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Yasushi Saito - One of the best experts on this subject based on the ideXlab platform.
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Effect of Pitavastatin on sterol and bile acid excretion in guinea pigs.
Arzneimittel-Forschung, 2011Co-Authors: T. Aoki, Masaki Kitahara, Hiroyuki Yamazaki, Takashi Maejima, Sato Fumiyasu, Yasushi SaitoAbstract:The influence of Pitavastatin (CAS 147526-32-7), a potent 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, exerted on fecal and biliary excretion of sterols and bile acids was investigated using guinea pigs. The cumulative amount of [3H] bile acid in bile 0 to 6 h after the injection of high density lipoprotein (HDL), which was labeled with [3H] cholesteryl ester (CE), was slightly decreased with atorvastatin (30 mg/kg, CAS 134523-00-5) and simvastatin (30 mg/kg, CAS 79902-63-9), and the same level as the control was maintained with Pitavastatin (3 mg/kg). The amount of excretion of [3H] sterol into bile was significantly increased with atorvastatin and simvastatin, and exhibited a tendency to decline with Pitavastatin. The [3H] bile acid/[3H] sterol ratios were significantly lowered with atorvastatin and simvastatin by 41% and 29%, respectively, as compared to the control, and exhibited an upward tendency with Pitavastatin (22%). The total amounts of fecal [3H] bile acid from 0 to 7 days were significantly decreased with atorvastatin and simvastatin by 30% and 32%, respectively, and slightly increased with Pitavastatin by 8% Furthermore, mRNA expression of the hepatic microsomal cytochrome P-450 enzyme, cholesterol-NADPH: oxygen oxidoreductase (cholesterol 7 alpha-hydroxylase; CYP7A), which is a late limiting enzyme with a bile acid composition, was also decreased with atorvastatin and simvastatin by 54% and 38%, respectively, and slightly increased with Pitavastatin (14%). The change in CYP7A mRNA expression was well correlated with the amount of the fecal [3H] bile acid. The bile acid excreting efficacy of Pitavastatin was relatively high as compared with atorvastatin or simvastatin. It is suggested that this action may contribute to the powerful cholesterol lowering action of Pitavastatin.
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Treatment Options for Hypercholesterolemia and Combined Dyslipidemia: Focus on Pitavastatin
2011Co-Authors: Yasushi SaitoAbstract:Pitavastatin is one of the most effective treatment agents for lowering serum low-density lipoprotein cholesterol (LDL-C) levels. Because Pitavastatin is scarcely metabolized, the risk of drug-drug interactions during multidrug therapy is low, and the LDL-C target is achieved in the majority of patients. The incidence of adverse events associated with Pitavastatin treatment has so far been comparable to or lower than that associated with other statins, and glucose metabolism is not affected by the drug. Pitavastatin promotes plaque regression and improves the plaque composition in patients with acute coronary syndrome. The serum level of high-density lipoprotein cholesterol (HDL-C) during treatment with Pitavastatin was demonstrated to be inversely associated with the incidence of cardiovascular events. Because of its effective and sustained action to increase HDL-C, Pitavastatin is expected to contribute to the prevention of cardiovascular events, in addition to its potent LDL-C lowering effect, especially in patients with low serum HDL-C levels.
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Pitavastatin: an overview.
