Mg Of Pitavastatin Research Articles

The effect of statins on the risk of anti-tuberculosis drug-induced liver injury among patients with active tuberculosis: A cohort study

BackgroundTuberculosis (TB) remains prevalent worldwide, and anti-TB drugs are associated with drug-induced liver injury (DILI). Statins have pleiotropic effects which may decrease inflammation and achieve immunomodulation. However, few studies have investigated the pleiotropic effects of statins on the risk of DILI. The purpose of this study was to investigate whether statins prevent anti-tuberculosis DILI among active TB patients on standard anti-TB drug therapy. MethodsWe conducted a hospital-based retrospective cohort study using claims data from the Integrated Medical Database of National Taiwan University Hospital (NTUH-iMD). Patients with a positive TB culture were included. The use of statins was defined as a daily equivalent dose >0.5 mg of pitavastatin. Deterioration in liver function was evaluated according to elevated liver enzyme levels. The primary and secondary endpoints were the DILI and the severe DILI. The prognostic value of statins was evaluated by Kaplan–Meier analysis, and Cox proportional hazards models. ResultsA total of 1312 patients with a diagnosis of TB and receiving anti-TB treatment were included. During the study period, 193 patients had the DILI and 140 patients had the severe DILI. Kaplan–Meier analysis showed a significant difference between the usual statin users and controls in the DILI. In multivariable Cox proportional hazards analysis, statins showed a protective effect against the primary and secondary endpoints. In addition, the protective effect of statins showed a dose–response relationship against the DILI. ConclusionStatin treatment had a protective effect against the risk of anti-TB DILI with a positive dose–response relationship.

Does Pitavastatin Therapy for Patients with Type 2 Diabetes and Dyslipidemia Affect Serum Adiponectin Levels and Insulin Sensitivity?

(1) Background: We aimed to demonstrate the effects of pitvastatin therapy on the serum levels of total adiponectin and high-molecular-weight (HMW) adiponectin in type 2 diabetes and the correlation with insulin sensitivity. (2) Methods: This study was designed as an open-labelled randomized trial. Patients with diabetes who were prescribed pitavastatin therapy were enrolled and randomized to either treatment with 2 mg of pitavastatin once daily (n = 44) (PITA group) or diet and exercise only, except their antidiabetic medications (n = 49), for 24 weeks. (3) Results: In lipid profiles, the reduction in total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) was significantly increased in the PITA group (TC; 207.5 ± 20 vs. 195.5 ± 30.0 ng/dL, p < 0.001, LDL-C; 132.0 ± 15.8 vs. 123.1 ± 25.7 mg/dL, p < 0.001). Adiponectin and HMW adiponectin were elevated in the PITA group, compared to the control group without significance. The PITA group showed a lower level of HOMA-IR and HOMA-β levels. However, there was no significance (HOMA-IR; p = 0.5921 -at 12 weeks and p = 0.3645 at 24 weeks; HOMA-β; p = 0.8915 at 12 weeks and p = 0.7313 in 6 months). (4) Conclusions: The present study did not show a significant change in serum adiponectin or HMW adiponectin from baseline in serum adiponectin following pitavastatin therapy. Although statin has been considered as a risk for dysglycemia, pitavastatin did not affect insulin sensitivity.

Evaluation of the Pharmacokinetic Drug-Drug Interaction between Micronized Fenofibrate and Pitavastatin in Healthy Volunteers.

Dyslipidemia is a major risk factor for development of atherosclerosis and cardiovascular disease (CVD). Effective lipid-lowering therapies has led to CVD risk reduction. This study evaluated the possible pharmacokinetic interactions between fenofibrate, a peroxisome proliferators-activated receptors α agonist, and pitavastatin, a 3-hydoxy-3-methylglutaryl-coenzyme A reductase inhibitor, in healthy Korean subjects. The study design was an open-label, randomized, multiple-dose, three-period, and six-sequence crossover study with a 10-day washout in 24 healthy volunteers. It had three treatments: 160 mg of micronized fenofibrate once daily for 5 days; 2 mg of pitavastatin once daily for 5 days; and 160 mg of micronized fenofibrate with 2 mg of pitavastatin for 5 days. Serial blood samples were collected at scheduled intervals for up to 48 h after the last dose in each period to determine the steady-state pharmacokinetics of both drugs. Plasma concentrations of fenofibric acid and pitavastatin were measured using a validated high-performance liquid chromatography with the tandem mass spectrometry method. A total of 24 subjects completed the study. Pitavastatin, when co-administered with micronized fenofibrate, had no effect on the Cmax,ss and AUCτ,ss of fenofibric acid. The Cmax,ss and AUCτ,ss of pitavastatin were increased by 36% and 12%, respectively, when co-administered with fenofibrate. Combined treatment with pitavastatin and micronized fenofibrate was generally well tolerated without serious adverse events. Our results demonstrated no clinically significant pharmacokinetic interactions between micronized fenofibrate and pitavastatin when 160 mg of micronized fenofibrate and 2 mg of pitavastatin are co-administered. The treatments were well tolerated during the study, with no serious adverse events.

