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Cortisol (hydrocortisone) is the most prominent glucocorticosteroid, and it is essential for the maintenance of several body functions. Like other glucocorticosteroids, cortisol is synthesized from the common precursor cholesterol in the zona fasciculata of the cortex of the adrenal gland. For the transport of cortisol in blood, about 90% of cortisol is bound to corticosteroid-binding globulin (CBG) and to albumin.

Only a small amount of cortisol circulates unbound in blood and is free to interact with its receptors.3 The most important physiological effects of cortisol are the increase of blood glucose levels (enhancement of gluconeogenesis, catabolic action) and its anti-inflammatory and immunosuppressive action.3 Synthesis and secretion of cortisol by the adrenal gland are controlled by a negative feedback mechanism within the hypothalamus-pituitary-adrenal cortex-axis.

If the cortisol level is low, corticotropin-releasing hormone (CRH) is secreted by the hypothalamus, which causes the pituitary to release adrenocorticotropic hormone (ACTH). This stimulates the synthesis and secretion of cortisol by the adrenal gland. Cortisol itself acts in a negative feedback mechanism on the pituitary gland and the hypothalamus. In addition, stress is followed by increased cortisol secretion.

3 Serum cortisol concentrations normally show a diurnal variation.3 Maximum concentrations are usually reached early in the morning and then concentrations decline throughout the day to an evening level that is about half of the morning concentration; therefore, for interpretation of results, it is important to know the collection time of the serum sample. The cortisol status of a patient is used to diagnose the function or malfunction of the adrenal gland, the pituitary, and the hypothalamus.

4,5 Thereby, cortisol serum concentrations are used for monitoring several diseases with an overproduction (eg, Cushing syndrome)6,7 or underproduction (eg, Addison disease) of cortisol and for monitoring several therapeutic approaches (eg, dexamethasone suppression therapy in Cushing syndrome and hormone replacement therapy in Addison disease).

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Phenytoin is 90% bound, but only the free fraction circulates through plasma membranes and is biologically active. Because of rapid equilibration between free and bound portions of drugs, free levels are potentially important only in AEDs that are highly bound (ie, phenytoin but not carbamazepine). Measurement of the free fraction is not cost-effective on a routine outpatient basis, but may be clinically relevant in exceptional circumstances associated with alterations in the binding of phenytoin.

1 Binding kinetics may be altered in uremia, hepatic disease, late pregnancy or postpartum, cases of head injury associated with a hypermetabolic state, and certain instances of polypharmacy, described below.2-4 Determination of free levels may also be helpful in overdosages, since only the free portion can be cleared by dialysis. In renal disease, total phenytoin levels may generate falsely high values, leading to inadequate dosage.

Dialysis may increase the amount of free phenytoin available.5 In hepatic disease, phenytoin competes with endogenous bilirubin for binding sites,6 and thus the need for a free level may be greatest if the total bilirubin level is high and albumin low. Available liver function tests are not predictive of free phenytoin levels in patients with liver disease.4 Drugs which compete for binding sites on albumin and which may displace phenytoin include valproic acid, acetazolamide, high doses of salicylic acid, phenylbutazone, ceftriaxone, nafcillin, and sulfamethoxazole.

7 In a clinical setting in which one of these drugs is used with phenytoin and toxicity is suspected despite normal phenytoin levels, a free level may be useful. The free phenytoin level can be approximated by the total phenytoin level in cerebrospinal fluid or saliva or other body fluids that are albumin-poor.

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