 | lld:lifeskim |
pubmed-article:17087362 | lifeskim:mentions | umls-concept:C2003888 | lld:lifeskim |
pubmed-article:17087362 | lifeskim:mentions | umls-concept:C0023779 | lld:lifeskim |
pubmed-article:17087362 | lifeskim:mentions | umls-concept:C0577631 | lld:lifeskim |
pubmed-article:17087362 | lifeskim:mentions | umls-concept:C0449258 | lld:lifeskim |
pubmed-article:17087362 | lifeskim:mentions | umls-concept:C0445223 | lld:lifeskim |
pubmed-article:17087362 | lifeskim:mentions | umls-concept:C1552599 | lld:lifeskim |
pubmed-article:17087362 | lifeskim:mentions | umls-concept:C1704787 | lld:lifeskim |
pubmed-article:17087362 | pubmed:issue | 8 | lld:pubmed |
pubmed-article:17087362 | pubmed:dateCreated | 2006-11-7 | lld:pubmed |
pubmed-article:17087362 | 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. | lld:pubmed |
pubmed-article:17087362 | pubmed:language | eng | lld:pubmed |
pubmed-article:17087362 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17087362 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:17087362 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17087362 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17087362 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17087362 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17087362 | pubmed:month | Aug | lld:pubmed |
pubmed-article:17087362 | pubmed:issn | 0016-254X | lld:pubmed |
pubmed-article:17087362 | pubmed:author | pubmed-author:SawayamaYasun... | lld:pubmed |
pubmed-article:17087362 | pubmed:author | pubmed-author:HayashiJunJ | lld:pubmed |
pubmed-article:17087362 | pubmed:author | pubmed-author:FurusyoNorihi... | lld:pubmed |
pubmed-article:17087362 | pubmed:author | pubmed-author:MaedaShinjiS | lld:pubmed |
pubmed-article:17087362 | pubmed:author | pubmed-author:OkadaKyokoK | lld:pubmed |
pubmed-article:17087362 | pubmed:author | pubmed-author:OhnishiHachir... | lld:pubmed |
pubmed-article:17087362 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17087362 | pubmed:volume | 97 | lld:pubmed |
pubmed-article:17087362 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17087362 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17087362 | pubmed:pagination | 245-55 | lld:pubmed |
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pubmed-article:17087362 | pubmed:year | 2006 | lld:pubmed |
pubmed-article:17087362 | pubmed:articleTitle | Both hepatitis C virus and Chlamydia pneumoniae infection are related to the progression of carotid atherosclerosis in patients undergoing lipid lowering therapy. | lld:pubmed |
pubmed-article:17087362 | pubmed:affiliation | Department of General Medicine, Kyushu University Hospital. | lld:pubmed |
pubmed-article:17087362 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17087362 | pubmed:publicationType | Randomized Controlled Trial | lld:pubmed |
pubmed-article:17087362 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:17087362 | lld:pubmed |