Oxandrolone indications

Risk of peliosis hepatis, liver cell tumors, blood lipid changes associated with atherosclerosis. Discontinue if cholestatic hepatitis, jaundice, abnormal liver function tests, or hypercalcemia occurs. Cardiovascular disease. COPD. Edematous conditions. Hepatic or renal dysfunction. Monitor hepatic function, serum lipids, Hgb/Hct, and bone age (children) periodically. Monitor for signs of virilization in women; discontinue if mild virilism occurs to prevent irreversible condition. Elderly. Young children. Nursing mothers: not recommended.

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.

Oxandrolone indications

oxandrolone indications

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