Absorption of the synthetic steroids given orally is rapid. The tx/2 in plasma of most is 1-3 h but the maximum biological effect occurs after 2-8 h. Administration is usually 2 or 3 times a day. They are metabolised principally in the liver (some undergoing hepatic first-pass metabolism, see above) and some are excreted unchanged by the kidney. The t1^ is prolonged in hepatic and renal disease and is shortened by enzyme induction to an extent that can be clinically important.
Topical application (skin, lung, joints) allows absorption which can be enough to cause systemic effects.
In the blood, adrenal steroids are carried in the free (biologically active) form (5%) and also bound (95% in the case of hydrocortisone) to transcortin (a globulin with high affinity, but low binding capacity) and, when this is saturated, to albumin (80% in the case of hydrocortisone). The concentration of transcortin is increased by oestrogens, e.g. pregnancy, hormonal contraception, other oestrogen therapy; if these substances are taken, the total plasma hydrocortisone will be found to be raised, but the amount of free hydrocortisone may be normal, being controlled by the physiological feedback mechanism. Patients may be wrongly suspected of having Cushing's syndrome if the fact that they are taking oestrogen is unrecognised and only the total is measured (as is usual).
In patients with very low serum albumin, steroid doses should be lower than usual owing to the reduced binding capacity. In addition, low albumin concentration may be caused by liver disease, which also augments the effects of steroids by delaying metabolism (t'/2 of prednisolone may be doubled).
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