Oxandrolone mechanism of action

Oxandrolone is a synthetic anabolic steroid that helps to restore lean muscle mass and increase visceral protein stores. Oxandrolone is the only anabolic steroid approved by the Federal Drug Administration (FDA) for the treatment of cachexia. Oxandrolone has also been found to demonstrate a significant improvement in wound healing over a 12 week period in eight out of eight patients with weight loss and non healing chronic wounds [18]. In another study by Yeh et al. [19], oxandrolone was found improve appetite and increase weight gain in patients with COPD associated weight loss. No studies to date were found that specifically address the use of this agent in the nursing home population. Oxandrolone is contraindicated for use in patients with prostate or breast cancer and may lead to hirsutism and fluid retention. Oxandrolone should also be used with caution in patients with hepatic disease [4].

Oxandrolone, an anabolic androgenic steroid, has been shown repeatedly to lower plasma triglycerides in hypertriglyceridemic patients. This study was performed to determine which of seven subfractions of triglyceride-rich lipoproteins are affected by the action of oxandrolone with respect to both their plasma levels and composition. Concurrently, we have determined the levels and composition of HDL subfractions and the plasma levels of the major HDL apoprotein, apoA-I. Oxandrolone was administered to two hypertriglyceridemic subjects, one with type III and one with type V hyperlipoproteinemia until plasma triglycerides were below the target level of 270 mg/dl. Two months and two weeks were required for the type III and type V patients, respectively. In both subjects, the treatment caused a reduction in the plasma levels of all seven subclasses of triglyceride-rich lipoproteins without altering their overall composition. LDL were at least temporarily increased. The reduction of VLDL subfractions caused by oxandrolone was accompanied by a progressive and consistent effect on HDL subfractions in both hypertriglyceridemic subjects; in the type III patient, oxandrolone reduced HDL2 from low pretreatment levels further until they became undetectable. The type V subject had no detectable HDL2 levels prior to treatment. In both subjects, oxandrolone lowered the levels of HDL3. This lowering effect was caused by a preferential reduction of the less dense, major HDL3 subfraction, . HDL3L, causing the denser, smaller HDL3 subfraction, HDL3D, to become the predominant HDL class. The lowering of HDL levels was reflected by a decrease in the plasma levels of the major HDL apoprotein, apoA-I. This first report on the simultaneous reduction of VLDL and the larger, less dense HDL subclasses suggest that oxandrolone lowers plasma triglycerides by a mechanism other than increased lipolysis.

A very typical case of severe cholestasis due to anabolic steroid use.  Because the steroids were being used without medical supervision, the dose and actual duration of use of each preparation was unclear, but cholestasis usually arises within 4 to 12 weeks of starting a C-17 alkylated androgenic steroid.  The jaundice can be severe and prolonged and accompanied by severe pruritus and marked weight loss.  The serum enzymes are typically minimally elevated except for a short period immediately after stopping therapy.  The pattern of enzyme elevations can be hepatocellular, cholestatic or mixed.  Liver biopsy shows a “bland” cholestasis with minimal inflammation and hepatocellular necrosis.  Ma Huang has also been implicated in cases of drug induced liver injury, but is associated with an acute hepatocellular pattern of injury.

Oxandrolone mechanism of action

oxandrolone mechanism of action

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