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PubMed1991

Cortisol escape from suppression by dexamethasone during depression is strongly predicted by basal cortisol hypersecretion and increasing age combined.

We determined baseline 0800h plasma cortisol concentrations, 24-hr urinary free cortisol (UFC) excretion, the post-dexamethasone cortisol values at 0800h and 1600h, and the 0800h dexamethasone concentrations in 60 depressed patients categorized according to the DSM-III. Up to 59% of the variability in the 0800h post-dexamethasone cortisol values could be explained by the multiple regression on UFC, 0800h basal plasma cortisol, age (all positively related), and dexamethasone concentrations (negatively related). The 1600h post-dexamethasone cortisol data were best explained (i.e., 55% of the variance) by the multiple regression on basal plasma cortisol, UFC (positive) and dexamethasone (negative). After controlling for UFC, baseline plasma cortisol, and age no significant effects of the depressive state (diagnostic classification or severity of illness) on the post-dexamethasone cortisol values could be detected. It can be deduced that cortisol non-suppression during depression is related strongly to baseline cortisol hypersecretion and increasing age. These factors are additive and contribute independently towards cortisol escape from suppression by dexamethasone.

Adult↗

PubMed1993

The relationship between cortisol production rate and serial serum cortisol estimation in patients on medical therapy for Cushing's syndrome.

OBJECTIVE: The aim was to determine the target range into which mean daily serum cortisol should be lowered in patients on medical therapy for Cushing's syndrome, using isotopically estimated cortisol production rates as 'gold standard'. DESIGN: Patients with Cushing's syndrome on medical treatment were given 12 ng of tritiated cortisol intravenously and a 24-hour urine collection was made in a single day. On the same day, serum cortisol was measured at 0900, 1200, 1500, 1800, 2100, and at 2400 h in in-patients. In addition, serum cortisol was measured at the same times as above in a group of healthy volunteers. SUBJECTS: Twenty-two patients on medical therapy for Cushing's syndrome were studied on a total of 29 occasions. In addition, serum cortisol profiles were obtained in 12 healthy volunteers. RESULTS: The median serum cortisol in patients with Cushing's syndrome was 400 (range 66-839) nmol/l, and in the healthy volunteers 178 (range 137-299) nmol/l. The median isotopic cortisol production rate in the patients with Cushing's syndrome was 84 mumol/24 h, range 10-343 (normal range 22-83) mumol/24 h. In the patients with Cushing's syndrome, the correlation of mean serum cortisol to cortisol production rate was +0.77 (P < 0.001). Normal rates were found when mean serum cortisol levels were between 150 and 300 nmol/l. CONCLUSIONS: The aim of drug therapy for Cushing's syndrome should be to lower the mean serum cortisol through the day into the range 150-300 nmol/l.

Cushing Syndrome↗

PubMed2001

A nonlabeled method to evaluate cortisol production rate by modeling plasma CBG-free cortisol disposition.

This study aimed to develop a nonlabeled method for the measurement of cortisol production rate to evaluate adrenal function. The cortisol production rate determination requires that of cortisol clearance, which is not a parameter but a variable resulting from the saturable binding of cortisol to corticosteroid-binding globulin (CBG). Our method is based on evaluation of the plasma clearance of the CBG-free cortisol fraction. This parameter was evaluated from a pharmacokinetic model of total plasma cortisol disposition that takes into account specific binding of the corticoid to CBG in the plasma. We have shown that the CBG-free cortisol kinetics and CBG-binding parameters thus evaluated are not statistically different from those obtained by the radioisotopic method and equilibrium dialysis, suggesting that the plasma CBG-free cortisol clearance is independent of the total plasma cortisol concentrations and represents the actual parameter of cortisol elimination. We validated this modeling approach by using it to calculate the in vivo entry rate of cortisol mimicked by the perfusion of cortisol at a known rate.

Animals↗

PubMed1989

Uptake of cortisol by the perfused rat liver: validity of the free hormone hypothesis applied to cortisol.

