During conventional pharmacologic dose corticosteroid therapy, ACTH production is inhibited with subsequent suppression of cortisol production by the adrenal cortex. Recovery time for normal HPA activity is variable depending upon the dose and duration of treatment. During this time the patient is vulnerable to any stressful situation. Although it has been shown that there is considerably less adrenal suppression following a single morning dose of prednisolone (10 mg) as opposed to a quarter of that dose administered every six hours, there is evidence that some suppressive effect on adrenal activity may be carried over into the following day when pharmacologic doses are used. Further, it has been shown that a single dose of certain corticosteroids will produce adrenal cortical suppression for two or more days. Other corticoids, including methylprednisolone, hydrocortisone, prednisone, and prednisolone, are considered to be short acting (producing adrenal cortical suppression for 1¼ to 1½ days following a single dose) and thus are recommended for alternate day therapy.
Transdermal patches (adhesive patches placed on the skin) may also be used to deliver a steady dose through the skin and into the bloodstream. Testosterone-containing creams and gels that are applied daily to the skin are also available, but absorption is inefficient (roughly 10%, varying between individuals) and these treatments tend to be more expensive. Individuals who are especially physically active and/or bathe often may not be good candidates, since the medication can be washed off and may take up to six hours to be fully absorbed. There is also the risk that an intimate partner or child may come in contact with the application site and inadvertently dose himself or herself; children and women are highly sensitive to testosterone and can suffer unintended masculinization and health effects, even from small doses. Injection is the most common method used by individuals administering AAS for non-medical purposes. 
do glucocorticoids decrease gene transcription of L-selectin thereby decreasing
the neutrophil's ability to replace shed L-selectin to maintain its attachment
to the endothelial surface?
The exact details of how glucocorticoids turn off gene transcription for L-selectin is not completely understood. However, glucocorticoids are very well known to bind to glucocorticoid receptors (in particular GR-alpha) found in the cytoplasm of the Upon binding, the glucocorticoid/GR complex results in a conformational change that results in the dissociation of other proteins that free the glucocorticoid/GR complex to enter into the nucleus. After entering the nucleus it can bind to glucocorticoid responsive elements (GRE) in the region just above the target gene (L-selectin in this case) where it can either turn on gene transcription or inhibit it. It is likely that this is where the inhibition occurs since mRNA levels for L-selectin are decreased with glucocorticoid This process does not occur immediately which explains why the progressive loss of L-selectin starts 5-24 hours post administration of the glucocorticoid and coincides with the rise in PMNs in the WBC count.