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Since their introduction in the late 1980s, the 3- hydroxy-3 -methilglutaryl coenzyme A (HMG -CoA) reductaze inhibitors or statins, have revolutionized the treatment of hyperlipidemia. Despite the well-recognized benefits of statins, there is evidence that low density lipoprotein cholesterol (LDL-C) reductions as specified by National Cholesterol Education Program (NCEP) are not being met. The aim of the study was to assess the efficacy of Zo-20 ("GMP", Georgia) in achieving the target level for LDL-C in patients with CAD and hypercholesterinemia. 100 patients received 20-40 mg Zo-20 during the 3 months period, all parameters of the blood plasma lipids and adverse events were monitored during the study. 78% of patients reached the target goal for LDL-C, using 28,2 mg Zo-20 daily. No serious adverse events associated with study drug treatment were revealed. Zo-20 seems to be very effective and safety in treatment of patients with CAD and lipid disorders.
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This unexpected beneficial impact provides another scientific credence to the hypothesis that immune mechanisms play a role in the development of vitiligo and that the use of statins as immuno-modulator could be of use not only for treatment relative to organ transplant but in other pathologies such as vitiligo.
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An intricate relationship between CD1d, MHC, and lipid species were found on the membrane of human B cells. General significance Organization of CD1d on the plasma membrane might be critical for its biological functions.
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The aim of the study was to determine the effect of the often applied drugs in cardiovascular diseases (metoprolol, acetylsalicylic acid, simvastatin and molsidomine) on antioxidative/oxidative balance in vivo. The determination of oxidative status was based on measurements of concentration of: thiobarbituric acid reactive substances (TBARS - lipid peroxidation products), protein carbonyl groups (marker of proteins oxidative injury), nitrotyrosine (marker of NO-mediated tissue damage) and sulfhydryl groups (protein oxidation product). The assays were performed in the plasma and whole blood of rabbits after three weeks of daily intragastric administration of the drugs mentioned above. It was shown that all drugs except acetylsalicylic acid caused an increase in the plasma and hemolysate levels of TBARS. No changes in nitrotyrosine concentration were observed after drug administration. The content of carbonyl groups did not change after administration of metoprolol, but increased significantly after simvastatin and molsidomine administration. Blood sulfhydryl group concentration was not changed by metoprolol but it significantly decreased after acetylsalicylic acid and increased significantly after molsidomine administration.
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Sixty-seven subjects with primary hypercholesterolemia were enrolled in an open study with "low dosages" of inhibitors of 3-hydroxy-3methylglutaril coenzyme A reductase. Patients were randomized in comparative and parallel study with simvastatin 10 mg (30 subjects) and pravastatin 20 mg (27 subjects) once in the evening for a treatment period of 12 months. At the end of the treatment the plasma concentrations of total and LDL cholesterol were reduced respectively by 21% (p < 0.001) and 29% (p < 0.001), plasma triglyceride concentration was reduced by 16%, high density lipoprotein (HDL) was increased by 2.9%. The efficacy of drugs was increasing during the study: at the third month 63% of subjects and at the twelfth month 89% of subjects showed a LDL < 160 mg/dL. In this study the drugs were well-tolerated, but 11 subjects showed a slight and transitory increase of CK. A treated group with simvastatin showed a similar decrease of the total cholesterol and LDL as that one treated with pravastatin. Pravastatin in comparison with simvastatin reduced significantly plasma triglycerides. There was no significant difference between the groups in the frequency of drug-related adverse effects. In conclusion "low dosages" of simvastatin and pravastatin in long term treatment were very efficacious in the reduction of total and LDL cholesterol. In our study, the decrease of total and LDL cholesterol was time-dependent, with the greatest reduction after sixth months. There were no significant differences between 10 mg of simvastatin and 20 mg of pravastatin on reduction of total and LDL cholesterol levels. Triglycerides decreased significantly only with pravastatin.