Effect of Ezetimibe on LDL-C Lowering and Atherogenic Lipoprotein Profiles in Type 2 Diabetic Patients Poorly Controlled by Statins.

BackgroundThere exists a subpopulation of T2DM in whom first-line doses of statin are insufficient for optimally reducing LDL-C, representing a major risk of CVD. The RESEARCH study focuses on LDL-C reduction in this population along with modifications of the lipid profiles leading to residual risks.MethodsLipid changes were assessed in a randomized, multicenter, 12-week, open-label study comparing a high-potency statin (10mg of atorvastatin or 1mg of pitavastatin) plus ezetimibe (EAT: n = 53) with a double dose of statin (20mg of atorvastatin or 2mg of pitavastatin) (DST: n = 56) in DM subjects who had failed to achieve the optimal LDL-C targets. Lipid variables were compared with a primary focus on LDL-C and with secondary focuses on the percentage of patients who reached the LDL-C targets and changes in the levels of RLP-C (remnant like particle cholesterol) and sd-LDL-C, two characteristic atherogenic risks of DM.ResultsThe reduction of LDL-C (%), the primary endpoint, differed significantly between the two groups (-24.6 in EAT vs. -10.9 in DST). In the analyses of the secondary endpoints, EAT treatment brought about significantly larger reductions in sd-LDL-C (-20.5 vs. -3.7) and RLP-C (-19.7 vs. +5.5). In total, 89.4% of the patients receiving EAT reached the optimized treatment goal compared to 51.0% of the patients receiving DST. The changes in TC (-16.3 vs. -6.3) and non-HDL-C (-20.7 vs. -8.3) differed significantly between the two groups.ConclusionEzetimibe added to high-potency statin (10 mg of atorvastatin or 1 mg of pitavastatin) was more effective than the intensified-dose statin (20 mg of atorvastatin or 2 mg of pitavastatin) treatment not only in helping T2DM patients attain more LDL-C reduction, but also in improving their atherogenic lipid profiles, including their levels of sd-LDL-C and RLP-C.We thus recommend the addition of ezetimibe to high-potency statin as a first line strategy for T2DM patients with insufficient statin response.Trial RegistrationThe UMIN Clinical Trials Registry UMIN000002593

Efficacy and Safety of Pitavastatin in Japanese Male Children with Familial Hypercholesterolemia.

The purpose of this study was to evaluate the efficacy and safety of LIVALO tablets (pitavastatin) in Japanese male children with heterozygous familial hypercholesterolemia (FH). A multicenter, randomized, double-blind, parallel study was conducted in 14 male children 10-15 years of age with heterozygous FH. Pitavastatin (1 mg/day or 2 mg/day) was administered orally for 52 weeks.The primary endpoint was the percent change in the LDL-cholesterol (LDL-C) concentrations from baseline to endpoint (repeated measures ANCOVA at Weeks 8 and 12). Secondary endpoints included the percentage of patients who achieved the target LDL-C concentration and percent changes in the levels of lipoprotein and lipid parameters at the visit performed at 52 weeks. The percent change in LDL-C from baseline (mean 258 mg/dL for all patients) to the endpoint was -27.3% (95%CI; -34.0, -20.5) and -34.3% (95%CI; -41.0, -27.5) in the patients receiving 1 mg and 2 mg of pitavastatin, respectively. Stable reductions in the total cholesterol (TC), non-HDL cholesterol (non-HDL-C), apolipoprotein B (Apo-B) and LDL-C levels and non-HDL-C/HDL-C and Apo-B/Apo-A1 ratios were observed up to 52 weeks in both groups. One patient in each dose group (14%) reached the treatment target level of 130 mg/dL.Adverse events were observed in seven (100%) patients receiving 1 mg and five (71%) patients receiving 2 mg of pitavastatin, although none were considered related to the study treatment. One patient in the 1 mg group reported a musculoskeletal AE; however, it was attributed to recent excessive exercise. Pitavastatin significantly reduced the LDL-C levels and was well tolerated when administered at usual adult doses in 14 male children 10-15 years of age with heterozygous FH. Pitavastatin is a promising therapeutic agent for pediatric dyslipidemia with few safety concerns.

