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Effect For Coenzyme Q10 To Prevent Hepatic Injury From Atorvastatin And Rosuvastatin

Posted on:2013-12-18Degree:MasterType:Thesis
Country:ChinaCandidate:X L ZhaoFull Text:PDF
GTID:2234330374959040Subject:Internal Medicine
Abstract/Summary:PDF Full Text Request
Objective: To evaluate the impact of double dose of stains on liverfunctions of the patients who had taken common dose of statins beforetreatment. And to determine whether coenzyme Q10supplementation wouldprevent statin-induced hepatopathy, and observe if it was associated with theanti-inflammatory action of the coenzyme Q10.Methods:The patients who were diagnosed as coronary heart disease inthe Second Hospital of Hebei Medical University from July2011to Februray2012were collected. All patients had taken common dose of statins beforetreatment, and no elevation of the transaminase levels of them were observed.A total of69patients including41male and28female were randomly dividedinto two groups: statins group (atorvastatin40mg once per night orrosuvastatin20mg once per night), the patients were42-74(61.6±9.0) yearsold.; statins and coenzyme Q10group (atorvastatin40mg once per night andcoenzyme Q1020mg Bid or rosuvastatin20mg once per night and coenzymeQ1020mg Bid), the patients were40-76(59.4±9.2) years old. They were allgiven routine treatment. The liver functions, blood routine and high-sensitivityC-reactive protein (hs-CRP) of the patients were measured beforeadministration and1week and4weeks after administration. Statins wasdiscontinued when transaminase levels rised to three times the upper limit ofnormal. Exclusion criteria: serious diseases such as acute and serious infection,electrolyte imbalance, serious endocrine disorders, serious metabolicabnormalities of the kidney. The patients with obviously abnormal liverfunction (aspartate aminotransferase AST, alanine aminotransferase ALT>3times the upper limit of normal), and those allergic to statins or the patientswith other definite contradiction were excluded. The data were analyzed bySSPS13.0statistical software. Results:Compared with the level before therapy, the ALT levels ofstatins group at1week after treatment elevated significantly; while the ALTlevels at1month after treatment were slightly declined compared with theALT levels at1week after treatment. In the statins and coenzyme Q10group,ALT levels increased significantly after1week’s treatment, while ALT levelsreduced to the levels before therapy at1month after treatment. No statisticalsignificance of ALT levels were observed between statins group and statinsand coenzyme Q10group at three time points. Compared with the level beforetherapy, AST of statins group at1week after treatment increased significantly;while AST at1month after treatment were not significantly different fromAST after1week’s treatment. The AST levels of statins and coenzyme Q10group after treatment were not significantly different from the AST levelsbefore therapy. No statistical significance of AST levels was observed in thetwo groups at three time points. The hs-CRP levels after treatment weresignificantly lower than the levels before therapy in both groups. No statisticalsignificance of hs-CRP levels was observed between statins group and statinsand coenzyme Q10group at any time points. The WBC levels of statins groupafter treatment were not significantly different from the levels before therapy.No significant difference of WBC levels was observed between statins groupand statins and coenzyme Q10group at three time points. The level of ALT wastwo times the upper limit of normal after treatment in6.7%patients of statinsgroup, while there were16.7%patients whose ALT levels were three timesthe upper limit of normal. ALT levels were two times the upper limit of normalin4.0%patients of statins group after1month’s treatment. ALT levels in19.4%patients of statins and coenzyme Q10were two times the upper limit ofnormal after1week’s treatment, while there were19.4%of the patients whoseALT levels were three times the upper limit of normal. ALT levels in3.4%patients of statins group were three times the upper limit of normal after1month’s treatment. AST levels in6.7%patients of statins group were twotimes the upper limit of normal after1week’s treatment, while there were3.3%of the patients whose AST levels were three times the upper limit of normal. AST levels in4.1%patients of statins group were two times the upperlimit of normal after1month’s treatment. AST levels in8.3%patients ofstatins and coenzyme Q10were two times the upper limit of normal at1weekafter treatment, while there were13.9%of the patients whose AST levels werethree times the upper limit of normal. The patients that had discontinued thestatin were not included in the patients that transaminase levels rised to threetimes the upper limit of normal at1month after treatment. In statins group andstatins and coenzyme Q10group, the proportion of patients whose ALT or ASTlevels increased2times or3times were not different significantly.Conclusion: The patients who had taken common dose of statins beforetreatment were given double dose of statins now. Hepatic enzymes levels weretwo times the upper limit of normal in18.2%of the patients, while13.6%patients’ hepatic enzymes levels were three times the upper limit of normal at1week after treatment. In1.85%patients, hepatic enzymes level three timesthe upper limit of normal at1month after treatment was observed. Doubledose of statins combined with regular doses of coenzyme Q10could preventthe statin-induced hepatopathy, but it was not different significantly. Statins atdouble dosage could effectively reduce high-sensitivity C-reactive protein(hs-CRR) levels, and it was not associated with the anti-inflammatory actionof the coenzyme Q10.
Keywords/Search Tags:atorvastatin, rosuvastatin, coenzyme Q10, liver injury, prevention
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