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• W2016253197 abstract "We measured plasma markers of cholesterol synthesis (lathosterol) and absorption (campesterol, sitosterol, and cholestanol) in order to compare the effects of maximal doses of rosuvastatin with atorvastatin and investigate the basis for the significant individual variation in lipid lowering response to statin therapy. Measurements were performed in participants (n = 135) at baseline and after 6 weeks on either rosuvastatin (40 mg/day) or atorvastatin (80 mg/day) therapy. Plasma sterols were measured using gas-liquid chromatography. Rosuvastatin and atorvastatin significantly (P < 0.001) altered plasma total cholesterol (C) levels by −40%, and the ratios of lathosterol/C by −64% and −68%, and campesterol/C by +52% and +72%, respectively, with significant differences (P < 0.001) between the treatment groups for the latter parameter. When using absolute values of these markers, subjects with the greatest reductions in both synthesis (lathosterol) and absorption (campesterol) had significantly greater reductions in total C than subjects in whom the converse was true (−46% versus −34%, P = 0.001), with similar effects for LDL-C. Rosuvastatin and atorvastatin decreased markers of cholesterol synthesis and increased markers of fractional cholesterol absorption, with rosuvastatin having significantly less effect on the latter parameter than atorvastatin. In addition, alterations in absolute values of plasma sterols correlated with the cholesterol lowering response. We measured plasma markers of cholesterol synthesis (lathosterol) and absorption (campesterol, sitosterol, and cholestanol) in order to compare the effects of maximal doses of rosuvastatin with atorvastatin and investigate the basis for the significant individual variation in lipid lowering response to statin therapy. Measurements were performed in participants (n = 135) at baseline and after 6 weeks on either rosuvastatin (40 mg/day) or atorvastatin (80 mg/day) therapy. Plasma sterols were measured using gas-liquid chromatography. Rosuvastatin and atorvastatin significantly (P < 0.001) altered plasma total cholesterol (C) levels by −40%, and the ratios of lathosterol/C by −64% and −68%, and campesterol/C by +52% and +72%, respectively, with significant differences (P < 0.001) between the treatment groups for the latter parameter. When using absolute values of these markers, subjects with the greatest reductions in both synthesis (lathosterol) and absorption (campesterol) had significantly greater reductions in total C than subjects in whom the converse was true (−46% versus −34%, P = 0.001), with similar effects for LDL-C. Rosuvastatin and atorvastatin decreased markers of cholesterol synthesis and increased markers of fractional cholesterol absorption, with rosuvastatin having significantly less effect on the latter parameter than atorvastatin. In addition, alterations in absolute values of plasma sterols correlated with the cholesterol lowering response. There is extensive evidence that HMG-CoA reductase inhibitors (statins) significantly lower total cholesterol and LDL cholesterol (C) levels and reduce coronary heart disease (CHD) risk (1Baigent C. Keech A. Kearney P.M. Blackwell L. Buck G. Pollicino C. Kirby A. Sourjina T. Peto R. Collins R. et al.Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins.Lancet. 2005; 366: 1267-1278Abstract Full Text Full Text PDF PubMed Scopus (5820) Google Scholar). Although reductions of up to 60% in LDL-C levels have been reported (2Schachter M. Chemical, pharmacokinetic and pharmacodynamic properties of statins: an update.Fundam. Clin. Pharmacol. 