Atherosclerosis. Supplements, 2011Co-Authors: Yasushi SaitoAbstract:Compared to other statins, Pitavastatin is a highly potent 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase inhibitor and an efficient hepatocyte low-density lipoprotein-cholesterol (LDL-C) receptor inducer. Its characteristic structure (heptenoate as the basic structure, a core quinoline ring and side chains that include fluorophenyl and cyclopropyl moieties) provides improved pharmacokinetics and significant LDL-C-lowering efficacy at low doses. Unlike other statins, the cyclopropyl group on the Pitavastatin molecule appears to divert the drug away from metabolism by cytochrome P450 (CYP) 3 A4 and allows only a small degree of clinically insignificant metabolism by CYP2C9. As a result, Pitavastatin is minimally metabolized; most of the bioavailable fraction of an oral dose is excreted unchanged in the bile and is reabsorbed by the small intestine ready for enterohepatic recirculation. This process probably accounts for Pitavastatin's increased bioavailability relative to most other statins and contributes to its prolonged duration of action. In addition to its potent LDL-C-lowering efficacy, a number of pleiotropic benefits that might lead to a reduction in residual risk have been suggested in vitro. These include beneficial effects on endothelial function, stabilisation of the coronary plaque, anti-inflammatory effects and anti-oxidation. With regard to the clinical safety and efficacy of Pitavastatin, the Phase IV Collaborative study of Hypercholesterolemia drug Intervention and their Benefits for Atherosclerosis prevention (CHIBA study) showed similar changes in lipid profile with Pitavastatin and atorvastatin in Japanese patients with hypercholesterolemia. However, a subgroup analysis of the CHIBA study showed that Pitavastatin produced more significant changes from baseline in LDL-C, TG, and HDL-C in patients with hypercholesterolemia and metabolic syndrome. The clinical usefulness of Pitavastatin has been further demonstrated in a number of Japanese patient groups with hypercholesterolemia, including those with insulin resistance, low levels of high-density lipoprotein-cholesterol (HDL-C), high levels of C-reactive protein, and chronic kidney disease. Finally, the Japan Assessment of Pitavastatin and AtorvastatiN in Acute Coronary Syndrome (JAPAN-ACS) study showed that Pitavastatin induces plaque regression in patients with ACS, which suggests potential benefits for Pitavastatin in reducing CV risk.
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Critical appraisal of the role of Pitavastatin in treating dyslipidemias and achieving lipid goals
Vascular health and risk management, 2009Co-Authors: Yasushi SaitoAbstract:Pitavastatin is a potent HMG-CoA reductase inhibitor and efficient hepatocyte low-density lipoprotein cholesterol (LDL-C) receptor inducer, producing robust reduction of the serum LDL-C levels, even at a low dose. Pitavastatin and its lactone form are minimally metabolized by CYP enzymes, and are therefore associated with minimal drug–drug interactions (DDIs). Pitavastatin 2 to 4 mg has potent LDL-C-reducing activity, equivalent to that of atorvastatin 10 to 20 mg; several clinical trials have revealed consistently superior high-density lipoprotein cholesterol (HDL-C) elevating activity of Pitavastatin than that of atorvastatin. Pitavastatin-induced HDL-C elevation has been shown to be sustained, even incremental, in long-term clinical trials. Pitavastatin was as well-tolerated as atorvastatin or simvastatin in double-blind randomized clinical trials. Two-year long-term safety and effectiveness of pitavastain has been confirmed in a large-scale, prospective post-marketing surveillance. The safety and efficacy profile of Pitavastatin is favorable for the treatment of dyslipidemia, especially in metabolic syndrome patients. In addition to control of LDL-C, adequate control of triglyceride (TG) and HDL-C, hypertension and hyperglycemia is also necessary in metabolic syndrome patients. Pitavastatin produces adequate control of LDL-C and TG, along with potent and incremental HDL-C elevation, with a low frequency of DDIs.
