Oxandrolone indications

Rivaroxaban is administered orally. Plasma protein binding of rivaroxaban in human plasma is approximately 92% to 95%; albumin is the main binding component. The volume of distribution at steady state is approximately 50 L in heathy subjects. Oxidative degradation catalyzed by CYP3A4/5 and CYP2J2 and hydrolysis are the major sites of biotransformation. Unchanged rivaroxaban was the predominant moiety in plasma with no major or active circulating metabolites. In a Phase I study, after the administration of [14C]-rivaroxaban, 36% was recovered in the urine as unchanged drug and 7% was recovered in the feces as unchanged drug. Unchanged drug is excreted into urine, mainly via active tubular secretion and to a lesser extent via glomerular filtration (approximate 5:1 ratio). Rivaroxaban is a substrate of the efflux transporter proteins P-glycoprotein and ABCG2 (also abbreviated BCRP). Rivaroxaban’s affinity for influx transporter proteins is unknown. Rivaroxaban is a low-clearance drug, with a systemic clearance of approximately 10 L/hour. The terminal elimination half-life of rivaroxaban is 5 to 9 hours in healthy patients aged 20 to 45 years.
 
The anticoagulant effect of rivaroxaban cannot be monitored with standard laboratory testing or be readily reversed. Dose-dependent inhibition of factor Xa activity was observed in humans and the Neoplastin prothrombin time (PT), activated partial thromboplastin time (aPTT), and HepTest are prolonged dose-dependently. Anti-factor Xa activity is also influenced by rivaroxaban. No data exist on the use of the International Normalized Ratio (INR). The predictive value of these coagulation parameters for bleeding risk or efficacy has not been established.
 
Affected cytochrome P450 isoenzymes and drug transporters: CYP3A4, CYP3A5, CYP2J2, P-glycoprotein (P-gp), ABCG2
Rivaroxaban is a substrate of CYP3A4/5, CYP2J2, and the P-gp and ATP-binding cassette G2 (ABCG2) transporters. Inhibitors and inducers of these CYP450 enzymes or transporters may result in changes in rivaroxaban exposure. Avoid use of rivaroxaban with combined P-gp and strong CYP3A4 inhibitors, which cause significant increases in rivaroxaban exposure that may increase bleeding risk. In vitro studies indicate that rivaroxaban neither inhibits the major cytochrome P450 enzymes CYP1A2, 2C8, 2C9, 2C19, 2D6, 2J2, and 3A4 nor induces CYP1A2, 2B6, 2C19, or 3A4. In vitro data also indicates a low rivaroxaban inhibitory potential for P-glycoprotein and ABCG2 transporters. However, no significant pharmacokinetic interactions were observed in studies comparing concomitant rivaroxaban 20 mg and mg single dose of midazolam (substrate of CYP3A4), mg once-daily dose of digoxin (substrate of P-gp), or 20 mg once daily dose of atorvastatin (substrate of CYP3A4 and P-gp) in healthy volunteers.

Goserelin is a synthetic analogue of a naturally occurring luteinizing-hormone releasing hormone ( LHRH ). Bioavailability is almost complete. Goserelin is poorly protein bound and has a serum elimination half-life of two to four hours in patients with normal renal function. The half-life increases with patients with impaired renal function. There is no significant change in pharmacokinetics in subjects with liver failure. After administration, peak serum concentrations are reached in about two hours. It rapidly binds to the LHRH receptor cells in the pituitary gland thus leading to an initial increase in production of luteinizing hormone and thus leading to an initial increase in the production of corresponding sex hormones. This initial flare may be treated by co-prescribing/co-administering an androgen receptor antagonist such as bicalutamide ( Casodex ). Eventually, after a period of about 14–21 days, production of LH is greatly reduced due to receptor downregulation , and sex hormones are generally reduced to castrate levels. [8]

Shelton and Rajfer (2012) noted that androgen deficiency in aging men is common, and the potential sequelae are numerous.  In addition to low libido, erectile dysfunction, decreased bone density, depressed mood, and decline in cognition, studies suggest strong correlations between low testosterone, obesity, and the metabolic syndrome.  Because causation and its directionality remain uncertain, the functional and cardiovascular risks associated with androgen deficiency have led to intense investigation of testosterone replacement therapy in older men.  Although promising, evidence for definitive benefit or detriment is not conclusive, and treatment of LOH is complicated.

Patients 60 years or older appear to exhibit greater than expected INR response to the anticoagulant effects of warfarin. The cause of the increased sensitivity to the anticoagulant effects of warfarin in this age group is unknown but may be due to a combination of pharmacokinetic and pharmacodynamic factors. Limited information suggests there is no difference in the clearance of S-warfarin; however, there may be a slight decrease in the clearance of R-warfarin in the elderly as compared to the young. Therefore, as patient age increases, a lower dose of warfarin is usually required to produce a therapeutic level of anticoagulation [see Dosage and Administration ( , ) ].

Oxandrolone indications

oxandrolone indications

Patients 60 years or older appear to exhibit greater than expected INR response to the anticoagulant effects of warfarin. The cause of the increased sensitivity to the anticoagulant effects of warfarin in this age group is unknown but may be due to a combination of pharmacokinetic and pharmacodynamic factors. Limited information suggests there is no difference in the clearance of S-warfarin; however, there may be a slight decrease in the clearance of R-warfarin in the elderly as compared to the young. Therefore, as patient age increases, a lower dose of warfarin is usually required to produce a therapeutic level of anticoagulation [see Dosage and Administration ( , ) ].

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