2005; 19: 117-125Crossref PubMed Scopus (901) Google Scholar), there is large variation in the lipid-lowering response between individuals (3Pedro-Botet J. Schaefer E.J. Bakker-Arkema R.G. Black D.M. Stein E.M. Corella D. Ordovas J.M. Apolipoprotein E genotype affects plasma lipid response to atorvastatin in a gender specific manner.Atherosclerosis. 2001; 158: 183-193Abstract Full Text Full Text PDF PubMed Scopus (159) Google Scholar). These variations have been attributed to intrinsic factors, such as genetic variation, as well as extrinsic factors, such as compliance, time of administration, concomitant drug therapy, and dietary intake (4Thompson G.R. O'Neill F. Seed M. Why some patients respond poorly to statins and how this might be remedied.Eur. Heart J. 2002; 23: 200-206Crossref PubMed Scopus (58) Google Scholar). Total body cholesterol pools represent a balance between endogenous synthesis and dietary absorption (5Matthan N.R. Lichtenstein A.H. Approaches to measuring cholesterol absorption in humans.Atherosclerosis. 2004; 174: 197-205Abstract Full Text Full Text PDF PubMed Scopus (49) Google Scholar). It has been documented using formal cholesterol balance studies, which measure cholesterol synthesis and intestinal cholesterol absorption, that the plasma sterols lathosterol and desmosterol serve as markers of cholesterol synthesis, while campesterol, sitosterol, and cholestanol are markers of fractional cholesterol absorption (6Miettinen T.A. Tilvis R.S. Kesaniemi Y.A. Serum plant sterols and cholesterol precursors reflect cholesterol absorption and synthesis in volunteers of a randomly selected male population.Am. J. Epidemiol. 1990; 131: 20-31Crossref PubMed Scopus (561) Google Scholar). The benefit of statins has largely been linked to total cholesterol and LDL-C lowering, and it has been suggested that the degree of lowering may relate to reductions in synthesis markers, which may be offset by increases in markers of absorption. In small-scale cholesterol balance studies, Miettinen et al. (7Miettinen T.A. Gylling H. Synthesis and absorption markers of cholesterol in serum and lipoproteins during a large dose of statin treatment.Eur. J. Clin. Invest. 2003; 33: 976-982Crossref PubMed Scopus (120) Google Scholar, 8Vanhanen H. Kesaniemi Y.A. Miettinen T.A. Pravastatin lowers serum cholesterol, cholesterol-precursor sterols, fecal steroids, and cholesterol absorption in man.Metabolism. 1992; 41: 588-595Abstract Full Text PDF PubMed Scopus (59) Google Scholar–9Vanhanen H.T. Miettinen T.A. Cholesterol absorption and synthesis during pravastatin, gemfibrozil and their combination.Atherosclerosis. 1995; 115: 135-146Abstract Full Text PDF PubMed Scopus (48) Google Scholar) have documented that statins markedly lower cholesterol synthesis and bile acid production, but also significantly increase fractional intestinal cholesterol absorption. Duane (10Duane W.C. Effects of lovastatin and dietary cholesterol on sterol homeostasis in healthy human subjects.J. Clin. Invest. 1993; 92: 911-918Crossref PubMed Scopus (38) Google Scholar) reported similar observations. Miettinen, Strandberg, and Gylling (11Miettinen T.A. Strandberg T.E. Gylling H. Noncholesterol sterols and cholesterol lowering by long-term simvastatin treatment in coronary patients: relation to basal serum cholestanol.Arterioscler. Thromb. Vasc. Biol. 2000; 20: 1340-1346Crossref PubMed Scopus (198) Google Scholar) have also reported in a subset of CHD patients participating in the Scandinavian Simvastatin Survival Study (4S) that those in the highest quartile of the cholestanol/C ratio (indicative of high cholesterol absorption), while on simvastatin had no reduction in CHD events as compared with the placebo-treated group, with the converse also being the case. Moreover