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Differences in response to medications both in terms of clinical activity and side-effects have long been recognised by physicians. Genetics has been recently considered as a potential factor to explain part of this variability. Pharmacogenetics focuses on the variants within one or more candidate genes while pharmacogenomics evaluates the entire genome for associations with pharmacologic phenotypes. Genetic variants can effect drug metabolism, drug transport or drug targets. Drug metabolism is responsible 1. for the conversion of prodrugs into active compounds or conversion of drug to toxic or inactive metabolites mostly through reactions mostly catalysed by cytochromes (CYP) P450 (phase reactions) and 2. for transforming drugs to compounds that are more water soluble and more easily excreted (phase type II reactions). Genetic polymorphisms can modify the activity of several CYPs such as CYPs, 2D6, 2C9, 2C19 with altered responses to codeine, tamoxifen, clopidogrel, warfarin, ... or of enzymes of the phase II reactions with abnormal responses to drugs like irinotecan, 5-fluorouracil, azathioprine, ... Proteins involved in the transport of drugs in or out the cells such as chemiotherapeutic agenrs, simvastatin, ... can also be affected by genetics. Genetics can also modify drug targets by mutations affecting tumour cells rending these later more or less responsive to drugs. Genetic tests have been launched for screening polymorphisms before giving drugs such as warfarin and several biomarkers are available in oncology. However, many challenges exist. For example, we need more prospective studies to have a better knowledge of the clinical impact and the cost-effectiveness of these tests. It remains that in the future pharmacogenetics/genomics will probably help to personalise medicine by conferring to the clinician the possibility of giving the right drug to the right patients and by this way improving efficacy and safety of medications.
Organic anion-transporting polypeptides (OATP) 1B1 and OATP1B3 are drug transporters mediating the active hepatic uptake of their substrates. Because they exhibit overlapping substrate specificities, the contribution of each isoform to the net hepatic uptake needs to be considered when predicting drug-drug interactions. The relative contribution of OATP1B1- and OATP1B3-mediated uptake of statins into hepatocytes was estimated based on either relative transporter protein expression data or relative activity data. Therefore, kinetics of eight statins and OATP1B1- and OATP1B3-specific reference substrates was determined in OATP1B1- and OATP1B3-expressing human embryonic kidney 293 cells and in human cryopreserved hepatocytes. Absolute OATP1B1 and OATP1B3 protein abundance was determined by liquid chromatography-tandem mass spectrometry in all expression systems. Transporter activity data generated in recombinant cell lines were extrapolated to hepatocyte values using relative transporter expression factors (REF) or relative activity factors (RAF). Our results showed a pronounced OATP1B1 and comparatively low OATP1B3 protein expression in the investigated hepatocyte lot. Based on REF scaling, we demonstrated that the active hepatic uptake clearances of reference substrates, atorvastatin, pravastatin, rosuvastatin, and simvastatin were well predicted within twofold error, demonstrating that OATP1B1 and OATP1B3 were major contributors. For other statins, the net hepatic uptake clearance was underpredicted, suggesting the involvement of other hepatic uptake transporters. Summarized, we showed that REF- and RAF-based predictions were highly similar, indicating a direct transporter expression-activity relationship. Moreover, we demonstrated that the REF-scaling method provided a powerful tool to quantitatively assess the transporter-specific contributions to the net uptake clearance of statins in hepatocytes.
Anti-inflammatory qualities are held partially responsible for the reduction of cardiovascular events after statin treatment. We examined the phenotype of carotid atherosclerotic plaques harvested during carotid endarterectomy in relation to the previous use of different statins prescribed in clinical practice.
This review discusses the current evidence regarding the safety of ezetimibe/simvastatin combination. Current evidence regarding possible associated side effects (musculoskeletal, gastrointestinal, endocrine, hematological, renal, ophthalmologic, allergic, malignancy) and drug interactions of this combination is thoroughly discussed.
Our results indicate that manipulations of the isoprenoid biosynthesis pathway that promote the synthesis of nonsterol isoprenoids may provide an interesting therapeutic option for the treatment of MK deficiency.
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610 adults (49% men) with a mean age of 58 years; 91% of prescriptions were from general practitioners; prescribed drugs were simvastatin (54%), pravastatin (31%) and gemfibrozil (15%).
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Of the 15 CHC patients, 13 completed the study. Subjects were mostly Caucasian (8/15), mean age 49.1 ±9 years and the genotype distribution was 1=10, 2=2 and 3=3. No subject discontinued dosing due to adverse events. Mean HCV RNA change from baseline was from -0.005 to -0.236 log(10) IU/ml across study intervals. Three subjects had transient >1 log(10) HCV RNA declines. No subject achieved >2 log(10) HCV RNA decline.
