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PubMed1996

Fasting as a metabolic stress paradigm selectively amplifies cortisol secretory burst mass and delays the time of maximal nyctohemeral cortisol concentrations in healthy men.

Serum cortisol concentrations are increased in fasted or malnourished human subjects. The dynamic mechanisms underlying this adaptive response have been investigated in eight normal men by analyzing serum cortisol concentrations measured in blood obtained at 5-min intervals over 24 h on a control (fed) day and on the fifth day of a fast (water only) assigned in randomized order. A multiple parameter deconvolution method was used to simultaneously resolve endogenous cortisol secretion and half-life. Five days of fasting induced a 1.8-fold increase in the 24-h endogenous cortisol production rate (fed, 2504 +/- 308; fasted, 4528 +/- 488 nmol/L distribution volume; P < 0.006). This enhanced cortisol production rate was accounted for by a 1.6-fold increase in the mass of cortisol secreted per burst (fed, 115 +/- 12.1; fasted, 183 +/- 17.3 nmol/L; P < 0.02). Cortisol secretory event amplitudes (maximal rates of cortisol release attained within a burst) increased in seven of eight men, and mean secretory burst durations remained unchanged by fasting. Moreover, the number of computer-resolved cortisol secretory bursts per 24 h (fed, 22 +/- 1.4; fasted, 25 +/- 2.0; P = NS) and the interburst interval (fed, 65 +/- 4.0; fasted, 57 +/- 4.4 min) did not change significantly during a 5-day fast. The calculated half-life of endogenous cortisol was not significantly altered by fasting (fed, 108 +/- 9.7; fasted, 129 +/- 11 min). There was no significant change in the nyctohemeral pattern of varying adrenocortical secretory burst frequency in response to fasting. However, the mean (mesor) mass of glucocorticoid secreted per burst over 24 h rose significantly in response to fasting. In addition, by cosinor analysis, maximal serum cortisol concentrations occurred (95% confidence intervals) between 0930-1334 h in the fed state and between 1116-1612 h in the fasted state (P < 0.04). Fasting augmented the mesor (average value about which the diurnal rhythm oscillates; P < 0.0008 compared with fed state) and the amplitude (P < 0.04) of the 24-h serum cortisol concentration profile. Linear regression analysis disclosed a significant inverse relationship between mean serum cortisol and GH concentrations in fasted men (r = -0.76; P < 0.02). In conclusion, the present data indicate that starvation-induced enhancement of cortisol secretion in young healthy men is mediated by an increased glucocorticoid secretory burst mass, rather than changes in secretory burst frequency or duration or in cortisol half-life. In addition, fasting modifies the diurnal secretory pattern of cortisol by delaying maximal serum concentrations to the early afternoon. The inverse relationship between serum cortisol and GH responses to fasting suggests differential regulation of the corticotropic and somatotropic axis by the metabolic stress of fasting and/or feedback interactions between these two axes when they are both activated.

Adult↗

PubMed1999

Diagnosis of Cushing's syndrome: re-evaluation of midnight plasma cortisol vs urinary free cortisol and low-dose dexamethasone suppression test in a large patient group.

We studied plasma cortisol levels at 00:00 h and 08:00 h in 103 patients with Cushing's syndrome and 144 patients in whom this diagnosis had been excluded. These patients were hospitalized in our department from 1975 to 1996. Additionally, we measured these parameters in 20 healthy volunteers and in 5 patients with nonendocrine disease. Corresponding data of urinary free cortisol and low-dose dexamethasone suppression testing were included in the evaluation. Values (mean+/-SD) from patients with Cushing's syndrome: 510+/-232 nmol/l (range 165-1488) for plasma cortisol 00:00 h, 574+/-242 nmol/l (range 236-1612) for plasma cortisol 08:00 h, 991+/-885 nmol/24 h (range 154-4866) for urinary free cortisol and 479+/-304 nmol/l (range 34 - 1,393) for plasma cortisol after 1.5 mg dexamethasone. Values from the patients excluded from Cushing's syndrome: 99+/-76 nmol/l (range 5-371) for plasma cortisol 00:00 h, 393+/-136 nmol/l (range 119-812) for plasma cortisol 08:00 h, 126+/-84 nmol/24 h (range 30-485) for urinary free cortisol, and 64+/-82 nmol/l (range 5-395) for plasma cortisol after 1.5 mg dexamethasone. Values of the healthy volunteers respectively patients with non-endocrine disease: 59+/-30 nmol/l (range 25-130) respectively 127+/-80 nmol/l (range 62-265) for plasma cortisol 00:00 h and 388+/-144 nmol/l (range 157-651) respectively 498+/-113 nmol/l (range 302-581) for plasma cortisol 08:00 h. None of the Cushing patients exhibited a 00:00 h plasma cortisol below 140 nmol/l and only one had a urinary free cortisol below 200 nmol/24 h, whereas 4 were complete dexamethasone suppressors. The diagnostic value of these parameters was examined based on various cutoffs. We recommend determination of midnight plasma cortisol as an efficient and simple additional procedure for the diagnosis of Cushing's syndrome. The sensitivity and specificity of this procedure is similar to urinary free cortisol and slightly above the low-dose dexamethasone suppression testing in our hospitalized patients.

