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Cortisol plasma

Normally, circulating glucocorticoids (of which cortisol is the most prominent in humans) cause feedback inhibition of ACTH release so that cortisol secretion is, to some extent, self-limiting. However, many patients suffering from major depression have an increased concentration of plasma cortisol but reduced ACTH secretion. The latter abnormality seems to be partly due to a reduction in the number of CRF receptors in the pituitary, although it is thought that decreased ACTH secretion could provoke the adrenal hyperplasia which is common in depression. This would result in excessive secretion of cortisol and contribute to the inhibition of ACTH release (Musselman and Nemeroff 1993). [Pg.447]

Bleau H, Daniel C, Chevaher G, Van Tra H, Hontela A. 1996. Effects of acute exposure to mercury chloride and methyhnercury on plasma cortisol, T3, T4, glucose and Ever glycogen in rainbow trout (Oncorhynchus mykiss). Aquat Toxicol 34 221-235. [Pg.168]

True Cushing s syndrome also must be distinguished from other conditions that share some clinical presentations (as well as elevated plasma cortisol concentrations), such as depression, alcoholism, obesity, and chronic illness—the so-called pseudo-Cushing s states. [Pg.694]

The midnight plasma cortisol determination and combined dexamethasone suppression plus CRH test are used less commonly. [Pg.694]

Overnight Give 1 mg oral Plasma cortisol greater Simple to perform and inexpensive. [Pg.696]

Measure plasma cortisol after surgery to determine if the patient displays persistent hypercortisol ism (surgical treatment failure) or hypocortisolism (adrenal insufficiency requiring steroid replacement therapy). [Pg.699]

The observed Li+-induced stimulation of corticotropin (ACTH) secretion from cells in culture, requiring extracellular Ca2+, involves a corresponding and apparently associated increase in the concentration of Ins(l)P, indicating some interaction with phosphoinositide metabolism [176], Pretreatment with Li+ desensitizes the cells, reducing this Li+-induced stimulation of ACTH secretion. Li+ initially raises plasma cortisol levels in manic-depressives however the levels are subsequently reduced with chronic Li+ treatment in both patients and controls [177]. This effect is probably secondary to the stimulation and subsequent desensitization of ACTH secretion by Li+, as observed in cultured cells. [Pg.31]

Rapid and sustained elevation of plasma cortisol levels altered plasma cholesterol and sodium levels... [Pg.191]

The presence of hypercortisolism can be established with a midnight plasma cortisol, late-night (11 PM) salivary cortisol, 24-hour urine free cortisol, and/or low-dose dexamethasone suppression test. [Pg.217]

Cyproheptadine can decrease ACTH secretion monitoring should include morning plasma cortisol and 24-hour urinary free cortisol concen-... [Pg.219]

Shannon, C., Champoux, M., and Suomi, S.J., Rearing condition and plasma cortisol in rhesus monkey infants, Am. J. Primatol., 46, 311, 1998. [Pg.507]

Neuroendocrine Tobacco smoking is acutely related to elevations in plasma arginine vasopressin, neurophs I, j8-endorphin, and j8-lipotropin (Pomerleau et al. 1983). Cigarette smoking elevates plasma cortisol levels via a central mechanism in the hypothalamus or brain stem... [Pg.111]

Targovnik 1989). Smoking cessation causes a decrease in plasma cortisol and epinephrine levels. However, effects on the adrenal medulla are biphasic, with small doses evoking release of plasma catecholamines and large doses inhibiting it (Talyor 1996). [Pg.112]

Plasma cortisol levels are increased and the normal diurnal variation is lost. [Pg.361]

In addition to behavior changes, exposure to the alarm odor also has physiological effects. For instance, in pearl dace, Semotilus margarita, the levels of plasma cortisol and glucose increase 15 minutes after the alarm and are back to normal after 5 hours. The brain concentrations of dopamine, norepinephrine, 5-hydroxytryptamine, or tryptophan did not change (Rehnberg et al., 1987). The fish recovered physiologically much sooner than the behavioral activation For example. Von Frisch (1941) observed that minnows avoided the site of their encounter with alarm substance for many hours, even days. [Pg.194]

Pearl dace Semotiltis margarita Both sexes Alarm pheromone ll Plasma cortisol, glucose Rehnberg etal., 1987... [Pg.206]

Catostomus macrocheilus. However, both rinses induced elevated levels of plasma cortisol and glucose, commonly referred to as a stress response. This experiment demonstrates that the behavioral and physiological responses are not necessarily coupled (Rehnberg and Schreck, 1987). [Pg.359]