Effects of Pitavastatin on the Intima-Media Thickness of the Carotid Artery in Patients with Ischemic Stroke: The Pitavastatin Efficacy Study on Surrogate Markers and Imaging for Stroke (PESSMIST)

Pitavastatin is a strong statin that was developed in Japan. The clinical impact of pitavastatin treatment in patients with ischemic stroke has not been reported. We conducted a prospective, open label, clinical case-control study to determine the secondary preventive effects of pitavastatin for patients with cerebral infarction and hyperlipidemia. The pitavastatin group included 20 Japanese patients diagnosed with cerebral infarction and hyperlipidemia without previous statin intake. The control group included 22 patients diagnosed with cerebral infarction without hyperlipidemia. The pitavastatin group of patients received 2 mg of pitavastatin once a day after dinner. The mean age of the patients was 69.3 and 75.5 years for the pitavastatin and control groups, respectively, and the age of the pitavastatin group was significantly younger than that of the control group (P

Short-Term Effect of Pitavastatin Treatment on Glucose and Lipid Metabolism and Oxidative Stress in Fasting and Postprandial State Using a Test Meal in Japanese Men

Introduction. The objective of this study was to clarify how pitavastatin affects glucose and lipid metabolism, renal function, and oxidative stress. Methods. Ten Japanese men (average age of 33.9 years) were orally administered 2 mg of pitavastatin for 4 weeks. Postprandial glucose, lipoprotein metabolism, and oxidative stress markers were evaluated at 0 and 4 weeks of pitavastatin treatment (2 mg once daily) with a test meal consisting of total calories: 460 kcal, carbohydrates: 56.5 g (226 kcal), protein: 18 g (72 kcal), lipids: 18 g (162 kcal), and NaCl: 1.6 g. Metabolic parameters were measured at 0, 60, and 120 minutes after test meal ingestion. Results. After administration of pitavastatin, serum total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B, arachidonic acid, insulin, and adjusted urinary excretion of uric acid decreased, whereas creatinine clearance (C Cr) and uric acid clearance (C UA) increased. And postprandial versus fasting urine 8-hydroxydeoxyguanosine remained unchanged, while postprandial versus fasting isoprostane decreased after pitavastatin treatment. Next, we compared postprandial glucose and lipid metabolism after test meal ingestion before and after pitavastatin administration. Incremental areas under the curve significantly decreased for triglycerides (P < 0.05) and remnant-like particle cholesterol (P < 0.01), while those for apolipoprotein E (apoE), glucose, insulin, and high-sensitivity C-reactive protein remained unchanged. Conclusion. Pitavastatin improves postprandial oxidative stress along with hyperlipidemia.

Very rapid effect of pitavastatin on microvascular function in comparison to rosuvastatin: reactive hyperemia peripheral arterial tonometric study

Background:It has been reported that pitavastatin improves endothelial function faster than other statins. Recently introduced reactive hyperemia peripheral arterial tonometry (RH-PAT) provides objective and quantitative assessment of peripheral microvascular function.Purpose:This study aimed to investigate whether peripheral microvascular function improved 2 hours after pitavastatin in subjects with coronary artery disease (CAD) using RH-PAT, and the results were compared with those of rosuvastatin.Methods:This study included 94 subjects with CAD, assigned to a group given 2 mg of pitavastatin (n = 36), a group given 2.5 mg of rosuvastatin (n = 38), and a control group (n = 20). RH-PAT examinations were performed before and 2 hours after statin administration.Results:The RH-PAT index increased 2 hours after pitavastatin administration from 1.82 ± 0.45 to 2.16 ± 0.62 (P = 0.02), whereas there were no differences in the RH-PAT index in the rosuvastatin group (1.79 ± 0.71 to 1.91 ± 0.53, P = 0.09) and the control group (1.68 ± 0.36 to 1.84 ± 0.58, P = 0.4). No significant changes were observed at 2 hours in serum cholesterol levels in each group.Conclusion:The present study demonstrated that peripheral microvascular function improved 2 hours after a single clinical dose of pitavastatin, but not after rosuvastatin.