Miettinen, Strandberg, and Gylling (11Miettinen T.A. Strandberg T.E. Gylling H. Noncholesterol sterols and cholesterol lowering by long-term simvastatin treatment in coronary patients: relation to basal serum cholestanol.Arterioscler. Thromb. Vasc. Biol. 2000; 20: 1340-1346Crossref PubMed Scopus (198) Google Scholar) have also reported that plasma sterols serve as markers of LDL-C lowering response to statins. Despite these data, there has been some controversy in the field as to whether statins actually increase intestinal cholesterol absorption. An alternative explanation to account for the relative increase in campesterol and beta sitosterol, putative markers of fractional cholesterol absorption, may be that statins are more active in reducing the biliary excretion of cholesterol and sterols. In addition, there is limited epidemiological data available on head-to-head comparisons between different statins and their effects on overall cholesterol homeostasis. The current study is a posthoc analysis of a subset of patients who participated in the Statin Therapies for Elevated Lipid Levels Compared Across Doses to Rosuvastatin (STELLAR) trial, which compared the effects of rosuvastatin in the reduction of LDL-C with other statins (12Jones P.H. Hunninghake D.B. Ferdinand K.C. Stein E.A. Gold A. Caplan R.J. Blasetto J.W. Effects of rosuvastatin versus atorvastatin, simvastatin, and pravastatin on non-high-density lipoprotein cholesterol, apolipoproteins, and lipid ratios in patients with hypercholesterolemia: additional results from the STELLAR trial.Clin. Ther. 2004; 26: 1388-1399Abstract Full Text PDF PubMed Scopus (99) Google Scholar, 13Jones P.H. Davidson M.H. Stein E.A. Bays H.E. McKenney J.M. Miller E. Cain V.A. Blasetto J.W. Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR* Trial).Am. J. Cardiol. 2003; 92: 152-160Abstract Full Text Full Text PDF PubMed Scopus (1293) Google Scholar). The aim of the current study was to investigate the effects of maximal dose rosuvastatin and atorvastatin treatment on markers of cholesterol synthesis and absorption. In addition, we investigated whether changes in synthesis and absorption markers correlated with changes in total cholesterol, LDL-C, HDL-C, triglycerides, and small dense (sd) LDL-C. The novel aspect of the current study is that it compares the effects of the most potent statin treatments available, 40 mg/day of rosuvastatin and 80 mg/day of atorvastatin, on plasma lipid and sterol changes from baseline. The current investigation was performed in a subset of 135 patients participating in the STELLAR study; the inclusion criteria was the availability of both a baseline- and a 6-week plasma sample for the measurement of the synthesis and absorption markers. The details of the design and conduct of the STELLAR study and of the patient population have been previously published (12Jones P.H. Hunninghake D.B. Ferdinand K.C. Stein E.A. Gold A. Caplan R.J. Blasetto J.W. Effects of rosuvastatin versus atorvastatin, simvastatin, and pravastatin on non-high-density lipoprotein cholesterol, apolipoproteins, and lipid ratios in patients with hypercholesterolemia: additional results from the STELLAR trial.Clin. Ther. 2004; 26: 1388-1399Abstract Full Text PDF PubMed Scopus (99) Google Scholar, 13Jones P.H. Davidson M.H. Stein E.A. Bays H.E. McKenney J.M. Miller E. Cain V.A. Blasetto J.W. Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR* Trial).Am. J. Cardiol. 