Atorvastatin pharmacokinetics furadantin

2001;40(4):263-81. doi: 10.2165/00003088-200140040-00003.Raittinen P, Niemistö K, Pennanen E, Syvälä H, Auriola S, Riikonen J, Lehtimäki T, Ilmonen P, Murtola T.Sci Rep. 2020 Jul 21;10(1):12016. doi: 10.1038/s41598-020-68868-5.Rombolà L, Scuteri D, Marilisa S, Watanabe C, Morrone LA, Bagetta G, Corasaniti MT.Life (Basel). The mean dose-response relationship was log linear, and almost all individual dose-response curves paralleled the mean curve. In vitro, atorvastatin acid is a substrate for P-glycoprotein, organic anion-transporting polypeptide (OATP) C and H+-monocarboxylic acid cotransporter. Steady-state atorvastatin pharmacokinetic parameters were estimated on the last day of each dosing period. LDL-apolipoprotein B and LDL-cholesterol were measured directly after ultracentrifugation, and LDL-cholesterol also was estimated by the method of Friedewald. 2020 May 20;14:1953-1961. doi: 10.2147/DDDT.S233732. Please enable it to take advantage of the complete set of features! Name must be less than 100 characters doi: 10.1016/j.amjcard.2005.06.007.Drug Des Devel Ther. Epub 2019 Sep 30.Molecules. doi: 10.2165/00003088-200342130-00005. 2020 May 20;14:1953-1961. doi: 10.2147/DDDT.S233732. Wiley Unable to load your delegates due to an error 2019 Dec;21(12):2635-2642. doi: 10.1111/dom.13849. Atorvastatin is a cholesterol-lowering medication that blocks the production of cholesterol in the body. A few case studies have reported rhabdomyolysis when the pharmacokinetics of atorvastatin have been affected by interacting drugs. At each dose, an individual's LDL-cholesterol response was not correlated with AUC(0-24). Steady-state atorvastatin pharmacokinetic parameters were estimated on the last day of each dosing period. Atorvastatin increases the bioavailability of digoxin, most probably by inhibition of P-glycoprotein, but does not affect the pharmacokinetics of ritonavir, … Following initiation of dosing, statistically significant decreases in total cholesterol, LDL-cholesterol (beta quant), and LDL-apolipoprotein B were observed within 24 hours and in LDL-C (Friedewald) within 72 hours. Atorvastatin acid and its metabolites undergo glucuronidation mediated by uridinediphosphoglucuronyltransferases 1A1 and 1A3. Atorvastatin showed ATP-dependent transport in BCRP-expressing membrane vesicles and it inhibited rosuvastatin transport with Ki of 6.3 ± 2.9 μM (mean ± SD). Women appear to have a slightly lower plasma exposure to atorvastatin for a given dose. Atorvastatin se usa junto con la dieta para reducir los niveles sanguíneos del colesterol "malo" (lipoproteínas de baja densidad, o LDL, por sus siglas en Inglés), para aumentar los niveles del colesterol "bueno" (lipoproteínas de alta densidad, o HDL, por sus siglas en Inglés), y para reducir los triglicéridos (un tipo de grasa en su sangre). Springer LDL-cholesterol (Friedewald) reductions of 34%, 43%, and 57% were produced by atorvastatin doses of 5, 20, and 80 mg, respectively. On the other hand, SLCO1B1 c.388G or ABCG2 c.421A variant alleles did not significantly affect the pharmacokinetics of atorvastatin. Following discontinuation of drug dosing, statistically significant increases were observed in total cholesterol and LDL-cholesterol (Friedewald) within 48 hours and in LDL-cholesterol (beta quant) and LDL-apolipoprotein B within 72 hours. The mean dose-response relationship has been shown to be log-linear for atorvastatin, but plasma concentrations of atorvastatin acid and its metabolites do not correlate with LDL-cholesterol reduction at a given dose. The total plasma clearance of atorvastatin acid is 625 mL/min and the half-life is about 7 hours. In vivo, cytochrome P450 (CYP) 3A4 is responsible for the formation of two active metabolites from the acid and the lactone forms of atorvastatin. Serial plasma lipid and lipoprotein analyses were performed during the initiation and discontinuation of atorvastatin therapy, as well as at steady state. 2019 Jul 24;24(15):2685. doi: 10.3390/molecules24152685. However, atorvastatin acid is subject to extensive first-pass metabolism in the gut wall as well as in the liver, as oral bioavailability is 14%.

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