Cortisol levels measurement

Kanter et al. reported an increase concentration of the corticosteroid binding globulin (CBG) (Kanter et al. 2001). Most cortisol is bound to CBG, and is biologically inactive. A greater concentration of CBG is consistent with low levels of measurable free cortisol, and provides a putative explanation for how cortisol levels could be measurably low even though other aspects of HPA axis functioning do not seem hypoactive. However, the extent to which CBG levels are a contributing cause of low cortisol requires further examination. 

Check plasma cortisol levels at baseline and 30-60 min after drug is administered normal adrenal function indicated by an increase of at least 70 mcg/1 or a measured level of 20 meg... 

Clinically, ACTH stimulation of the adrenals is used diagnostically to detect adrenal insufficiency plasma cortisol levels are measured before and 60 minutes following an intravenous injection of cosyntropin. Adrenocortical insufficiency is known as Addison s disease Addison s classic description, in 1855, namely general debility, remarkable feebleness of the heart, irritability of the stomach, and a peculiar change of the colour of the skin , summarizes the clinical features of this disease, which is uniformly fatal if undetected and untreated. Therapeutically, corticotropin therapy has been essentially abandoned in favor of the direct administration of glucocorticoids. However, ACTH is still rarely used in the treatment of the infantile spasm seizure disorder. 

ACTH stimulation of the adrenals will fail to elicit an appropriate response in states of adrenal insufficiency. A rapid test for ruling out adrenal insufficiency employs cosyntropin (see below). Plasma cortisol levels are measured before and either 30 minutes or 60 minutes following an intramuscular or intravenous injection of 0.25 mg of cosyntropin. A normal plasma cortisol response is a stimulated peak level exceeding 20 g/dL. A subnormal response indicates primary or secondary adrenocortical insufficiency that can be differentiated using endogenous plasma ACTH levels (which are increased in primary adrenal insufficiency and decreased in the secondary form). 

No abnormalities were found in Brian s urine and his blood cell count was normal. However, his blood glucose was 8.1 mmol l-1 (normal value 3.5-6.7 mmol l-1) and a glucose tolerance test later indicated impaired glucose tolerance. Tests for plasma insulin and thyroid hormones (T3, T4 and TSH) showed normal levels. Two further tests were then performed. A 24-hour urine sample was collected and Brian s free cortisol excretion was found to be considerably higher than normal. A second test, the dexamethasone suppression test, was also carried out. In this test, the patient is given a dose of dexamethasone at 11 -12 p.m. and plasma cortisol is measured early next morning. 

Experimental studies in rats indicate that the adrenal response as measured by plasma cortisol levels is unaltered by keeping injured animals at 30°C, though this temperature reduces significantly the catabolic response (Cl, T5). 

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. 

It is felt, however, that true adrenocortical exhaustion is a very uncommon condition (C3) and low plasma values imresponsive to ACTH are found in only a minority of very ill people (M6). The adrenal cortex usually responds to prolonged stress by hypertrophy and measurements of cortisol after prolonged stress show that they are frequently high (C12). True adrenal exhaustion or insufficiency can be diagnosed only when the plasma cortisol levels are constantly low and do not respond to ACTH stimulation. 

Weller RA. Comparison of fluorescent polarization immunoassay and radioimmunoassay in measuring cortisol levels in prepubertal depressed children. Am J Psychiatry 1992 149 1395-6. 

Noncompartmental analysis to assess systemic effects in humans. The degree of systemic side effects can easily be measured for most inhalation drugs. This includes, for example, the change in plasma potassium levels [97,98] and increase in heart rate for beta-2-adrenergic drugs. Other parameters, such as lymphocyte numbers, the suppression of 24-hour urine cortisol [70,99] and 24-hour serum cortisol levels [100] (a more sensitive parameter) have been used for inhaled glucocorticoids. 

Fig. 2 (a, b) Cortisol and aldosterone production were measured over 48 h in response to physiological stimuli (n=2 experiments). K+ signifies an increase in potassium from 4 to 10 mM ACTH = 10 nM, Angiotensin 11 = 100 nM. (c, d) Exposures to etomidate, ketoconazole, or resveratrol (n= 3 experiments, means shown SEM). Significant difference relative to 10 pM forskolin treatments (mean shown as upper dotted line) as determined by one-way ANOVA. Lower dotted line shows mean cortisol levels produced without stimulation... 

Failure of 1 mg of dexamethasone taken at 23 00 to suppress the serum cortisol level at 08 00 the following morning, or failure to suppress urinary cortisol secretion oveniight (as measured by an early morning urine cortisol creatinine ratio) is another pointer towards the presence of Cushing s syndrome. 

Two years later, the Mt. Sinai research group published three papers on their findings in three different medical journals.2 To sum up their conclusions The cause of intrauterine growth retardation in the infants was apparently not dust and smoke inhaled by the pregnant mothers, but maternal psychological stress and cortisol secretion effects, as indicated by measures of below-normal cortisol levels in their infants. 

Sixteen healthy subjeets were given a single 1-mg inhaled dose of budesonide after taking ketoeonazole 200 mg daily for 2 days. Plasma cortisol levels and urinary cortisol excretion were used as a measure of how much budesonide was absorbed systemically, and ketoconazole was found to cause a 37% decrease in the AUC0.24 of cortisol. ... 

A hormonal measure based on the functioning of the hypothalamic-pituitary-adrenocortical axis cortisol level can be viewed as the level of reactivity of the organism to stress (Gunnar, 2000)... 

The majority of the plasma cortisol is protein bound, only a small proportion being in the free state. This free cortisol is filtered at the glomerulus and passes into the urine where it can be measured, for example by radioimmunoassay. Urinary free cortisol determinations therefore correlate with the plasma free cortisol and the cortisol secretion rate. Increased urinary free cortisol levels are found in cases of Cushing s syndrome. 

The application from van der Hoeven et al. (1997) used an ADS cartridge online SPE to measure cortisol and prednisolone in plasma and arachidonic acid in urine. A precolumn packed with a C18 alkyl-diol support (LiChrosphere RP-18 ADS, 25 /an, Merck) was used. To reduce run time, column switching was programmed as heart-cut , diverting only the analyte fraction into the analytical column. Another LiChrosphere column (125 x 4 mm inner diameter, Merck) handled separation. After the injection of 100 fiL plasma, the lower limit of detection for prednisolone was 1 ng/mL while cortisol was readily quantitated at its endogenous level of 100 ng/mL. The run time was 5 min. For arachidonic acid, a Hypersil ODS column (200 x 3.0 mm inner diameter, 5 /.an) was used. The injection volume was 200 //I. and run time was 9.5 min. The detection limit was 1 ng/mL and recovery was 77%. 

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