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In G1 to G4, TC, HDL, apoA, TG, LDL, Lpa, apoB increased, but only TC, HDL, apoA were significantly different as compared with G5 (P=0.020, P=0.001, P=0.001, P=0.911, P=0.249, P=0.681, P=0.053). The tumor in G1 grew fastest, and its growth rate was significantly different as compared with G2, G4, G5 except G3 (P=0.001, P=0.806, P=0.001, P=0.010). The tumor growth rate of G3 was lower than group G1, but higher than G2, G4, G5 with significant difference (P=0.001, P=0.002, P=0.016). The tumor of G5 grew faster than G2 and G4, but without significant differences (P=0.051, P=0.070). The tumor of G4 grew slowest without significant difference as compared to G2 (P=0.438). Compared with pre-administration, at the third week, the TC of G1 was increased [(3.8±0.4) mmol/L], while the other 4 groups decreased [G2 (2.8±1.8) mmol/L, G3 (2.9±0.7) mmol/L, G4 (1.4±0.9) mmol/L, G5 (2.1±0.2) mmol/L]. G4 decreased significantly (P=0.004). At the fifth week, the TC of all the 5 groups decreased, while the lipids of G4 were higher as compared to those at the third week. The TG, Lpa, ApoA were significantly decreased at the third week (all P<0.05), while no significant differences were found in HDL and apoB.
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Doxorubicin efficacy in cancer therapy is hampered by the dose-dependent side effects, which may be overcome by reducing the drug's dose and increasing its efficacy. In the present work, we suggest that the activation of the nuclear factor-kappaB (NF-kappaB) pathway and of nitric-oxide (NO) synthase increases the doxorubicin efficacy in human colon cancer HT29 cells. To induce NF-kappaB, we took into account the effect of doxorubicin itself and of the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor simvastatin; as NF-kappaB inhibitors, we chose the sesquiterpene lactones parthenolide and artemisinin. Simvastatin increased the NF-kappaB activity and NO synthesis, elicited the tyrosine nitration of the multidrug resistance-related protein 3, and enhanced the doxorubicin intracellular accumulation and cytotoxicity. Simvastatin potentiated the effect of doxorubicin on the NF-kappaB pathway and the inducible NO synthase expression. The effects of simvastatin were due to the inhibition of the small G-protein RhoA and of its effector Rho kinase. Parthenolide and artemisinin prevented all of the statin effects by inducing RhoA/Rho kinase activation. On the other hand, they did not reduce the NF-kappaB translocation and doxorubicin intracellular content when RhoA was silenced by small interfering RNA (siRNA). It is interesting that RhoA siRNA was sufficient to increase NF-kappaB translocation, NO synthase activity, doxorubicin accumulation, and cytotoxicity also in non-stimulated cells. Our results suggest that artemisinin, a widely used antimalarial drug, may impair the response to doxorubicin in colon cancer cells; on the contrary, simvastatin and RhoA siRNA may represent future therapeutic approaches to improve doxorubicin efficacy, reducing the risk of doxorubicin-dependent adverse effects.
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A retrospective study of 84 patients aged > or = 65 years, admitted in the last 6 months in Medical Clinic IV, was conducted. Admission criteria in the study were: age > or = 65 years old and high serum levels of cholesterol, triglycerides and LDL-C/HDL-C ratio. The patient population was divided into two groups: Group I of 40 patients treated for dyslipidemia only with diet and Group II with 44 patients in which was associated treatment with hydroxymethylglutaryl coenzyme A reductase inhibitors, 10 mg/day. The patients were controlled when admitted in the study and then at 3 and 6 weeks afterwards.
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In a randomized controlled trial, addition of simvastatin to standard therapy did not reduce rebleeding, but was associated with a survival benefit for patients with Child-Pugh class A or B cirrhosis. Survival was not the primary end point of the study, so these results require validation. The incidence of rhabdomyolysis in patients receiving 40 mg/d simvastatin was higher than expected. European Clinical Trial Database ID: EUDRACT 2009-016500-24; ClinicalTrials.gov ID: NCT01095185.