The mechanism by which cortisol in plasma enters hepatic cells was investigated using the isolated perfused rat liver. To determine whether hepatic uptake of cortisol from serum can be accounted for entirely by the pool of unbound (free) cortisol, we compared observed uptake rates with the equilibrium-free fraction of cortisol in serum and the rates of dissociation of cortisol from its serum binding proteins (determined using a rapid filtration assay based on transfer of [3H] cortisol to dextran-coated charcoal). More than 95% of the cortisol in both human and rat serum dissociated spontaneously from its binding proteins within 5 sec at 37 C. The fractional unidirectional hepatic uptakes of cortisol from pooled human serum and pooled rat serum were 59.4 +/- 5.4% and 59.5 +/- 1.0% (mean +/- SE), respectively, at the physiological flow rate of 1 ml/min.g liver. The corresponding free cortisol fractions in these sera were 4.53 +/- 0.15% and 8.16 +/- 0.23%, respectively. The fractional unidirectional hepatic uptake of cortisol from protein-free buffer averaged 99.9% (n = 5) at a flow rate of 3 ml/min.g liver. By calculating the appropriate rate constants and applying the Kety-Renkin-Crone equation to the above data, it can be shown that all of the cortisol taken up from serum by the perfused rat liver can be accounted for by the pool of free cortisol, which turns over very rapidly. The physiological significance of this finding is discussed in terms of a general mathematical model of hormone transport that delineates the conditions under which the free hormone hypothesis is and is not valid.

Animals↗

PubMed1980

Investigation of the secretion and metabolism of cortisol during a 100 km race using [4-14C] and [11 alpha-3H] cortisol.

A mixture of [11 alpha-3H] and [4-14C] cortisol was administered orally to healthy men, following which urine was collected for 24 h. Four subjects acted as basal controls, going about their normal (sedentary) work; a further 3 resting subjects also received 100 mg cortisol orally (high cortisol controls) and 6 subjects competed in a 100 km race. Decreases in the carbon-14 specific activity of the cortisol metabolite excreted by the runners suggested that they secreted cortisol at 2-4 times the rate of the basal controls. This change was mirrored by the excretion of urine free cortisol but not by that of 17-hydroxycorticosteroids. The isotope ratio (3H:14C) of 11-hydroxy metabolites of cortisol from the runners was intermediate between those of the basal and high cortisol controls, from which we conclude that though the fractional oxidation of cortisol to cortisone is reduced by increasing the cortisol pool, it is not affected by exercise per se. This and other results show that although continuous running for 6-8 h, involving energy expenditure in excess of 25 megajoules, leads to a moderate increase in the rate of cortisol secretion, running per se does not appear to markedly affect the metabolism of cortisol.

17-Hydroxycorticosteroids↗

PubMed2001

Exploration of the awakening cortisol response in relation to diurnal cortisol secretory activity.

Adrenocortical activity can be assessed by measurement of free cortisol in saliva. Cortisol status has important health implications in both physical and psychological terms. Assessment of cortisol status is complicated by the marked diurnal cortisol cycle. This cycle is characterised by an increase in secretory activity following awakening to achieve the morning acrophase. Thereafter it falls with a declining trend over the remainder of the day. For between subject studies the timing of sampling in relation to this cycle is an important consideration. We report a comprehensive study of the diurnal free cortisol cycle designed to analyse its components and to investigate their reliability and inter-relatedness. We instructed 42 healthy volunteers to collect saliva samples at home on two consecutive days. On each day the first sample was collected immediately upon awakening, followed by a further three samples at 15-minute intervals which collectively comprised the "awakening samples". A further four sample's were collected through the day at 3-hour intervals, all synchronized to awakening time. The cortisol response to awakening was calculated in two ways. Overall cortisol production in the first 45 minutes after awakening was calculated as area under the cortisol curve with reference to zero (AUC). The dynamic of the cortisol response to awakening was calculated as area under the cortisol response curve (AURC) with reference to the first awakening sample. In addition the underlying cortisol secretory activity was assessed based upon the diurnal three-hourly samples. All three parameters of adrenocortical activity showed reasonable stability across the two sampling days indicating all were reliable indexes of trait characteristic. AUC was representative of underlying diurnal activity but AURC was not. Measurement at any time point, 3, 6, 9 or 12 hours post-awakening was representative of the underlying 12-hour diurnal activity.

Adrenal Cortex↗

PubMed2002

Measurement of cortisol secretion rate by stable isotope methodology following oral administration of 13C-labeled cortisol to a human subject.

