Effects of atorvastatin on serum lipids, lipoproteins, and hemostasis

Kushiya, Fumihiko; Wada, Hideo; Ooi, Kinue; Sakurai, Yuko; Sakaguchi, Akane; Noda, M.; Abe, Yasunori; Nakasaki, Takahiro; Tsukada, Tetsuya; Shiku, Hiroshi

doi:10.1002/ajh.20191

Cited by 8 publications

(7 citation statements)

References 32 publications

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“…CCL11, CCL13, CCL17, CCL22 and CCL26) levels in CD patients treated with atorvastatin. In addition, in our CD patient group atorvastatin shows no effect on adhesion molecules linked to leukocyte trafficking, such as E-selectin, P-selectin and ICAM-3, whereas in cardiovascular disease patients these adhesion molecules can be reduced by the statin therapy [35], [36], [37]. One can only speculate that the reason for these differences may reflect different effects of statins in relation to dosage, and co-treatments, and may reflect differences between the statin used, since all statins may not have the same therapeutic potential.…”

Section: Discussionmentioning

confidence: 75%

Atorvastatin Reduces Plasma Levels of Chemokine (CXCL10) in Patients with Crohn's Disease

Grip

Janciauskiene

2009

PLoS ONE

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BackgroundIn Crohn's disease high tissue expression and serum levels of chemokines and their receptors are known to correlate with disease activity. Because statins can reduce chemokine expression in patients with coronary diseases, we wanted to test whether this can be achieved in patients with Crohn's disease.Methodology/Principal FindingsWe investigated plasma levels of chemokines (CCL2, CCL4, CCL11, CCL13, CCL17, CCL22, CCL26, CXCL8, CXCL10) and endothelial cytokines (sP-selectin, sE-selectin, sICAM-3, thrombomodulin) in ten Crohn's disease patients before and after thirteen weeks' daily treatment with 80 mg atorvastatin. Of the 13 substances investigated, only CXCL10 was found to be significantly reduced (by 34%, p = 0.026) in all of the treated patients. Levels of CXCL10 correlated with C-reactive protein (r = 0.82, p<0.01).Conclusions/SignificanceCXCL10 is a ligand for the CXCR3 receptor, the activation of which results in the recruitment of T lymphocytes and the perpetuation of mucosal inflammation. Hence the reduction of plasma CXCL10 levels by atorvastatin may represent a candidate for an approach to the treatment of Crohns disease in the future.Trial RegistrationClinicalTrials.gov NCT00454545

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Section: Discussionmentioning

confidence: 75%

Atorvastatin Reduces Plasma Levels of Chemokine (CXCL10) in Patients with Crohn's Disease

Grip

Janciauskiene

2009

PLoS ONE

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“…However, the possible effects of artovastatin on hemostatic proteins, such as antithrombin, remain controversial. Thus, while one study reported that atorvastatin treatment decreases the levels of the thrombin–antithrombin complex (30), a different one found a decrease in the circulating levels of antithrombin after atorvastatin treatment (31). Thus, it was interesting to evaluate the effects of atorvastatin in our model.…”

Section: Discussionmentioning

confidence: 99%

Intracellular retention of hepatic serpins caused by severe hyperlipidemia

Hernández-Espinosa

Ayala

Castells

et al. 2006

Liver International

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“…Although Drs Bach and Endler also found that FXIIa levels were associated with hypercholesterolemia [1], higher FXIIa levels did not associate significantly with CHD. This may be because of the intake of cholesterol‐lowering drugs, such as statins or colestimide, by the patients, which are known to have the potential to lower plasma FXII levels [11,12]. Thus, FXIIa may be decreased in patients treated with lipid‐lowering agents, and this may interfere with the results of analyses such as those by Drs Bach and Endler.…”

Section: Comparison Of the Fxii Activity (A) And Antigen (B) Levels mentioning

confidence: 99%

Lower factor XII activity is a risk marker rather than a risk factor for cardiovascular disease: a rebuttal

Kanaji

2008

Journal of Thrombosis and Haemostasis

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To cite this article: Kanaji T. Lower factor XII activity is a risk marker rather than a risk factor for cardiovascular disease: a rebuttal. J Thromb Haemost 2008; 6: 1053-4. See also Bach J, Endler G, Mannhalter C, Hellstern P. Coagulation factor XII activity, activated factor XII, distribution of factor XII C46T gene polymorphism and coronary risk: reply to a rebuttal. This issue, pp 1055-6; Bach J, Endler G, Winkelmann BR, Boehm BO, Maerz W, Mannhalter C, Hellstern P. Coagulation factor XII (FXII) activity, activated FXII, distribution of FXII C46T gene polymorphism and coronary risk. J Thromb Haemost 2008; 6: 291-6. In a recent paper published by this journal, Drs Bach and Endler conducted a large prospective surveillance study to examine the relationships between plasma levels of factor (F) XII activity, activated FXII (FXIIa), the 46C>T ()4c>t) polymorphism in the FXII gene, and coronary heart disease (CHD) [1]. They observed that patients with CHD had significantly lower FXII activity than the controls and concluded that lower FXII activity is an independent risk factor for CHD. Doggen et al. [2] have also reported that patients with myocardial infarction have lower FXII activity than control subjects. They speculated that lower FXII activity may enhance thrombus formation by decreasing fibrinolysis. In contrast, we speculate that reduced FXII activity is not the cause of thrombosis, but the result of it. Our reasoning is as follows. We previously showed the existence of the FXII sequence variant 46C>T ()4c>t), where the T allele creates a novel methionine initiating codon that reduces the translation efficiency of FXII [3]. As a result, the FXII 46C>T polymor-phism is not merely a marker, rather it is a strong determinant of plasma FXII levels. Notably, despite the importance of FXII genotype on FXII levels, the studies by Drs Bach and Endler and others did not observe an association between the FXII 46T/T genotype and CHD. This would suggest that lower FXII activity is not a risk factor, rather it simply represents a risk marker. Supporting this notion is that we performed a case-control study involving deep vein thrombosis (DVT) patients and normal controls to examine the effect of the 46C>T genotype on plasma FXII activity and antigen [4]. We first observed that there was a 46T ()4 t) allele-specific dose-dependent effect on plasma FXII activity and antigen levels, with the T/T patients and controls having lower levels than C/C patients and controls, respectively, while the C/T patients and controls had intermediate levels (Tables 1A and 1B) as we have previously shown [3]. We further found that the patients of the C/C, C/T, and T/T genotypes had lower FXII activity and antigen levels than the controls with the same genotypes; this was statistically significant for the T/T and/or C/T subjects (Tables 1A and 1B). None the less, carriers of 46C/C ()4C/C), indicating a high level of FXII, had an increased risk of DVT (odds ratio 46C/C carriers 2.69, 46T/T as reference) [4]. We also obtained seemingly con...

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Effects of atorvastatin on serum lipids, lipoproteins, and hemostasis

Cited by 8 publications

References 32 publications

Atorvastatin Reduces Plasma Levels of Chemokine (CXCL10) in Patients with Crohn's Disease

Atorvastatin Reduces Plasma Levels of Chemokine (CXCL10) in Patients with Crohn's Disease

Intracellular retention of hepatic serpins caused by severe hyperlipidemia

Lower factor XII activity is a risk marker rather than a risk factor for cardiovascular disease: a rebuttal

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