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multicenter collaborative randomized parallel group comparative study of Pitavastatin and atorvastatin in japanese hypercholesterolemic patients collaborative study on hypercholesterolemia drug intervention and their benefits for atherosclerosis prev
Atherosclerosis, 2008Co-Authors: Koutaro Yokote, Hideaki Bujo, Hideki Hanaoka, Masaki Shinomiya, Keiji Mikami, Yoh Miyashita, Tetsuo Nishikawa, Tatsuhiko Kodama, Norio Tada, Yasushi SaitoAbstract:Abstract Aims To compare the efficacy and safety of Pitavastatin and atorvastatin in Japanese patients with hypercholesterolemia. Methods and results Japanese patients with total cholesterol (TC)≥220mg/dL were randomized to receive Pitavastatin 2mg ( n =126) or atorvastatin 10mg ( n =125) for 12 weeks. The primary endpoint was percent change from baseline in non-HDL-C level after 12 weeks of treatment. Reduction of non-HDL-C by Pitavastatin treatment (39.0%, P =0.456 vs. atorvastatin) was non-inferior to that by atorvastatin (40.3%). Both Pitavastatin and atorvastatin also significantly reduced LDL-C by 42.6% and 44.1%, TC by 29.7% and 31.1%, and TG by 17.3% and 10.7%, respectively, at 12 weeks without intergroup differences. HDL-C showed a significant increase at 12 weeks with Pitavastatin treatment (3.2%, P =0.033 vs. baseline) but not with atorvastatin treatment (1.7%, P =0.221 vs. baseline). Waist circumference, body weight and BMI were significantly correlated with percent reduction of non-HDL-C in the atorvastatin group, whereas Pitavastatin showed consistent reduction of non-HDL-C regardless of the body size. In patients with metabolic syndrome, LDL-C was reduced significantly more in patients receiving Pitavastatin when compared with those receiving atorvastatin. AST, ALT and γGTP increased significantly in patients receiving atorvastatin but not in those receiving Pitavastatin. Both treatments were well tolerated. Conclusion Pitavastatin 2mg and atorvastatin 10mg are equally effective in improving the lipid profile and were well tolerated in Japanese patients with hypercholesterolemia.
Tamio Teramoto - One of the best experts on this subject based on the ideXlab platform.
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Efficacy and safety of Pitavastatin in Japanese patients with hypercholesterolemia: LIVES study and subanalysis
Expert review of cardiovascular therapy, 2011Co-Authors: Koutaro Yokote, Hitoshi Shimano, Mitsuyoshi Urashima, Tamio TeramotoAbstract:The Livalo Effectiveness and Safety (LIVES) study was an observational study to examine the efficacy and safety of Pitavastatin, a newly developed drug, in approximately 20,000 Japanese patients with hypercholesterolemia. During a 2-year follow-up period, no significant problems concerning safety were observed upon treatment with Pitavastatin. Pitavastatin demonstrated potent and stable lowering of the LDL-cholesterol level. The LIVES study subanalyses revealed significant and continuous elevation of HDL-cholesterol in association with Pitavastatin treatment and also showed that the drug did not adversely affect glycemic control as evaluated by the glycohemoglobin A(1c) level. Moreover, Pitavastatin treatment was associated with an increase in estimated glomerular filtration rate in subjects with chronic kidney disease. These results suggest the usefulness of Pitavastatin in hypercholesterolemic patients from various backgrounds. The ongoing LIVES study extension is expected to provide further data on cardiovascular outcome in subjects treated with Pitavastatin.
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effects of Pitavastatin livalo tablet on the estimated glomerular filtration rate egfr in hypercholesterolemic patients with chronic kidney disease sub analysis of the livalo effectiveness and safety lives study
Journal of Atherosclerosis and Thrombosis, 2010Co-Authors: Kenjiro Kimura, Hitoshi Shimano, Koutaro Yokote, Mitsuyoshi Urashima, Tamio TeramotoAbstract:Aim: In addition to the risk of progression to end-stage renal disease (ESRD), chronic kidney disease (CKD) is also known to be associated with an elevated risk of cardiovascular disease (CVD). Statins may improve renal function in CKD patients.Methods: The database of the LIVALO Effectiveness and Safety (LIVES) Study, a large-scale (n=20,279), long-term (104 weeks), prospective post-marketing surveillance study of hypercholesterolemic patients treated with Pitavastatin, was used to evaluate the effects of Pitavastatin on the estimated glomerular filtration rate (eGFR).Results: Of the 19,925 patients enrolled in the aforementioned study, data from 3,119 patients were analyzed to evaluate the effects of Pitavastatin treatment for 104 weeks on the eGFR. In this subanalysis, 958 patients with a baseline eGFR of less than 60 mL/min/1.73 m2 (30.7%) were analyzed. A significant increase of the eGFR (+5.4 mL/min/1.73 m2) was observed after 104 weeks of pitavastain treatment (p < 0.001; one-sample t-test). In the analysis of the time-course of changes in the eGFR in response to Pitavastatin treatment, the eGFR was elevated by 2.4 mL/min/1.73 m2 after 12 weeks' treatment, and by 5.6 mL/min/1.73 m2 after 104 weeks' treatment (p < 0.001; repeated measures ANOVA). The results of multivariate analysis identified the presence/absence of proteinuria and the amount change of HDL-C as clinical factors associated with increased eGFR during Pitavastatin treatment.Conclusions: Increased eGFR was noted after 104 weeks of treatment with Pitavastatin, which suggests a possible effect of the statin on CKD.