2003; 92: 152-160Abstract Full Text Full Text PDF PubMed Scopus (1293) Google Scholar). Briefly, the STELLAR study was an open-label, randomized, parallel group study in hypercholesterolemic patients conducted in 182 US centers. The primary objective was to compare the efficacy of rosuvastatin in the reduction of LDL-C with other statins across dose ranges. Secondary objectives included a comparison of the effects of the statins on other lipoprotein parameters such as HDL-C, apolipoprotein (apo) A-I and B, and lipid ratios (12Jones P.H. Hunninghake D.B. Ferdinand K.C. Stein E.A. Gold A. Caplan R.J. Blasetto J.W. Effects of rosuvastatin versus atorvastatin, simvastatin, and pravastatin on non-high-density lipoprotein cholesterol, apolipoproteins, and lipid ratios in patients with hypercholesterolemia: additional results from the STELLAR trial.Clin. Ther. 2004; 26: 1388-1399Abstract Full Text PDF PubMed Scopus (99) Google Scholar, 13Jones P.H. Davidson M.H. Stein E.A. Bays H.E. McKenney J.M. Miller E. Cain V.A. Blasetto J.W. Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR* Trial).Am. J. Cardiol. 2003; 92: 152-160Abstract Full Text Full Text PDF PubMed Scopus (1293) Google Scholar). Men and nonpregnant women (adults aged 18 or more) with hypercholesterolemia (LDL-C > 160 mg/dl) were asked to follow a National Cholesterol Education Program step 1 diet for 6 weeks. Those who were compliant with the diet and had fasting calculated LDL-C levels between 160 mg/dl and 250 mg/dl and triglycerides (TG) < 400 mg/dl were randomized to the different statin doses as described (12Jones P.H. Hunninghake D.B. Ferdinand K.C. Stein E.A. Gold A. Caplan R.J. Blasetto J.W. Effects of rosuvastatin versus atorvastatin, simvastatin, and pravastatin on non-high-density lipoprotein cholesterol, apolipoproteins, and lipid ratios in patients with hypercholesterolemia: additional results from the STELLAR trial.Clin. Ther. 2004; 26: 1388-1399Abstract Full Text PDF PubMed Scopus (99) Google Scholar, 13Jones P.H. Davidson M.H. Stein E.A. Bays H.E. McKenney J.M. Miller E. Cain V.A. Blasetto J.W. Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR* Trial).Am. J. Cardiol. 2003; 92: 152-160Abstract Full Text Full Text PDF PubMed Scopus (1293) Google Scholar). The relevant institutional review boards approved the STELLAR study protocol, and all participants gave informed consent. Blood samples were collected on at least three occasions before randomization and after 4 and 6 weeks of treatment and sent to a central lab (Medical Research International, Highland Heights, KY) for the measurement of lipid and lipoprotein parameters that included LDL-C, HDL-C, and TG as described (12Jones P.H. Hunninghake D.B. Ferdinand K.C. Stein E.A. Gold A. Caplan R.J. Blasetto J.W. Effects of rosuvastatin versus atorvastatin, simvastatin, and pravastatin on non-high-density lipoprotein cholesterol, apolipoproteins, and lipid ratios in patients with hypercholesterolemia: additional results from the STELLAR trial.Clin. Ther. 2004; 26: 1388-1399Abstract Full Text PDF PubMed Scopus (99) Google Scholar, 13Jones P.H. Davidson M.H. Stein E.A. Bays H.E. McKenney J.M. Miller E. Cain V.A. Blasetto J.W. Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR* Trial).Am. J. Cardiol. 2003; 92: 152-160Abstract Full Text Full Text PDF PubMed Scopus (1293) Google Scholar). Plasma samples were stored at −80°C at Medical Research International. For the current study, available serum samples were sent on dry ice to the Cardiovascular Research Laboratory, Tufts University, in Boston, MA. In the rosuvastatin 40 mg and atorvastatin 80 mg arms of the STELLAR study, 66 and 69 patients, respectively, were randomized and had data recorded at baseline and after 6 weeks treatment. In our laboratory we have previously measured sdLDL-C as previously described (14Ai M. Otokozawa S. Asztalos B.F. Nakajima K. Stein E. Jones P.H. Schaefer E.J. Effects of maximal doses of atorvastatin versus rosuvastatin on small dense low-density lipoprotein cholesterol levels.Am. J. Cardiol. 