Adult↗

PubMed2004

Circulating adrenocorticotropic hormone (ACTH) and cortisol concentrations in normal, appropriate-for-gestational-age newborns versus those with sepsis and respiratory distress: Cortisol response to low-dose and standard-dose ACTH tests.

In this crossover study, we compared the peak responses of cortisol to low-dose (1 microg/1.73 m(2)) and standard-dose (250 microg/1.73 m(2)) adrenocorticotropic hormone (ACTH) stimulation tests in 90 full-term newborns (37 to 42 weeks gestational age, birthweight > 2,500 g, aged 4 to 7 days): 30 with sepsis syndrome, 30 with respiratory distress (RD) and 30 normal infants. Basal cortisol and ACTH were measured in a fasting venous sample. Serum cortisol concentrations were measured 30 minutes after low-dose ACTH and 60 minutes after standard-dose ACTH by radioimmunoassay (RIA). The mean basal circulating cortisol concentration and peak cortisol responses to low-dose and standard-dose ACTH tests were higher in stressed infants with sepsis and RD compared to normal. Basal but not ACTH-stimulated cortisol concentrations were significantly higher in newborns with sepsis versus those with RD. Circulating cortisol concentrations after the low-dose ACTH test were correlated significantly with those obtained after the standard-dose ACTH test (r = 0.814, P <.001). Clinical subgrouping of septic newborns showed that those with leukopenia (5/10 died) and with meningitis (6/12 died) had significantly lower basal and peak cortisol responses to the low-dose ACTH test (but not the standard-dose ACTH test) versus those with leukocytosis (3/20 died) and without meningitis (2/18 died), respectively. In addition, septic newborns who died had significantly lower circulating cortisol concentrations and lower cortisol responses to the low-dose ACTH test (but not the standard-dose test) versus those who survived the stress. On an individual basis, only 2 septic newborns (both died) had low basal cortisol levels (<5 microg/dL) and cortisol responses less than 15 microg/dL after the low-dose ACTH test. Four more septic newborns had basal cortisol above 5 microg/dl but cortisol responses below 20 microg/dL after the low-dose ACTH test. These 4 newborns (4/30) with inadequate adrenocortical response to low-dose ACTH during sepsis had high mortality (3/4 died) and represented a subgroup of septic newborns that should be diagnosed, using a low-dose ACTH test, and treated early. These data suggest that the low-dose ACTH test may be more disciminatory than the standard-dose test among babies under stress. Increasing the cut-point level of basal cortisol in stressed infants to the lowest level of cortisol response to low-dose ACTH in normal newborns, followed by the use of a low-dose ACTH test, appears to select some newborns who need and may improve on corticosteroid therapy. Further studies are required to investigate whether supplementation with stress doses of hydrocortisone may improve the outcome in these patients.

Adrenocorticotropic Hormone↗

PubMedDate not supplied

Kinetics of intravenously dosed cortisol in four men. Consequences for calculation of the plasma cortisol production rate.