Pitavastatin Increases HDL Particles Functionally Preserved with Cholesterol Efflux Capacity and Antioxidative Actions in Dyslipidemic Patients

Although statins increase the plasma concentration of high-density lipoprotein cholesterol (HDL-C), it has not been elucidated whether the increased HDL particles possess normal antiatherosclerotic properties. Pitavastatin functions to increase the plasma HDL-C level and decrease the lowdensity lipoprotein cholesterol (LDL-C) level. In the present study, we sought to examine the qualitative changes in HDL during pitavastatin treatment. A total of 30 patients with dyslipidemia were treated with 2 mg of pitavastatin for four weeks. The cholesterol efflux capacity and activities of the antioxidative enzymes paraoxonase-1 (PON-1) and platelet-activating factor acetylhydrolase (PAF-AH) were evaluated using polyethethylene glycol-treated HDL fractions before and after pitavastatin treatment. Pitavastatin treatment decreased the serum LDL-C level by 39% and increased the serum HDL-C level by 9% (p＜0.05). In addition, pitavastatin increased the phospholipid content of HDL by 7.8% (p＜0.05). The pitavastatin-induced increase in the HDL-C level coincided with an increase in the cholesterol efflux capacity of the isolated HDL fraction of 8.6% (p＜0.05). The post-pitavastatin treatment activity of HDL-associated PON-1 (paraoxonase and arylesterase) was increased by 9% (p＜0.05) and 11% (p＜0.05), respectively, while the HDL-associated PAF-AH activity was not affected by pitavastatin. In addition to its LDL-C-lowering effects, pitavastatin elevates the HDL-C level and enhances the cholesterol efflux capacity and antioxidative properties of HDL. Pitavastatin therefore increases the amount of functional HDL without attenuating HDL quality.

Randomized comparison of pitavastatin and pravastatin treatment on the reduction of urinary albumin in patients with type 2 diabetic nephropathy

The effect of pitavastatin and pravastatin treatment on renal function was compared in type 2 diabetic patients with nephropathy in a randomized, controlled, open-label, parallel and multi-centre study. Type 2 diabetic patients with modest renal impairment (serum creatinine level <1.4 mg/dl) accompanied by albuminuria (30-600 mg/g creatinine) were randomly assigned to receive 2 mg of pitavastatin (n = 44) or 10 mg of pravastatin (n = 43) for 12 months. At 12 months, pitavastatin significantly reduced urinary albumin-to-creatinine ratio than pravastatin in subjects with macroalbuminuria (-67.2% vs. +14.5%, p = 0.0040), but not in subjects with microalbuminuria. There was no significant difference in the change in estimated glomerular filtration rate between the two groups. Pitavastatin is more effective than pravastatin for the reduction of albuminuria in type 2 diabetic patients with early stage of diabetic nephropathy.

A crossover study of rosuvastatin and pitavastatin in patients with type 2 diabetes

The effects of a low dose of rosuvastatin (ROS) and pitavastatin (PIT) on lipid profiles and inflammation markers were assessed in subjects with type 2 diabetes mellitus. A total of 90 Japanese type 2 diabetes patients with hyperlipidemia (low-density lipoprotein cholesterol [LDL-C] ≥140 mg/dL) were enrolled in this study. They were randomly assigned to four groups with open-label treatment with ROS (2.5 mg daily) or PIT (2 mg daily); two groups were sequentially treated with both drugs, with crossover of medication after 12 weeks, and the other two groups underwent treatment with either ROS or PIT for 24 weeks. The primary endpoints were the percentage changes in LDL-C, high-density lipoprotein cholesterol (HDL-C) and triglyceride, and the LDL-C/HDL-C ratio. Both ROS and PIT lowered LDL-C and triglyceride, and increased HDL-C. In particular, significantly greater reduction in LDL-C was seen with ROS (-44.1%) than with PIT (-36.9%, P<0.01) in the crossover group from ROS to PIT, and the same result was detected in the crossover group from PIT (-34.8%) to ROS (-44.7%). The ratio of LDL-C/HDL-C was significantly reduced with ROS treatment (from 3.45 to 1.85) compared with that with PIT (from 3.45 to 2.22, P<0.01). Both ROS and PIT lowered plasma levels of high-sensitivity C-reactive protein (hsCRP), tumor necrosis factor (TNF)-alpha, and plasminogen activator inhibitor-1 (PAI-1). In addition, the hsCRP level with the administration of ROS was significantly improved compared with the administration of PIT. There was no significant correlation between changes in LDL-C and hsCRP, TNF-alpha, and PAI-1 levels. ROS and PIT did not have an adverse effect on glycemic control in type 2 diabetes patients. Therapy with both statins improved lipid profiles and reduced proinflammatory responses; however, 2.5 mg of ROS have a potent LDL-C-lowering and hsCRP-lowering effect compared with 2 mg of PIT in patients with diabetes.