2008; 101: 315-318Abstract Full Text Full Text PDF PubMed Scopus (49) Google Scholar). Coefficients of variations within and between runs for all assays were less than 5%. Glycated albumin was measured according to the method described by Kouzuma et al. (15Kouzuma T. Uemastu Y. Usami T. Imamura S. Study of glycated amino acid elimination reaction for an improved enzymatic glycated albumin measurement method.Clin. Chim. Acta. 2004; 346: 135-143Crossref PubMed Scopus (145) Google Scholar). Plasma concentrations of lathosterol, campesterol, sitosterol, and cholestanol were assessed in all 135 subjects using gas-liquid chromatography according to methods previously described (16Matthan N.R. Giovanni A. Schaefer E.J. Brown B.G. Lichtenstein A.H. Impact of simvastatin, niacin, and/or antioxidants on cholesterol metabolism in CAD patients with low HDL.J. Lipid Res. 2003; 44: 800-806Abstract Full Text Full Text PDF PubMed Scopus (68) Google Scholar). Because these plasma sterols are mainly carried in the LDL fraction (7Miettinen T.A. Gylling H. Synthesis and absorption markers of cholesterol in serum and lipoproteins during a large dose of statin treatment.Eur. J. Clin. Invest. 2003; 33: 976-982Crossref PubMed Scopus (120) Google Scholar), it is common practice to adjust them for the total plasma cholesterol level by expressing them as a ratio to cholesterol. In the current study, plasma sterols were expressed corrected for plasma cholesterol levels as well as in absolute terms. Routine quality control assays show no significant differences when the results from fresh plasma samples were compared with values obtained after prior freezing at −80°C and subsequent thawing. The coefficients of variations between runs for plasma sterols were derived from routine quality control assays and were less than 5%. All continuous variables were checked for their distribution and expressed as means ± standard deviation if they were normally distributed, or, in case of nonlinear distributions, as medians and interquartile ranges. Correlation coefficients were based on pairwise comparisons. For the correlation and the regression models, nonlinear variables were log transformed. Comparisons between baseline plasma lipid and sterol levels and their changes after 6 weeks of treatment were based on a paired t-test or a Wilcoxon signed rank test for nonlinear variables. Comparisons between the statin treatments were based on an independent t-test or a Wilcoxon-Mann-Whitney test for nonlinear variables. Study subjects were divided into four groups based on having above or below median changes with statin treatment in the absolute values of lathosterol and either an increase or a decrease in absolute campesterol levels (high-increase, high-decrease, low-increase, and low-decrease synthesis-absorption changes). Total cholesterol changes were investigated among high/low synthesis and increase/decrease absorption change subgroups using a one-way ANOVA with Bonferroni corrections for post hoc testing. Linear regression analyses were used to characterize the variables associated with changes in lathosterol, campesterol, and cholestanol during treatment. In turn, changes in lathosterol, campesterol, and cholestanol, served as dependent variables while age, gender, statin treatment, baseline total cholesterol, and changes in total cholesterol served as independent variable. In addition, depending on the model, baseline levels of lathosterol, campesterol, and cholestanol were added as independent variables. Linear regression analyses were also used to investigate the association of baseline levels of plasma sterols with changes in total cholesterol and