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New evidence on Pitavastatin: efficacy and safety in clinical studies.
Expert opinion on pharmacotherapy, 2010Co-Authors: Tamio Teramoto, Hitoshi Shimano, Koutaro Yokote, Mitsuyoshi UrashimaAbstract:Importance of the field: Many clinical trials of Pitavastatin have been done since its launch. New insights on Pitavastatin from these trials are summarized and evaluated.Areas covered in this review: The results of clinical studies using Pitavastatin, from 2008 to 2009, the LIVES study, the JAPAN-ACS study, the CHIBA study, the PIAT study and Phase III clinical trials in the West are reviewed.What the reader will gain: In the LIVES study, Pitavastatin showed significant and continuous elevation of high-density lipoprotein cholesterol (HDL-C), estimated glomerular filtration rate (eGFR), as well as potential decrease in low-density lipoprotein cholesterol (LDL-C), in addition to long-term safety. Non-inferiority of Pitavastatin against atorvastatin in the percentage change in plaque volume was proved in the JAPAN-ACS study. Also, comparable effects on LDL-C reduction rate of Pitavastatin versus atorvastatin were confirmed in the CHIBA study and Phase III clinical trials in the West, and a greater increase...
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a randomized double blind trial comparing the efficacy and safety of Pitavastatin versus pravastatin in patients with primary hypercholesterolemia
Atherosclerosis, 2002Co-Authors: Yasushi Saito, Tamio Teramoto, Nobuhiro Yamada, Hiroshige Itakura, Yoshiya Hata, Noriaki Nakaya, Hiroshi Mabuchi, Motoo Tushima, Jun Sasaki, Nobuya OgawaAbstract:Pitavastatin (p-INN) is a novel and fully synthetic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, with a cholesterol-lowering action stronger than that of other statins currently in use. A 12-week, multi-center, randomized, double-blind, controlled study was conducted to confirm the efficacy and safety of Pitavastatin compared with pravastatin, an agent for using to reduce low density lipoprotein cholesterol (LDL-C) in hypercholesterolemic patients. Patients were recruited at 43 institutes in Japan. Following more than 4 weeks run-in period, 240 patients were randomized to receive 2 mg of Pitavastatin or 10 mg of pravastatin daily. At 12 weeks post-randomization, the Pitavastatin group showed significantly lower LDL-C levels by -37.6% from baseline compared with -18.4% in the pravastatin group (P<0.05). Pitavastatin also significantly lowered total cholesterol (TC) by -28.2% compared with -14.0% of pravastatin (P<0.05). The LDL-C target level of <140 mg/dl was attained in 75% of the patients treated with Pitavastatin, compared with 36% of those in the pravastatin group (P<0.05). Pitavastatin also significantly reduced triglycerides (TG), apo B, C-II and C-III, compared with pravastatin, and increased HDL-C, apo A-I and A-II, to the same extent of pravastatin. Safety was assessed by monitoring adverse events and measuring clinical laboratory parameters. The adverse event profile was similar for both treatment groups and neither treatment caused clinically relevant laboratory abnormalities. These results indicated that Pitavastatin was more effective than pravastatin, and both drugs were well-tolerated in the treatment of hypercholesterolemia.
Kohji Shirai - One of the best experts on this subject based on the ideXlab platform.