Plasma concentration measurements of 13C-labeled cortisol ([1,2,4,19-13C(4)]cortisol, cortisol-13C(4)) and its metabolite cortisone-13C(4) were made simultaneously with measurements of endogenous cortisol and cortisone by gas chromatography-mass spectrometry (GC-MS). After administering a small amount (3mg) of cortisol-13C(4) to a human subject, changes in cortisol secretion rates were estimated by deconvolution techniques from the measured plasma cortisol and cortisone levels and the rates of elimination and interconversion of cortisol and cortisone were obtained from the plasma concentration-time data of cortisol-13C(4) and cortisone-13C(4). The objective of this study was to look for a novel approach to quantitate rates of minute-to-minute cortisol secretion in man by taking into account the interconversion of cortisol and cortisone by 11beta-hydroxysteroid dehydrogenase (11beta-HSD).

11-beta-Hydroxysteroid Dehydrogenases↗

PubMedDate not supplied

Cortisol kinetics in elderly women with persistently high cortisol concentrations after proximal femur fracture.

OBJECTIVES: Elderly women with proximal femur fracture show abnormal persistence of increased cortisol concentrations, which could contribute to the high morbidity associated with this injury. Two weeks after injury, the authors found substantially increased urinary free cortisol excretion, which usually reflects the integrated concentration of free (bioactive) cortisol in plasma. However, there was a proportionally smaller increase in cortisol production rate. The authors have now tested the hypothesis that this was caused by a decreased metabolic clearance rate (MCR) rather than increased renal clearance, because the latter but not the former would invalidate free cortisol excretion as an index. SETTING: Orthopaedic wards in a teaching hospital. PATIENTS: Thirteen women aged seventy-one to ninety-two years who had sustained a proximal femur fracture approximately two weeks earlier were compared with ten healthy women aged sixty-seven to eighty-three years. These subjects are similar to those in the authors' previous study. MAIN OUTCOME MEASUREMENTS: The authors used single injections of [3H] cortisol to measure its MCR and estimated hepatic blood flow with indocyanine green. RESULTS: The patients with hip fractures had higher plasma cortisol concentrations than did the healthy subjects, as expected. Cortisol MCR was approximately 20 percent lower in the patients, and estimated hepatic blood flow was approximately 35 percent lower in the patients. Analysis of covariance showed that the difference in MCR was the result of the small difference in age between the groups rather than to injury per se. CONCLUSIONS: A lower cortisol MCR in the patients with hip fractures explains the authors' previous results and validates urinary free cortisol excretion as an index. The data suggest a roughly threefold mean increase in plasma cortisol bioactivity two weeks after hip fracture.

Aged↗

PubMed1993

Increased rates of cortisol production and urinary free cortisol excretion in elderly women 2 weeks after proximal femur fracture.

Cortisol production rate and urinary free cortisol excretion have been measured in healthy elderly women and elderly women about two weeks after upper femur fracture. Plasma cortisol was determined mid-morning, at the start of urine collection. All three variables were higher in the injured patients than in the control subjects. Urinary free cortisol excretion showed the greatest rise and was correlated with cortisol production rate in the patients. In the control subjects there was no correlation and nearly all the points fell below the regression line for the injured patients, indicating that urinary free cortisol excretion rose in relation to cortisol production rate after injury. Measurement of creatinine clearance showed that this was not due to an increased glomerular filtration rate, and a possible explanation is decreased metabolic clearance of cortisol. Plasma cortisol was not significantly correlated with either cortisol production rate or urinary free cortisol excretion.

Aged↗

PubMed1976

The effect of ACTH and cortisol on aldosterone and cortisol clearance and distribution in plasma and whole blood.