The kinetics of cortisol in the serum of 4 healthy men were studied following single i.v. doses of 2 and 0.8 mg of cortisol. The disappearance of cortisol was determined by blood sampling frequently over 2.5 h and analysing the apparently biexponential cortisol decay. The main results, shown as the mean (+/-SD), were: (a) the average distribution volume of cortisol at steady state (Vd,ss), which was 7.1 l/m2 body surface area. The extrapolated distribution volume (Vd,ext) was 8.4 l/m2, being 18% higher than the corresponding Vd,ss. (b) It was confirmed that plasma cortisol disappears biexponentially. Since the rapid phase remains unnoticed if cortisol is measured at an interval of 10 or more minutes, the obscured rapid-phase parameters can be found only if the known ratio of the two rate constants is used. (c) The fraction of cortisol, which during this fast phase irreversibly disappeared according to the two-compartment open model, was 5 to 8% larger than that found using the monocompartment model. (d) The half-life of the slow or beta phase was equal for the 2 and 0.8 mg experiments, namely t1/2(beta) = 66 +/- 18 min. The kinetics of cortisol in the same 4 men were also measured after an i.v. dose of radioactive cortisol (82 +/- 7 kBq 3H/m2). All urine was collected in 15 portions during the next 3 days, followed by measuring the cumulative radioactivity and analysing the triexponential increase of urinary radioactivity [1]. The main results with the urinary model were: (a) the half-life of cortisol elimination from the circulation was 40 +/- 11 min, (b) the maximal radioactivity (69 +/- 7% of the dose) in the first pool (liver) was found at 2 +/- 0.3 h, (c) the half-life of the cortisol metabolites in the body was 6.8 +/- 0.7 h. Forcing the measured cortisol concentrations in plasma to fit a monoexponential function, allowed us to compare the half-life of cortisol decay with that from the urinary model. It was found that these half-lives were similar with values between 30 and 40 min. Finally, the distribution volume has to be measured individually if a 24 h plasma cortisol profile is used for the calculation of the cortisol production rate.

Anti-Inflammatory Agents↗

PubMed1999

Evaluation of adrenal function in patients with hypothalamic and pituitary disorders: comparison of serum cortisol, urinary free cortisol and the human-corticotrophin releasing hormone test with the insulin tolerance test.

OBJECTIVE: This study aimed to evaluate the performance of screening tests (serum cortisol and 24-h urinary free cortisol) and the human-corticotrophin releasing hormone (h-CRH) test in the assessment of adrenal function in patients with hypothalamic-pituitary disorders. DESIGN: Summary receiver operating characteristics (SROC) curve analysis was applied with the insulin tolerance test (ITT) as reference test. A peak serum cortisol response to ITT > or = 500 nmol/l indicated adrenal sufficiency. The sensitivity at the intersect of the diagonal between sensitivity = 1 and (1-specificity) = 1 with the SROC curve, where sensitivity and specificity are equal, and the corresponding weighted kappa, an estimate of agreement with the ITT, served as parameters of test performance. The diagnostic yield, representing the proportion of tests obviating the need for an ITT, was also calculated. MEASUREMENTS: Serum cortisol at 0800 h (n = 122), at 1600 h (n = 116), 24-h urinary free cortisol (n = 115) and the peak serum cortisol to h-CRH (n = 129) were compared with the peak serum cortisol to ITT. PATIENTS: Eighty patients with hypothalamic-pituitary disorders in whom 75 ITT's were performed pre- and 57 post-operatively. RESULTS: Sensitivity at the intersect and weighted kappa were higher for 0800 h serum cortisol (0.873 and 0.763 respectively) than for 1600 h serum cortisol (0.769 and 0.561) and 24-h urinary free cortisol (0.777 and 0.576). These parameters were 0.868 and 0.756 for the h-CRH test. The diagnostic yield was 63.9% for 0800 h serum cortisol compared to 25.9% for 1600 h serum cortisol (P < 10(-8)), 23.5% for 24-h urinary free cortisol (P < 10(-8)) and 60.5% for the h-CRH test (NS). CONCLUSIONS: Serum cortisol measurement at 0800 h is better than 1600 h and 24-h urinary free cortisol to evaluate adrenal function in this patient category. The diagnostic applicability of the h-CRH test is not superior to 0800 h serum cortisol measurement.

Adenoma↗

PubMed1997

A putative cortisol receptor in the rainbow trout erythrocyte: stress prevents starvation-induced increases in specific binding of cortisol