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Efficacy and safety of Pitavastatin
Journal of symptoms and signs, 2015Co-Authors: Masahiro Ohira, Kohji Shirai, Ichiro TatsunoAbstract:3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) are widely used all over the world to reduce serum low-density lipoprotein cholesterol (LDL-C) levels. Pitavastatin is a new statin that exhibits potent serum LDL-C–lowering effect. Hence Pitavastatin belongs to a group of high-potency statins that include atorvastatin and rosuvastatin. Unlike most other currently available statins that are metabolized by the cytochrome P450 (CYP450) enzyme system, Pitavastatin is minimally metabolized by CYP450. This characteristic makes Pitavastatin an effective and safer statin. Pitavastatin reduces serum LDL-C by 30 to 40% and increases high-density lipoprotein cholesterol by 6 to 11%. Pitavastatin decreases apolipoprotein B, increases apolipoprotein A-I and reduces atherogenic lipoproteins. A large number of studies have not only confirmed the superior effect of Pitavastatin on lipid metabolism, but also indicated its pleiotropic effects in multiple tissues and organs such as blood vessels, heart, liver and kidney. Pitavastatin prevents cardiovascular and cerebrovascular events, and improves arterial stiffness, endothelial function and vascular plaque volume. Pitavastatin also improves cardiac systolic and diastolic functions by reducing oxidative stress. Pitavastatin is useful for two major liver diseases; non-alcoholic steatohepatitis and chronic hepatitis C. Pitavastatin exhibits anti-hepatitis C virus (anti-HCV) effect, and enhances the anti-HCV effect when used in combination with interferon-α. Chronic kidney disease is a serious health problem, and a large clinical study has shown that Pitavastatin increases estimated glomerular filtration in patients with chronic kidney disease. Physicians can use Pitavastatin safely in elderly patients, and in patients with Child-Pugh A cirrhosis, renal impairment, or type 2 diabetes. Moreover, Pitavastatin has a low risk of drug-drug interactions with other medicines. The adverse effect profile of Pitavastatin is the same as other statins. In conclusion, Pitavastatin is equivalent or superior to other statins in efficacy and safety. Thus, Pitavastatin is a very useful statin. Keywords: 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors; hyperlipidemia; efficacy; pleiotropic effects; safety; Pitavastatin. Received: May 27, 2014; Accepted: August 4, 2015; Published: April 9, 2015 Corresponding Author: Masahiro Ohira, MD, PhD, Center for Diabetes, Endocrinology and Metabolism, Sakura Hospital, Toho University Medical Center, 564-1 Shimoshizu, Sakura-City, Chiba, 285-0841, Japan. E-mail: 600137om@sakura.med.toho-u.ac.jp .
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effects of Pitavastatin a 3 hydroxy 3 methylglutaryl coenzyme a reductase inhibitor on cardio ankle vascular index in type 2 diabetic patients
Journal of Atherosclerosis and Thrombosis, 2009Co-Authors: Yoh Miyashita, Masahiro Ohira, Kei Endo, Atsuhito Saiki, Noriko Ban, Takashi Yamaguchi, Hidetoshi Kawana, Daiji Nagayama, Tomokazu Oyama, Kohji ShiraiAbstract:AIM: A novel device has been developed for measuring the cardio-ankle vascular index (CAVI) as an indicator of arterial stiffness. In this study, we evaluated the effect of Pitavastatin on CAVI in type 2 diabetic patients. METHODS: Forty-five type 2 diabetes mellitus patients with low-density lipoprotein cholesterolemia were enrolled and treated with Pitavastatin 2 mg/day for 12 months. Before and after Pitavastatin administration, HbA1c, serum lipids, serum malondialdehyde-LDL (MDA-LDL), urinary 8-hydroxy- 2'-deoxyguanosine (8-OHdG) and CAVI were measured. RESULTS: After Pitavastatin treatment for 12 months, significant decreases in 8-OHdG, MDA-LDL and CAVI were observed. DeltaCAVI significantly correlated with DeltaMDA-LDL. CONCLUSIONS: In type 2 diabetic patients, Pitavastatin may have an oxidative stress-reducing effect, especially in a state of enhanced oxidative stress, and CAVI may be useful as a routine test for the diagnosis and therapeutic monitoring of atherosclerosis.