The mechanisms of increased aldosterone and cortisol metabolic clearance rates (MCR) following ACTH or cortisol administration were studied in 13 subjects undergoing cardiac catheterization and in 9 healthy controls. In control subjects, the MCR (plasma) of both steroids increased by 29% (aldosterone: from 936 +/- 57 to 1204 +/- 55 l/day/m2, cortisol: from 205 +/- 12 to 264 +/- 17 l/day/m2 +/- SE) after ACTH (12 units/h) for 1 to 4 h, and by 20 and 32%, respectively, after cortisol (12 mg/h) for 1 to 2 h. In contrast, aldosterone MCR (whole blood) did not change with ACTH or cortisol administration (from 1276 +/- 57 to 1330 +/- 59 l/day/m2), indicating that the plasma MCR increase results from a redistribution of aldosterone from plasma to red cells. Aldosterone splanchnic extraction was 92 +/- 1% (n = 12) with normal morning cortisol levels, and extraction was unchanged after ACTH administration. For cortisol, however, the splanchnic extraction increased from 8 +/- 0.8% to 17.8 +/- 5.0%, and the MCR (whole blood) likewise increased by 15 to 31% (from 295 +/- 23 to 357 +/- 30 l/day/m2), after ACTH or cortisol administration. In vivo and in vitro measurements (at 37 C) of tracer aldosterone concentration in plasma and in red cells showed an increase in distribution to red cells with increasing cortisol concentrations. The results suggest that a fraction of aldosterone is bound in plasma and displaced by cortisol into red cells. There is an increased aldosterone plasma MCR, but unaltered whole blood MCR, since the liver extracts aldosterone almost completely from both plasma and red cells. The increase in cortisol MCR (plasma) results from both an increased splanchnic extraction as plasma binding sites approach saturation and a redistribution into red cells.

Adrenocorticotropic Hormone↗

PubMed2002

Free cortisol index as a surrogate marker for serum free cortisol.

BACKGROUND: The biologically active component of a hormone is the unbound or free fraction. Changes in cortisol-binding protein could give misleading results if only total cortisol is measured for the interpretation of dynamic function tests. METHODS: This study aimed to measure serum free cortisol using a steady-state gel-filtration method and then to evaluate the correlation between the serum free cortisol and the free cortisol index (FCI), defined as serum total cortisol/cortisol-binding globulin (CBG). RESULTS: Forty-eight serum samples from healthy volunteers undergoing a short Synacthen test were analysed for total cortisol, free cortisol and CBG. The FCI correlated well with a previously established, but more complex, calculation of serum free cortisol (R = 0.98, P <0.001) and with measured serum free cortisol (R = 0.90, P < 0.001). CONCLUSION: Free cortisol index is a reliable and user-friendly measure of serum free cortisol.

Adult↗

PubMed1998

Salivary cortisol--an alternative to serum cortisol determinations in dynamic function tests.

Salivary cortisol was measured as an alternative to serum cortisol as a marker for adrenocortical function following insulin tolerance test, corticotropin-releasing-hormone stimulation and adreno-corticotrophic hormone stimulation. During insulin tolerance test and corticotropin-releasing-hormone stimulation adreno-corticotrophic hormone was also measured. The tests were performed on healthy control subjects as well as on patients under investigation for various disturbances in the hypothalamic-pituitary-adrenocortical axis (insulin tolerance test: 3 controls on two occasions and 14 patients; corticotropin-releasing-hormone stimulation: 4 controls and 18 patients; adreno-corticotrophic hormone stimulation: 6 controls and 10 patients). Five patients underwent both insulin tolerance test and corticotropin-releasing-hormone stimulation. Using criteria for adequate cortisol response in serum, the patients were classified as good or poor responders. In 42 of the 45 tests performed the same conclusion as to cortisol status was drawn when based on serum and salivary cortisol responses. In healthy subjects and good responders the mean cortisol relative increase was greater in saliva than in serum in all three tests (p < 0.05). Characteristic of the results for the insulin tolerance test was a significant initial mean decrease (p < 0.05), not found in serum, and the highest observed salivary cortisol value was delayed for at least 30 minutes compared to that in serum. Plasma adreno-corticotrophic hormone correlated significantly with the cortisol concentrations determined 15 minutes later in serum (r = 0.54-0.64) and in saliva (r = 0.76-0.85). The more pronounced cortisol response in saliva than in serum and its closer correlation with adreno-corticotrophic hormone offer advantages over serum cortisol, suggesting salivary cortisol measurement may be used as an alternative parameter in dynamic endocrine test.

Adrenal Cortex↗

PubMed2006

Salivary cortisol in low dose (1 microg) ACTH test in healthy women: comparison with serum cortisol.