Lack of effect of genetic polymorphisms of SLCO1B1 on the lipid-lowering response to pitavastatin in Chinese patients

To investigate the SLCO1B1 388A>G and 521T>C polymorphisms in hyperlipidemia patients and evaluate the effect of the two polymorphisms on the lipid-lowering efficacy of pitavastatin. The functional polymorphisms of SLCO1B1 (388A>G and 521T>C) were genotyped in 140 Chinese patients with essential hyperlipidemia using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and one-step tetra-primers ARMS-PCR. Eighty-five patients were enrolled in the clinical trial and given 2 mg of pitavastatin daily for 8 weeks. Total cholesterol (TC), triglyceride (TG), high-density lipoprotein (HDL), and low-density lipoprotein (LDL) serum levels were measured at baseline, after 4 weeks and after 8 weeks of treatment. The allele frequencies of SLCO1B1 388A>G and 521T>C in essential hyperlipidemia patients were 71.1% and 11.1%, respectively. The 4- and 8-week treatment with pitavastatin significantly reduced TC, TG, and LDL levels, but there was no statistical difference among patients with wild type, SLCO1B1 388A>G or SLCO1B1 521T>C in the lipid-lowering efficacy of pitavastatin. The present study found that the allele frequencies of SLCO1B1 388A>G and 521T>C in Chinese patients with essential hyperlipidemia are comparable to those in healthy Chinese population. SLCO1B1 388A>G and 521T>C do not affect the lipid-lowering efficacy of pitavastatin.

Pitavastatin Improves Serum Resistin Levels in Patients with Hypercholesterolemia

Resistin in serum is associated with high risk in patients with atherosclerosis. This clinical study aimed to investigate whether pitavastatin can regulate the serum level of resistin, together with levels of other inflammatory cytokines and adipocytokines. Forty two outpatients (mean age 65.2 +/- 12.6 yr, M/F: 21/21) with hypercholesterolemia were administered 2 mg of pitavastatin and serum levels of resistin, together with serum levels of adiponectin, leptin, TNF-alpha and hsCRP, were measured before, and 12 weeks after enrollment. There was no significant gender-related difference in initial serum resistin levels. Pitavastatin significantly decreased LDL-cholesterol after 12 weeks. Initial levels of resistin showed a significant correlation with those of hsCRP (r=0.38, p=0.013), but not TNF-alpha or HOMA-R. Serum resistin, but not adiponectin and leptin, levels were significantly decreased, dropping from 17.1 +/- 9.9 ng/ dL to 15.2+/-10.0 (p=0.001) after 12 weeks of administration. The patient group with a baseline hsCRP > or = 0.1 at enrollment (n=17) had decreased levels of both resistin and hsCRP (p=0.011 and p=0.022, respectively). This study showed the pleiotropic effect of pitavastatin on the serum resistin concentration, suggesting that it may assist in the prevention of atherosclerosis.

Comparison of Effects of Pitavastatin and Atorvastatin on Plasma Coenzyme Q10 in Heterozygous Familial Hypercholesterolemia: Results From a Crossover Study

An open, randomized, four-phased crossover study using 4 mg of pitavastatin or 20 mg of atorvastatin was performed to compare their efficacy and safety, especially regarding plasma levels of coenzyme Q10 (CoQ10) in 19 Japanese patients with heterozygous familial hypercholesterolemia. Pitavastatin and atorvastatin caused significant and almost comparable reductions in serum levels of total cholesterol (-35.4 vs. -33.8%), low-density lipoprotein cholesterol (-42.8 vs. -40.7%), and triglyceride (-26.1 vs. -29.4%), and significantly increased serum levels of high-density lipoprotein cholesterol (12.1 vs. 11.4%). Under these conditions, plasma levels of CoQ10 were reduced by atorvastatin (-26.1%, P=0.0007) but not by pitavastatin (-7.7%, P=0.39), although no adverse events or abnormalities of liver and muscle enzyme were observed after either statin treatment. It remains to be seen whether the observed changes in CoQ10 levels are related to the long-term safety of this drug.