LDL-C levels and changes in lathosterol and campesterol with changes in total cholesterol and LDL-C. In these models, changes in total cholesterol and LDL-C respectively served as dependent variables, while age, gender, statin treatment, and alternatively baseline levels of plasma sterols and changes in plasma sterol served as independent variable. A P value smaller than 0.05 was considered statistical significant and all analyses were performed using STATA version 10.0. Gender distributions were similar among the treatment groups (rosuvastatin: 33 males, 33 females and atorvastatin: 33 males, 36 females, P = 0.80). The average age was somewhat higher in the atorvastatin group; however the difference did not reach statistical significance (56 ± 13 versus 60 ± 11 years, P = 0.08). Data on lipid and plasma sterol levels at baseline and after 6 weeks of treatment with maximal doses of either rosuvastatin or atorvastatin are presented in Table 1. Both therapies significantly decreased the levels of total cholesterol, LDL-C and triglycerides (P change < 0.001 for both treatments). These differences, however, were not significant among the statin treatment groups. On the other hand, a significant 9% increase in HDL-C was observed in the rosuvastatin treatment group (P change < 0.001), while a nonsignificant increase of 2% was seen for the atorvastatin-treated patients. In both groups, sdLDL-C levels decreased significantly (P change < 0.001 for both treatments), but the decrease was more profound in the rosuvastatin when compared with the atorvastatin-treated patients (−61% vs. −50%, P = 0.003). There was a wide individual response to therapy for LDL-C, HDL-C, and triglycerides (Fig. 1A).TABLE 1Lipid levels and levels of plasma sterols before and after treatment with rosuvastatin or atorvastatinRosuvastatin (n = 66)Atorvastatin (n = 69)Baseline6 weeksMean % changeP changeBaseline6 weeksMean % changeP changeP treatmentTotal cholesterol, mg/dl287 (29)173 (36)−40<0.001281 (31)169 (24)−40<0.0010.684LDL-C, mg/dl197 (28)89 (32)−55<0.001193 (26)91 (21)−53<0.0010.333HDL-C, mg/dl54.5 (11.5)59.5 (11.9)9<0.00153.5 (13.0)54.6 (12.7)20.2280.001Triglycerides, mg/dl171 [122–219]110 [92-138]−36<0.001169 [123–218]114 [94–144]−33<0.0010.738sdLDL-C, mg/dl69 (30)27 (16)−61<0.00162 (24)31 (15)−50<0.0010.003Lathosterol, μmol/L7.7 (3.1)1.7 (1.8)−78<0.0018.4 (3.0)1.6 (1.6)−81<0.0010.102Campesterol, μmol/L14.0 [10.3–20.0]13.7 [9.2–17.2]−20.00213.7 [11.3–19.4]14.4 [10.8–19.9]50.4770.001Sitosterol, μmol/L6.0 [4.5–8.6]5.9 [4.3–8.2]−20.0136.4 [5.0–8.5]7.1 [5.6–8.7]110.0420.001Cholestanol, μmol/L7.3 (2.9)6.5 (2.6)−110.0257.7 (2.4)7.1 (2.7)−80.0770.706Lathosterol/CaRatio of the plasma sterols to 102 umol/mmol of cholesterol.101 (38)36 (32)−64<0.001107 (39)34 (27)−68<0.0010.253Campesterol/CaRatio of the plasma sterols to 102 umol/mmol of cholesterol.178 [145–254]270 [203-405]52<0.001192 [146–254]331 [236–430]72<0.001<0.001Sitosterol/CaRatio of the plasma sterols to 102 umol/mmol of cholesterol.76 [59–109]127 [90-171]67<0.00182 [69–113]161 [122–204]96<0.001<0.001Cholestanol/CaRatio of the plasma sterols to 102 umol/mmol of cholesterol.95 (32)140 (56)47<0.001100 (30)156 (56)56<0.0010.263Lathosterol/campesterol ratio0.53 [0.32–0.82]0.09 [0.05–0.18]−83<0.0010.54 [0.36–0.84]0.10 [0.05–0.12]−81<0.0010.218C, cholesterol. Values are expressed as mean (SD) or median [interquartile range].a Ratio of the plasma sterols to 102 umol/mmol of cholesterol. Open table in a new tab C, cholesterol. Values are expressed as mean (SD) or median [interquartile range]. Treatment with both statins decreased lathosterol, the marker of cholesterol synthesis, in both absolute and relative terms (ratio lathosterol/C). The absolute values