The first example shows the circadian rhythm of the cortisol level. As an activator of gluconeogenesis (see p. 158), cortisol is mainly released in the early morning, when the liver s glycogen stores are declining. During the day, the plasma cortisol level declines. [Pg.372]

A rhythmic variation has been observed in levels of plasma hydroxy-corticosteroids (A9, B13, D9) and in the excretion of 17-ketosteroids (P7). As shown in Table 5, urinary excretions of potassium, sodium, chloride, 17-hydroxycorticosteroids and water have been reported to be greatest between 10 am to noon and lowest between 4 am and 6 am (S21). In this study it was shown that within 5 weeks subjects could acclimate to similar patterns for a 21-hour, rather than a 24-hour, day. Heilman and his associates reported that about half of the day s cortisol production is achieved in the early morning hours during sleep and that production is minimal between noon and 10 pm (H7). In one study the plasma cortisol in normal men was 24.6 5.5 /xg/100 ml at 7 am 13.1 3.4 fig/100 ml at 9 am 11.8 fig/100 ml at noon 9.1 2.3 jag/100 ml at 7 PM and 6.3 /ig/100 ml at 10 pm (A9). [Pg.14]

The administration of spironolactone (Aldactone) interferes in the determination of 11-hydroxy corticosteroid by methods that depend on formation of fluorescence in strong sulfuric acid (W15). In 5 patients, the administration of the drug produced as much as a 5-fold increase in the apparent plasma cortisol levels. Aspirin interferes in the determinations of homovanillic acid (HVA) by a fluorometric method. The HVA fluorophore occurs at 320 nm and 420 nm, and acetylsalicylic acid produces fluorescence at 305 to 405 nm (H12). [Pg.31]

Suppression tests For Cushing syndrome, give 1 mg at 11 pm. Draw blood for plasma cortisol determination the following day at 8 am. For greater accuracy, give 0.5 mg every 6 hours for 48 hours. Collect 24-hour urine to determine 17-hydroxycorticosteroid excretion. [Pg.257]

Endocrine effects Statins interfere with cholesterol synthesis and lower circulating cholesterol levels and, as such, might theoretically blunt adrenal or gonadal steroid hormone production. Small declines in total testosterone with no commensurate elevation in LH have been noted with the use of fluvastatin. Pravastatin showed inconsistent results with regard to possible effects on basal steroid hormone levels atorvastatin, lovastatin, rosuvastatin, and simvastatin did not reduce basal plasma cortisol concentration or basal plasma testosterone concentration or impair adrenal reserve. Appropriately evaluate patients who display clinical evidence of endocrine dysfunction. Exercise caution when administering HMG-CoA reductase inhibitors with drugs that affect steroid levels or activity, such as ketoconazole, spironolactone, and cimetidine. [Pg.619]

Metyrapone is a competitive inhibitor of 11 beta hydroxylation in the adrenal cortex, and effectively inhibits cortisol production. It is used in low doses, titrated to achieve plasma cortisol levels as close as possible to normal day-time values. Occasionally it is used in higher doses combined with replacement corticosteroid treatment. Its main side effects relate to overdosage and resulting hypoadrenalism, but it can also cause hirsutism and hypertension, due to accumulation of precursor steroids. Ketoconazole is also sometimes used to suppress adrenal steroid production, but its potential for hepatotoxicity limits its... [Pg.775]

Baker DG, West SA, Nicholson WE, Ekhator NN, Kasckow JW, Hill KK, Bruce AB, Orth DN, Geracioti TD Jr (1999) Serial CSF corticotropin-releasing hormone levels and adrenocortical activity in combat veterans with posttraumatic stress disorder [published erratum appears in Am J Psychiatry 1999 Jun 156(6) 986]. Am J Psychiatry 156 585-588 Bonne O, Brandes D, Segman R, Pitman RK, Yehuda R, Shalev AY (2003a) Prospective evaluation of plasma cortisol in recent trauma survivors with posttraumatic stress disorder. Psychiatry Res 119 171-175... [Pg.398]


See other pages where Cortisol plasma is mentioned: [Pg.538]    [Pg.545]    [Pg.258]    [Pg.454]    [Pg.241]    [Pg.278]    [Pg.696]    [Pg.696]    [Pg.91]    [Pg.127]    [Pg.892]    [Pg.903]    [Pg.102]    [Pg.219]    [Pg.115]    [Pg.26]    [Pg.176]    [Pg.236]    [Pg.302]    [Pg.768]    [Pg.223]    [Pg.376]    [Pg.379]    [Pg.390]    [Pg.396]   
See also in sourсe #XX -- [ Pg.194 ]




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