To date, a single report has appeared on the use of salivary cortisol for adrenal function testing with a low dose ACTH, although 1 microg has become preferred as a more physiological stimulus than the commonly used 250 microg ACTH test. Our present study was aimed to obtain physiological data on changes of free salivary cortisol after 1 microg ACTH stimulation. This approach was compared with the common method based on the changes of total serum cortisol. Intravenous, low-dose ACTH test was performed in 15 healthy women (aged 22-40 years) with normal body weight, not using hormonal contraceptives, in the follicular phase of the menstrual cycle. Blood and saliva for determination of cortisol were collected before ACTH administration and 30 and 60 min after ACTH administration. Basal concentration of salivary cortisol (mean +/- S.E.M., 15.9+/-1.96 nmol/l) increased after 1 microg ACTH to 29.1+/-2.01 nmol/l after 30 min, and to 27.4+/-2.15 nmol/l after 60 min. The differences between basal and stimulated values were highly significant (p<0.0001). The values of salivary cortisol displayed very little interindividual variability (p<0.04) in contrast to total serum cortisol values (p<0.0001) A comparison of areas under the curve (AUC) related to initial values indicated significantly higher AUC values for salivary cortisol than for total serum cortisol (1.89+/-0.88 vs. 1.22+/-0.19, p<0.01). Correlation analysis of serum and salivary cortisol levels showed a borderline relationship between basal levels (r=0.5183, p=0.0525); correlations after stimulation were not significant. Low-dose ACTH administration appeared as a sufficient stimulus for increasing salivary cortisol to a range considered as a normal adrenal functional reserve.

Adrenal Glands↗

PubMed2002

[Direct assay for urine cortisol with cortisol kit [TFB]].

We examined Cortisol Kit [TFB] for direct assay of urine cortisol. And the multiplication by dilution factor of urine cortisol values in this kit was examined. The coefficient of correlation of cortisol levels (46 urine samples) between Cortisol Kit [TFB] and Chemilumi ACS-Cortisol II, which is another kit for direct assay of urine cortisol, was r = 0.858, y = 1.86x + 38.2 (p < 0.001). There were differences between the both cortisol levels of each urine sample in spite of the good coefficient of correlation. The urine cortisol values obtained from the standard curve in addition of 50 microliters of zero standard were 50-80% of the values obtained from the standard curve in the package insert. These results suggest that the specificity of the antibodies of both direct assay kits for urine cortisol may be different each other, and the multiplication by 1.09, the dilution factor due to the addition of zero standard to only urine sample, is unnecessary although it is indispensable for urine samples to add zero standard. Cortisol Kit [TFB] was very convenient for its easy assay procedure and short incubation.

Evaluation Studies as Topic↗

PubMed1990

Differences between concentrations of salivary cortisol and cortisone and of free cortisol and cortisone in plasma during pregnancy and postpartum.

We measured cortisol and cortisone in plasma--both total and free--and in saliva during the course of pregnancy and postpartum. Antepartum and postpartum concentrations and morning and afternoon concentrations of both steroids were compared. The mean concentrations of cortisol and cortisone increased towards term and were significantly greater at the end of pregnancy than postpartum, except for free cortisol in plasma in the afternoon. The daily rhythm of both steroids was maintained throughout pregnancy and postpartum. The correlations between salivary and plasma free concentrations of cortisol and cortisone as well as of the sum of cortisol + cortisone were highly significant. The mean concentrations of cortisone in saliva accurately reflected both total and free concentrations in plasma. For cortisol, however, the change of the concentrations in saliva, was somewhat different from that in plasma. Moreover, the mass ratio of plasma free cortisol to salivary cortisol was about 2, whereas for cortisone the ratio was only about 0.5, probably owing to the conversion of cortisol to cortisone by 11 beta-hydroxysteroid dehydrogenase in the salivary gland. Furthermore, the passage of cortisol and cortisone from plasma to saliva should not be regarded as simple diffusion, because in the first half of pregnancy the sum of the concentrations of cortisol + cortisone in saliva significantly exceeded the sum of their free concentrations in plasma.

Adult↗

PubMed1984

Affinity of tixocortol pivalate (JO 1016), tixocortol, cortisol acetate and cortisol for dexamethasone receptors of mouse thymus cells and rat renomedullary interstitial cells in culture. Correlation with their biological activities.