The Effects of Statin and Fibrate on Lowering Small Dense LDL- Cholesterol in Hyperlipidemic Patients with Type 2 Diabetes

Small dense (sd)-low-density lipoprotein (LDL) is a potent atherogenic lipoprotein. The overall atherogenicity of this lipoprotein can be precisely assessed by quantifying sd-LDL rather than by measuring the LDL size. We studied the effects of representative lipid-lowering agents (statin and fibrate) on sd-LDL-cholesterol (C) in patients with type 2 diabetes. Sd-LDL-C was measured by the precipitation method established by Hirano and Ito. Large buoyant (lb)-LDL-C was calculated by subtracting sd-LDL-C from LDL-C. Type 2 diabetes patients (n=72) were administered lipid-lowering agents for three months: patients with hypercholesterolemia received 1 mg of pitavastatin and those with hypertriglyceridemia received 100 mg of micronized fenofibrate. Pitavastatin reduced LDL-C by 25% and reduced TG by 8%. The statin decreased sd-LDL-C by 26%, and lb-LDL-C by 22%. Fenofibrate reduced TG by 38% and increased HDL-C by 14%. The fibrate decreased sd-LDL-C by 23% without changing LDL-C. The pitavastatin-induced reduction of sd-LDL-C was significantly correlated with the reduction of LDL-C and apo B, whereas the fenofibrate-induced reduction of sd-LDL-C was correlated with the reduction of TG. Both statin and fibrate reduce the potency of atherogenic sd-LDL particles, but via different mechanisms: the former decreases total-LDL including sd-LDL, while the latter decreases sd-LDL specifically.

Prospective Study to Evaluate the Efficacy and Safety of Pitavastatin in Patients with Risk Factor of Cardiovascular Disease(PEACE Study)

Background and Objectives:Pitavastatin, a recently approved synthetic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, is known to effectively treat hypercholesterolemia. The goal of this study was to investigate the efficacy and safety of pitavastatin in hyperlipidemic Korean patients with coronary risk factors. Subjects and Methods:This was an 8-week, prospective, multicenter, open-label clinical trial. The study subjects were hyperlipidemic Korean patients (triglyceride 130 mg/dL, age; 45-75 years) with at least two coronary risk factors. After a 2-week wash out period, the eligible subjects were given 2 mg of pitavastatin once daily for 8 weeks. In the case of the patients with LDL-cholesterol ≥100 mg/dL after the first 4 weeks of treatment, the dose of pitavastatin was increased to 4 mg per day for the remaining 4 weeks. Results:Of the 131 patients initially enrolled, 105 completed the study. Among the lipid profiles, the total cholesterol, triglyceride, and LDL-cholesterol levels showed a significant reduction with mean reduction rates of -30.66%, -23.92%, and -41.06%, respectively, after 8 weeks. Interestingly, the HDL-cholesterol level was significantly increased in the subjects with a low HDL-cholesterol level (HDL-cholesterol <40 mg/dL) after 8 weeks of therapy (35.28±4.38 mg/dL to 40.39±6.45 mg/dL, 15.9%, p=0.001). The proportions of patients who achieved the LDL-cholesterol goal of the National Cholesterol Education Program Adult Treatment Panel III were 72.5% (37/51), 93.6% (44/47), and 100.0% (7/7) for the patients with goals of 100 mg/dL, 130 mg/dL, and 160 mg/dL, respectively. Five patients had mild adverse drug events, such as fatigue, itching, myalgia, and anorexia. No significant abnormalities were detected in the laboratory tests, including the liver function test and creatinine kinase level. Conclusion:The HMG-CoA reductase inhibitor, pitavastatin, was highly effective and generally well tolerated with an acceptable safety profile in hyperlipidemic Korean patients with coronary risk factors. (Korean Circulation J 2007;37:16-21)

A randomized, double-blind trial comparing the efficacy and safety of pitavastatin versus pravastatin in patients with primary hypercholesterolemia

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.