of the absorption markers, campesterol and cholestanol, did not change significantly in the atorvastatin-treated group, while a significant decrease was observed in the rosuvastatin group (campesterol: −2%, P change = 0.002 and cholestanol: −11%, P change = 0.025). The absolute concentration of the absorption marker sitosterol changed significantly in both groups (rosuvastatin −2%, P = 0.013 and atorvastatin +11%, P = 0.042). The treatment effects were significant for campesterol and sitosterol (P treatment = 0.001 for both observations), but not for cholestanol (P treatment = 0.706). When considering the relative effects (i.e., the ratio to cholesterol) of the statin therapies on campesterol, sitosterol, and cholestanol, all the absorption markers increased significantly within both treatment groups (P < 0.001); however, there was a greater increase observed for the ratios of campesterol and sitosterol to cholesterol in the atorvastatin-treated patients when compared with the rosuvastatin group (P treatment < 0.001 for both observations). The changes in the cholestanol/C ratio tended to be higher in the atorvastatin-treated group; however this difference did not reach statistical significance between treatment groups. Both statins had a significant impact on the lathosterol/campesterol ratio, showing a decrease of more than 80% (P change < 0.001 for both observations). There was a wide individual response for the plasma sterols lathosterol, campesterol, and cholestanol in absolute terms (Fig. 1B) as well as relative to total cholesterol (Fig. 1C) among the statin-treatment subgroups. The response of (absolute and relative) sitosterol to therapy showed the same typical pattern as the other absorption markers, campesterol and cholestanol (data not shown). The baseline correlations of lipids and lipoproteins with the plasma sterols are presented in Table 2. The marker of cholesterol synthesis, lathosterol, correlated with total cholesterol levels (r = 0.233, P < 0.01), LDL-C (r = 0.172, P < 0.05), triglycerides (r = 0.257, P < 0.01), and sdLDL-C (r = 0.310, P < 0.001). While the lathosterol/C ratio did not correlate with total cholesterol levels (r = −0.053), a negative correlation with HDL-C was observed (r = −0.207, P < 0.05) and the correlation with triglycerides and sdLDL-C remained significant (r = 0.195, P < 0.05 and r = 0.234, P < 0.01, respectively). The concentrations of campesterol and sitosterol correlated significantly with total cholesterol and LDL-C (campesterol: r = 0.174, P < 0.05 and r = 0.198, P < 0.05; and sitosterol: r = 0.261, P < 0.01 and r = 0.247, P < 0.01, respectively). In addition, concentrations of sitosterol also correlated significantly with HDL-C (r = 0.244, P < 0.01), while the sitosterol/C ratio correlated negatively with triglycerides and sdLDL-C (r = −0.206, P < 0.05 and r = −0.204, P < 0.05, respectively). Concentrations of cholestanol correlated with HDL-C (r = 0.284, P < 0.001), and there was a negative correlation with triglycerides and sdLDL-C (r = −0.187, P < 0.05 and r = −0.226, P < 0.01). The cholestanol/C ratio correlated negatively with total cholesterol, LDL-C, triglycerides, and sdLDL-C (r = −0.278, P < 0.01; r = −0.239, P < 0.01; r = −0.263, P < 0.01; and r = −0.273, P < 0.01). The lathosterol/C ratio did not correlate with total cholesterol, LDL-C, or HDL-C levels; however, there was a significant correlation with sdLDL-C (r = 0.237, P < 0.01).TABLE 2Baseline (n = 135) correlations of plasma lipids and lipoproteins with plasma sterolsTotal cholesterolLDL-CHDL-CTriglyceridessdLDL-CLathosterol0.233bP < 0.01.0.172cP < 0.05.