Affinity for the dexamethasone binding sites of tixocortol pivalate, (the ester of the 21 thiol derivatives of cortisol), a steroid with local anti-inflammatory activity similar to cortisol acetate and with no systemic activity, was investigated in comparison with other steroids: tixocortol (the thiol derivative yielded by esterase hydrolysis), cortisol acetate and cortisol. The rank order of relative affinity for dexamethasone receptor of mouse thymocytes (37 degrees C) was: dexamethasone (1), cortisol (0.20), tixocortol pivalate (0.16), tixocortol (0.065), cortisol acetate (0.05). The corresponding 21 oxygenated ester (cortisol pivalate) was found less potent (0.080). Using rat renomedullary interstitial cells in culture, tixocortol pivalate showed also a higher receptor affinity than tixocortol. Cortisol acetate was as potent as tixocortol pivalate. The biological activity of tixocortol pivalate measured by the inhibition of PGE2 secretion on the same model, was similar to cortisol acetate and cortisol (10(-6) M, 24 h incubation, 38-55% inhibition). Tixocortol was less active (26%). These results with tixocortol pivalate are in good agreement with previously reported in vivo studies and show a good correlation between its binding ability and biological effect.

Animals↗

PubMed1994

Measurement of urinary free cortisol by stable isotope dilution mass spectrometry using a new cortisol derivative.

The reaction of the bismethylenedioxy derivative of cortisol (cortisol-BMD) with heptafluorobutyric anhydride to give the corresponding 3,5-dienol heptafluorobutyrate (cortisol-BMD-HFB) has been shown to proceed with dehydration. Acid-promoted dehydration of either cortisol-BMD or cortisol-BMD-HFB, or concurrent dehydration of both, is the proposed reaction mechanism leading to a trienol heptafluorobutyrate, whose chromatographic properties and mass spectral data are consistent with the additional double bond in the C9-C11 position. Forming the 3,5-dienol heptafluorobutyrate of cortisol-BMD in benzene rather than acetone gave a compound whose chromatographic properties and mass spectral data were different to that of the 3,5,9(11)-trienol heptafluorobutyrate but consistent with that of a cortisol-BMD-HFB. The mass fragmentometry of this new cortisol derivative was found to be more suited to the technique of isotope dilution mass spectrometry than the 3,5,9(11)-trienol heptafluorobutyrate, and thus was applied to our intended goal of measuring urinary free cortisol by gas chromatography-mass spectrometry. An efficient and convenient solid-phase extraction technique is employed in our assay to isolate cortisol from 5 ml of urine.

Fluorocarbons↗

PubMed1975

Serum cortisol binding capacity and cortisol concentration in the pregnant baboon and its fetus during gestation.

The cortisol binding capacity of serum from 11 pregnant baboons (38 samples) and from 7 baboon fetuses delivered prematurely or at term was measured after removal of endogenous steroids. Values for maternal serum collected between 60 and 120 days after mating (59.0 +/- 6.4 mug/100 ml, mean +/- SD) were greater than those for serum collected at term (42.3 +/- 4.9 mug/100 ml). The cortisol-binding capacity of fetal serum collected between 100 and 132 days' gestation was similar to that of the corresponding maternal sample, but at term was only 50% of the maternal value. The rate of clearance of cortisol from both fetal and maternal serum may therefore increase progressively during the last trimester of pregnancy. This effect is likely to be more marked in the fetus. The cortisol binding capacity of 15 serum samples from 9 non-pregnant baboons was 33.4 +/- 5.5 mug/100 ml. Mestranol2 (administered 200 mug/day im for 15 days) significantly increased the serum cortisol binding capacity. The concentration of cortisol in maternal serum from 7 pregnant baboons (10 samples) was 44.0 +/- 8.4 mug/100 ml and was independent of the state of gestation. In fetal serum the cortisol concentration was 4 mug/100 ml before 168 days' gestation and reached 49 mug/100 ml after normal delivery at term. These findings suggest that the mechanisms for production of cortisol by the fetus mature as gestation progresses. The physiological significance of the marked difference between the cortisol concentration and the cortisol binding capacity of fetal serum awaits elucidation.

Animals↗