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The aim of this study was to evaluate the osteoinductive capacity of a poloxamine (Tetronic(®) 908, T) and α-cyclodextrin (αCD) supramolecular gel (T-CD) as scaffold in a critical size defect in rat calvaria. The T-CD gel was evaluated solely and after being loaded with simvastatin (SV) and bone morphogenetic protein (BMP-2) separately and in combinations in order to reduce the doses of the active substances. Three doses of SV (7.5, 75, 750 μg) and two doses of BMP-2 (3 and 6 μg) were tested. The histology and histomorphometrical analysis showed improved bone repair with T-CD compared to T, probably due to better release control of both SV and BMP-2. In addition, as T-CD eroded more slowly than poloxamine alone, it remained longer in the defect site. Although synergism was not obtained with BMP-2 and SV, according to the observed regeneration of the defect, the dose of BMP-2 and SV can be reduced to 3 μg and 7.5 μg, respectively.
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Evidence accumulating from biological and epidemiological studies suggests that high levels of serum cholesterol may promote the pathological processes that lead to Alzheimer's disease (AD). Lowering cholesterol in experimental animal models slows the expression of Alzheimer's pathology. These findings raise the possibility that treating humans with cholesterol lowering medications might reduce the risk of developing AD or help treat it. The statins (lovastatin, pravastatin, simvastatin, and others) are powerful cholesterol lowering agents of proven benefit in vascular disease. Several clinical studies comparing the occurrence of AD between users and non-users of statins suggested that risk of AD was substantially reduced among the users. However, because these studies were not randomized trials, they provided insufficient evidence to recommend statin therapy. Cochrane reviews are based on the best available information about healthcare interventions and they focus primarily on randomized controlled trials (RCTs). On the issue of prevention, two randomized trials have been carried out and neither showed any reduction in occurrence of AD in patients treated with statins compared to those given placebo. Statins cannot therefore be recommended for the prevention of AD. Regarding treatment of AD, the large RCTs which have assessed this outcome have not published their results. Initial analysis from the studies available indicate statins have no benefit on the outcome measure ADAS-Cog but have a significant beneficial effect on MMSE as an outcome. We need to await full results from the RCTs before we can be certain. In addition statins were not detrimental to cognition in either systematic review.
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A 5-mg dose of daily ezetimibe add-on treatment is effective in improving lipid profiles in Asian patients with severe hyperlipidaemia not reaching target with statin monotherapy.
Dose variation exceeded a proxy USP specification for more than one-third of sampled half-tablets of warfarin sodium, metoprolol succinate, and lisinopril and appeared to be greater for nonscored tablets as compared with scored tablets. Drug content variation in half-tablets appeared to be attributable primarily to weight variation occurring when tablets powder or fragment during the splitting process. Therefore, equal daily doses will be determined by the ability of patients to split tablets perfectly in half.
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The efficacy of the inhibitors of HMG CoA reductase shows considerable interindividual variation and intense research has focused in the recent years to identify the genetic loci and environmental factors responsible for this variability. A randomized, double-blind, placebo-controlled clinical trial with simvastatin, an HMG CoA reductase inhibitor, was conducted in 63 adolescents (47 treated versus 17 controls) with heterozygous FH. The patients were grouped according to known low-density lipoprotein (LDL) receptor gene mutation class. After 6 weeks of treatment with 20 mg/d of simvastatin, the mean reduction in plasma LDL-cholesterol in patients with a receptor-negative mutation (n=33) was 39% whereas, in the receptor-defective mutation group (n=14), it was 31% (P=0.01). Multiple regression analyses showed that there was a significant association between the apo E polymorphism and LDL-cholesterol response to simvastatin only among heterozygotes for a receptor-negative mutation. In subjects carrying a receptor-defective mutation, however, we observed that 51% of the variability in LDL-cholesterol response was explained by variations in the dosage of simvastatin expressed in mg/kg/day (P=0.0028). There was no significant association between LDL-cholesterol response and the dosage of simvastatin among heterozygotes for a receptor-negative mutation. The results of the present study have shown that the contribution of apo E polymorphism and the dosage of simvastatin to the LDL-cholesterol responsiveness is influenced by the nature of the LDL receptor gene mutation.
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Least squares mean percentage change in LDL-C and non-HDL-C was calculated using 38,052 patient exposures to rosuvastatin 5-40 mg, atorvastatin 10-80 mg and simvastatin 10-80 mg. Equipotent doses were estimated by linear interpolation between actual adjacent doses.
The efficacy of statins in combination with interferon therapy in patients with multiple sclerosis (MS) is reviewed.