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Pitavastatin Enhanced Lipoprotein Lipase Expression in 3T3-L1 Preadipocytes
Journal of atherosclerosis and thrombosis, 2005Co-Authors: Atsuhito Saiki, Yoh Miyashita, Tomokazu Oyama, Takeyoshi Murano, Fusako Watanabe, Kohji ShiraiAbstract:It is known that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) enhance the expression- of the low-density lipoprotein (LDL) receptor and lower the level of LDL cholesterol in the blood. But, a triglyceride (TG)-lowering effect is also observed during their administration. To clarify the possibility that statins enhance LPL activity and its mechanism, the effects of statins on the expression of LPL in adipocytes were studied. When statins (pravastatin, simvastatin, atorvastatin and Pitavastatin) were added to the culture medium of mouse 3T3-L1 preadipocytes at final concentrations of 1 μM for 3 days, LPL activity increased. Pitavastatin increased the activity the most. Western and Northern blotting showed that LPL protein and m-RNA were strongly expressed on the addition of Pitavastatin. With the addition of mevalonate (10 μM, 3 days), LPL activity weakened significantly. Statins, especially Pitavastatin, increased the expression of LPL in 3T3-L1 preadipocytes. The TG-lowering effect of Pitavastatin might be mediated by enhancement of LPL production in adipocytes.
Kimihiro Komori - One of the best experts on this subject based on the ideXlab platform.
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Pitavastatin Inhibits Intimal Hyperplasia in Rabbit Vein Graft
The Journal of surgical research, 2007Co-Authors: Hiromine Fujita, Hiroshi Banno, Dai Yamanouchi, Masayoshi Kobayashi, Kiyohito Yamamoto, Kimihiro KomoriAbstract:Background The autologous saphenous vein graft is currently the most suitable conduit for arterial bypass of the lower limbs. Various approaches have been attempted to control vein graft intimal hyperplasia, and several recent reports have suggested that statin use may be linked to improved patency of vein grafts. In this study, the efficacy of Pitavastatin was evaluated on intimal hyperplasia and midkine expression of experimental normocholesterolemic rabbit autologous vein graft. Materials And Methods Rabbits were fed regular rabbit chow, and in half of them, Pitavastatin (1 mg/kg/d) was administered. A week after starting the treatment, jugular vein was implanted into the carotid artery. At 2 and 4 wk after the operation, vein grafts were harvested, and intimal hyperplasia of vein grafts were assessed. Cell proliferation in neointima was determined by proliferative cell nuclear antigen and Ki-67 stain 2 wk after implantation. In addition, the effect of Pitavastatin on midkine, a heparin-binding growth factor, expressed in vein grafts was analyzed by Western blotting. Results The intimal hyperplasia in the Pitavastatin group was significantly suppressed compared with the control group. Both proliferative cell nuclear antigen and Ki-67 labeling index were significantly lower in the Pitavastatin group, and Pitavastatin significantly reduced midkine expression of vein graft. Conclusions These results demonstrate the efficacy of Pitavastatin in reducing the degree of intimal hyperplasia of rabbit autologous vein grafts under normocholesterolemic condition. The mechanism of inhibition of intimal hyperplasia might be associated with midkine suppression.
Yoh Miyashita - One of the best experts on this subject based on the ideXlab platform.
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effects of Pitavastatin a 3 hydroxy 3 methylglutaryl coenzyme a reductase inhibitor on cardio ankle vascular index in type 2 diabetic patients
Journal of Atherosclerosis and Thrombosis, 2009Co-Authors: Yoh Miyashita, Masahiro Ohira, Kei Endo, Atsuhito Saiki, Noriko Ban, Takashi Yamaguchi, Hidetoshi Kawana, Daiji Nagayama, Tomokazu Oyama, Kohji ShiraiAbstract:AIM: A novel device has been developed for measuring the cardio-ankle vascular index (CAVI) as an indicator of arterial stiffness. In this study, we evaluated the effect of Pitavastatin on CAVI in type 2 diabetic patients. METHODS: Forty-five type 2 diabetes mellitus patients with low-density lipoprotein cholesterolemia were enrolled and treated with Pitavastatin 2 mg/day for 12 months. Before and after Pitavastatin administration, HbA1c, serum lipids, serum malondialdehyde-LDL (MDA-LDL), urinary 8-hydroxy- 2'-deoxyguanosine (8-OHdG) and CAVI were measured. RESULTS: After Pitavastatin treatment for 12 months, significant decreases in 8-OHdG, MDA-LDL and CAVI were observed. DeltaCAVI significantly correlated with DeltaMDA-LDL. CONCLUSIONS: In type 2 diabetic patients, Pitavastatin may have an oxidative stress-reducing effect, especially in a state of enhanced oxidative stress, and CAVI may be useful as a routine test for the diagnosis and therapeutic monitoring of atherosclerosis.