−0.0680.251bP < 0.01.0.310dP < 0.001. The non linear variables were log transformed for the correlations.Campesterol0.174cP < 0.05.0.190cP < 0.05.0.133−0.105−0.105Sitosterol0.261bP < 0.01.0.247bP < 0.01.0.244bP < 0.01.−0.137−0.138Cholestanol0.017−0.0200.284dP < 0.001. The non linear variables were log transformed for the correlations.−0.187cP < 0.05.−0.226bP < 0.01.Lathosterol/CaRatio of the plasma sterols to 102 umol/mmol of cholesterol.−0.053−0.059−0.207cP < 0.05.0.195cP < 0.05.0.234bP < 0.01.Campesterol/CaRatio of the plasma sterols to 102 umol/mmol of cholesterol.−0.0100.0590.027−0.159−0.152Sitosterol/CaRatio of the plasma sterols to 102 umol/mmol of cholesterol.0.0940.1320.160−0.206cP < 0.05.−0.204cP < 0.05.Cholestanol/CaRatio of the plasma sterols to 102 umol/mmol of cholesterol.−0.278bP < 0.01.−0.239bP < 0.01.0.122−0.263bP < 0.01.−0.273bP < 0.01.Lathosterol/campesterol ratio0.010−0.046−0.1570.255bP < 0.01.0.273bP < 0.01.a Ratio of the plasma sterols to 102 umol/mmol of cholesterol.b P < 0.01.c P < 0.05.d P < 0.001. The non linear variables were log transformed for the correlations. Open table in a new tab Table 3shows the correlations between changes in plasma lipids and sterols per treatment group. Changes in lathosterol levels significantly correlated with changes in total cholesterol, LDL-C, and sdLDL-C in both treatment groups (rosuvastatin: r = 0.406, P < 0.001; r = 0.346, P < 0.01; and r = 0.337, P < 0.01, respectively, and atorvastatin: r = 0.390, P < 0.001; r = 0.331, P < 0.01; and r = 0.274 and P < 0.05, respectively). Changes in campesterol correlated with changes in total cholesterol and LDL-C in both treatment groups, while only reaching significance in the atorvastatin group (r = 0.311, P < 0.01 and r = 0.298, P < 0.05 respectively). Interestingly, changes of cholestanol correlated positively with LDL-C (r = 0.258, P < 0.05) in the rosuvastatin-treated patients, while a nonsignificant negative correlation was observed in the atorvastatin-treated patients. When the changes in cholestanol were adjusted for total cholesterol levels, the correlation with LDL-C shifted to a negative correlation in the rosuvastatin-treated patients, while the negative correlation with total and LDL-C became stronger and statistical significant in the atorvastatin-treated patients (r = −0.376, P < 0.01 and r = −0.317, P < 0.01).TABLE 3Correlations between changes in plasma lipids and lipoproteins and plasma sterols per statin treatmentRosuvastatin (n = 66)Atorvastatin (N = 69)Δ TCΔ LDL-CΔ HDL-CΔ TGΔ sdLDL-CΔ TCΔ LDL-CΔ HDL-CΔ TGΔ sdLDL-CΔ Lathosterol0.406bP < 0.001.0.346dP < 0.01.0.2000.0490.337dP < 0.01.0.390bP < 0.001.0.331dP < 0.01.0.0420.2160.274cP < 0.05.Δ Campesterol0.2330.2310.022−0.026−0.0820.311dP < 0.01.0.298cP < 0.05.0.0710.1640.188Δ Sitosterol0.2290.2140.1700.012−0.1040.252cP < 0.05.0.1860.1490.1620.268cP < 0.05.Δ Cholestanol0.2400.258cP < 0.05.0.047−0.140−0.087−0.168−0.1280.080−0.1120.008Δ Lathosterol/CaRatio of the plasma sterols to 102 umol/mmol of cholesterol. TC, total cholesterol; TG, triglycerides.0.301cP < 0.05.0.2380.1270.0.690.285cP < 0.05.0.1440.1390.044−0.0110.126Δ Campesterol/CaRatio of the plasma sterols to 102 umol/mmol of cholesterol. TC, total cholesterol; TG, triglycerides.−0.124−0.104−0.2390.106−0.1180.055−0.028−0.0120.1700.168Δ Sitosterol/CaRatio of the plasma sterols to 102 umol/mmol of cholesterol. TC, total cholesterol; TG, triglycerides.−0.216−0.242−" @default.
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• W2016253197 title "Comparison of the effects of maximal dose atorvastatin and rosuvastatin therapy on cholesterol synthesis and absorption markers" @default.
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• W2016253197 doi "https://doi.org/10.1194/jlr.p800042-jlr200" @default.
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