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Cortisol analogs

Dexamethasone suppression test Administration of dexamethasone (a cortisol analog) normally will suppress pituitary ACTH production, resulting in suppression of adrenal cortisol production and a decrease in urinary free cortisol. [Pg.235]

Cortisone and hydrocortisone (cortisol) are enzymatically interconvertible, and so one finds metabolites from both. Glucocorticoids having a ketone group at Cn (e.g., cortisone, prednisone, and meprednisone) must be reduced in the liver to their corresponding 11 J-hydroxyl analogs (hydrocortisone, prednisolone, and meprednisolone) in order to be pharmacologically active. [Pg.231]

The synthetic analogs of cortisol are useful in the treatment of a diverse group of diseases unrelated to any known disturbance of adrenal function (Table 39-2). The usefulness of corticosteroids in these disorders is a function of their ability to suppress inflammatory and immune responses and to alter leukocyte function, as previously described and as described in Chapter 55. These agents are useful in disorders in which host response is the cause of the major manifestations of the disease. In instances in which the inflammatory or immune response is important in controlling the pathologic process, therapy with corticosteroids may be dangerous but justified to prevent irreparable damage from an inflammatory response—if used in conjunction with specific therapy for the disease process. [Pg.884]

The primary glucocorticoids used pharmacologically are listed in Table 29-1. These drugs are either chemically identical to the naturally occurring hormones, or they are synthetic analogs of cortisol. The clinical choice of a particular agent depends on the problem being treated and the desired effect in each patient. [Pg.421]

Adrenal failure has been reported more than one year after withdrawal of steroid treatment. A preoperative test to detect patients who will fail to respond to surgery is important. The adrenal may be stimulated by injections of ACTH or synthetic analogs with measurement of changes in plasma cortisol levels (M4). This test, however, only gives information about the adrenal capacity to secrete and tells nothing of the ability of the pituitary adrenal axis to respond to stress. [Pg.278]

Fig. 2. Schematic representation of tests using exogenous ACTH, dbcAMP and pregnenolone (indicated by black horizontal arrows) of the functional integrity of teleost adrenocortical cells exposed to an adrenotoxicant (TOX). A lack of secretory response to ACTH (pattern A, black vertical arrow with X to show disrupted pathways) indicates a general dysfunction of the secretory pathways, possibly involving the ACTH receptor. No response to ACTH but a secretory response to dbcAMP, an analog of cAMP (pattern B), indicates that the steps downstream from cAMP are functional (white arrow bar) but steps upstream are disrupted by the toxicant. No response to ACTH or dbcAMP with a response to pregnenolone (pattern C) indicates that steps downstream from this precursor of cortisol are functional. Note that the concentrations of ACTH, dbcAMP and pregnenolone used in these functional in vitro tests should be physiological rather than pharmacological. Fig. 2. Schematic representation of tests using exogenous ACTH, dbcAMP and pregnenolone (indicated by black horizontal arrows) of the functional integrity of teleost adrenocortical cells exposed to an adrenotoxicant (TOX). A lack of secretory response to ACTH (pattern A, black vertical arrow with X to show disrupted pathways) indicates a general dysfunction of the secretory pathways, possibly involving the ACTH receptor. No response to ACTH but a secretory response to dbcAMP, an analog of cAMP (pattern B), indicates that the steps downstream from cAMP are functional (white arrow bar) but steps upstream are disrupted by the toxicant. No response to ACTH or dbcAMP with a response to pregnenolone (pattern C) indicates that steps downstream from this precursor of cortisol are functional. Note that the concentrations of ACTH, dbcAMP and pregnenolone used in these functional in vitro tests should be physiological rather than pharmacological.
In bony fishes, corticosteroids are secreted from the interrenal tissues (analogous to the adrenal cortex) located in the head kidney region121 182. Cortisol is the major steroid released from these cells in response to neuroendocrine stimulation emanating from the hypothalamus and the pituitary (see Chapter 12). The release of cortisol in response to stress has been characterized in several species and also in response to different stressors and this topic has been extensively reviewed1011 70 182. Cortisol... [Pg.365]

A possible explanation for the anti-inflammatory action of cortisol based on the prevention of release of plasma kinins has been published. A number of 8-dehydro analogs of corticosteroids have been synthesized and their thymolytic and salt retaining properties measured. The compound found to have the highest thymolytic activity was 1 (11.4 x hydrocortisone). Again the fallacy of projecting biological activity from one series of steroids to another was demonstrated by the large decrease in activity exhibited by the 8-dehydro steroid 2 as compared with 16a-methylprednisolone (3). [Pg.208]

The separation of endogenous 17- or 18-hydroxylated corticosteroids of the 21-hydroxylated 4-pregnen series was obtained by capillary electrophoresis of their charged borate chelate complexes (323). Aldosterone, 18-hydroxycorti-costerone, 18-hydroxy-deoxycorticosterone, cortisone, cortisol and 11-deoxycor-tisol are separated and resolved with 400 mM borate buffer at pH 9.0. The corticosteroid/borate chelation complex as indicated by CE data correlated well with 11 B-NMR. The separation of corticosteroids and benzothiazin analogs were studied by MEKC and a comparison with CZE was made (324). Bile salts, which have a similar carbon skeleton to the corticosteroids, were used for the separation of these steroids. A short analysis time, 15 min, and a high number of theoretical plates (150,000-350,000) were obtained. Sodium cholate was found to be very effective. The MEKC method was applied to the determination of the drug substance in tablets and cream formulations. An internal standard method was used for quantitation. The purity of the drug substance was also determined. [Pg.348]

Mitotane is an antineoplastic agent. The primary action is on the adrenal cortex. The production of adrenal steroids is reduced. The biochemical mechanism of action is nnknown. Data suggest that the drug modifies the peripheral metabolism of steroids and directly suppresses the adrenal cortex. Use of mitotane alters the peripheral metabolism of cortisol, even though plasma levels of corticosteroids do not fall. The drug causes increased formation of 6-beta-hydroxycortisol. Mitotane, a chlorophenothane (DDT) analog with antineoplastic properties (1 to 6 g p.o. daily in divided doses), is used in the treatment of inoperable adrenocortical cancer. [Pg.448]

In healthy individuals, the adrenal gland rhythmically secretes cortisol in normal amounts [27]. However, under unusually stressful conditions, the adrenal gland increases its release of cortisol that superimposes the basic rhythmic secretions. Here it should be noted that in addition to cortisol, several other hormones experience analogous stress-induced rhythmic secretion [8]. The stress-induced rhythmically secreted hormones of... [Pg.364]

Cyclic siliconides are analogous to acetonides in structure, and can most readily be made with dichlorodimethyl-silane (DMCS) in pyridine [35,36], Cyclic siliconide derivatives of steroids can similarly be made by reacting the dihydroxyacetone side chain of, e.g., cortisone, cortisol or betamethasone with dimethyldiacetoxysilane (DMDAS) and triethylamine [37] as shown in Figure 5. Other reagents for preparing cyclic siliconides include tetramethoxysilane and triethoxysilane [38]. [Pg.145]

The most important synthetic corticosteroid is prednisolone, which is the analog of cortisol. [Pg.2094]


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See also in sourсe #XX -- [ Pg.312 ]




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