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multicenter collaborative randomized parallel group comparative study of Pitavastatin and atorvastatin in japanese hypercholesterolemic patients collaborative study on hypercholesterolemia drug intervention and their benefits for atherosclerosis prev
Atherosclerosis, 2008Co-Authors: Koutaro Yokote, Hideaki Bujo, Hideki Hanaoka, Masaki Shinomiya, Keiji Mikami, Yoh Miyashita, Tetsuo Nishikawa, Tatsuhiko Kodama, Norio Tada, Yasushi SaitoAbstract:Abstract Aims To compare the efficacy and safety of Pitavastatin and atorvastatin in Japanese patients with hypercholesterolemia. Methods and results Japanese patients with total cholesterol (TC)≥220mg/dL were randomized to receive Pitavastatin 2mg ( n =126) or atorvastatin 10mg ( n =125) for 12 weeks. The primary endpoint was percent change from baseline in non-HDL-C level after 12 weeks of treatment. Reduction of non-HDL-C by Pitavastatin treatment (39.0%, P =0.456 vs. atorvastatin) was non-inferior to that by atorvastatin (40.3%). Both Pitavastatin and atorvastatin also significantly reduced LDL-C by 42.6% and 44.1%, TC by 29.7% and 31.1%, and TG by 17.3% and 10.7%, respectively, at 12 weeks without intergroup differences. HDL-C showed a significant increase at 12 weeks with Pitavastatin treatment (3.2%, P =0.033 vs. baseline) but not with atorvastatin treatment (1.7%, P =0.221 vs. baseline). Waist circumference, body weight and BMI were significantly correlated with percent reduction of non-HDL-C in the atorvastatin group, whereas Pitavastatin showed consistent reduction of non-HDL-C regardless of the body size. In patients with metabolic syndrome, LDL-C was reduced significantly more in patients receiving Pitavastatin when compared with those receiving atorvastatin. AST, ALT and γGTP increased significantly in patients receiving atorvastatin but not in those receiving Pitavastatin. Both treatments were well tolerated. Conclusion Pitavastatin 2mg and atorvastatin 10mg are equally effective in improving the lipid profile and were well tolerated in Japanese patients with hypercholesterolemia.
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Pitavastatin Enhanced Lipoprotein Lipase Expression in 3T3-L1 Preadipocytes
Journal of atherosclerosis and thrombosis, 2005Co-Authors: Atsuhito Saiki, Yoh Miyashita, Tomokazu Oyama, Takeyoshi Murano, Fusako Watanabe, Kohji ShiraiAbstract:It is known that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) enhance the expression- of the low-density lipoprotein (LDL) receptor and lower the level of LDL cholesterol in the blood. But, a triglyceride (TG)-lowering effect is also observed during their administration. To clarify the possibility that statins enhance LPL activity and its mechanism, the effects of statins on the expression of LPL in adipocytes were studied. When statins (pravastatin, simvastatin, atorvastatin and Pitavastatin) were added to the culture medium of mouse 3T3-L1 preadipocytes at final concentrations of 1 μM for 3 days, LPL activity increased. Pitavastatin increased the activity the most. Western and Northern blotting showed that LPL protein and m-RNA were strongly expressed on the addition of Pitavastatin. With the addition of mevalonate (10 μM, 3 days), LPL activity weakened significantly. Statins, especially Pitavastatin, increased the expression of LPL in 3T3-L1 preadipocytes. The TG-lowering effect of Pitavastatin might be mediated by enhancement of LPL production in adipocytes.