Binding sites for the steroid hormone cortisol, with characteristics typical of a steroid receptor, were detected in the rainbow trout (Oncorhynchus mykiss) erythrocyte. Binding of [3H]cortisol to a washed and purified erythrocyte suspension was saturable (Bmax=0.33±0.06 fmol per 2x10(6) cells; approximately 100±18 sites per cell; mean ± s.e.m., N=6), of high affinity (Kd=4.7±0.4 nmol l-1) and reversible in the presence of an excess of unlabelled ligand. Maximum levels of specific binding were observed within 60 min of the addition of [3H]cortisol at 4 °C and were stable for 23 h. Within 20 min of the addition of excess unlabelled ligand, 60 % of specifically bound [3H]cortisol had dissociated. Both dexamethasone and cortisol completely displaced specifically bound [3H]cortisol at 100-fold excess, whereas a 1000-fold excess of unlabelled cortisone, 11-ketotestosterone, oestradiol-17ß, testosterone and 17,20ß-dihydroxy-4-pregnen-3-one failed to displace specifically bound [3H]cortisol completely. Specific binding sites for [3H]cortisol were located predominantly (92 %) within the cytosolic fraction of the erythrocyte, with a trace amount of specific binding (8 %) detectable in the membrane fraction. No specific binding of [3H]cortisol was apparent in the erythrocyte nuclear fraction. A 7 day period of confinement stress resulted in no significant change in the number of erythrocyte cortisol-binding sites in rainbow trout, although plasma cortisol levels were significantly elevated in the stressed fish. However, in control unconfined fish, there was a progressive and significant increase in the amount of specifically bound cortisol per cell during the course of the experiment (from 0.097±0.030 to 0.260±0.070 fmol per 2x10(6) cells). A similar result was obtained when the experiment was repeated for confirmation. In both experiments, food was withheld from control and confined fish because of the negative impact of stress on appetite. The possibility that the increase in the number of erythrocyte cortisol-binding sites was related to the withdrawal of food was tested by quantifying the amount of specifically bound cortisol in erythrocytes over a 14 day period in unstressed rainbow trout maintained on normal rations and in unstressed fish from which food was withheld. A significant increase in the amount of specifically bound cortisol was observed with time in the fasted fish (from 0.33±0.07 to 0.53±0.03 fmol per 2x10(6) cells). These data suggest that the abundance of erythrocyte cortisol-binding sites in trout is a function of nutritional status and that stress opposes a fasting-induced increase in the number of binding sites.

Journal Article↗

PubMed2001

[ACTH stimulation test for the determination of salivary cortisol and of cortisol responses as markers of the training status/fitness of warm-blooded sports horses].

Previous work (Marc et al., 2000) suggested that plasma cortisol responses to treadmill exercise or ACTH injection are a reliable marker for performance evaluation in warmblood horses. For practical purposes blood sample collections and treadmill exercise tests are somewhat troublesome and time consuming. The goal of this study was thus to evaluate the use of saliva for cortisol determination (by direct EIA) as a marker for performance and to investigate the reliability and repeatability of plasma cortisol responses to a single i.v. injection of ACTH (50 micrograms or 250 micrograms). Furthermore, the effect of training horses for 8 weeks 3 times per week covering the same distance (increasing from 3.5 km during the first week to 8 km during the last week) either by trotting (approximately 240 m/min) or by cantering (375 m/min) was investigated. For this purpose initially ten four-year-old Hannovarian geldings, all reared in the same State stud, were used. Mean overall correlation between salivary cortisol and plasma cortisol concentrations was 0.64 when samples of various points of time were used. However, in spite of attempts to standardize saliva sample collection, correlation between salivary cortisol levels and plasma cortisol levels at distinct points of time in different tests were low and significant (r = 0.85, p < 0.02) only in one test. Thus, salivary cortisol measurements for diagnostic purposes are not reliable or useful. The repeatability of plasma cortisol responses to ACTH for untrained and trained horses were r = 0.86 and r = 0.8 respectively (p < or = 0.01 and p < or = 0.05 respectively). Training horses either by trotting or cantering did not affect the cortisol response either to treadmill exercise or to stimulation by ACTH. It is concluded that the relationship between salivary cortisol levels and plasma cortisol levels is not close enough to allow the use of salivary cortisol determination as marker of the training status/fitness of horses. The repeatability of the cortisol response to ACTH is similar to the cortisol response to treadmill exercise. Based on plasma cortisol responses to ACTH or treadmill exercise training horses by cantering at low speed is not superior to training by trotting for the fitness of horses.

Adrenocorticotropic Hormone↗

PubMed2000

Blood levels of corticosteroid-binding globulin, total cortisol and unbound cortisol in patients undergoing coronary artery bypass grafting surgery with cardiopulmonary bypass.

Previous studies have demonstrated a persistent rise in serum cortisol concentrations after cardiac surgery. To further investigate this finding and to evaluate the effect of hemodilution that occurs with the onset of cardiopulmonary bypass (CPB), concentrations of cortisol-binding globulin (CBG), total and unbound cortisol, and packed cell volume (PCV) were studied in 28 patients undergoing coronary artery bypass graft surgery. All patients received a standardized general anesthetic using a balanced technique with sufentanil, isoflurane, and midazolam. Blood was collected preoperatively, intraoperatively during CPB, and postoperatively in the evenings on the day of surgery and on the first and second postoperative day. Cortisol and CBG concentrations were measured by radioimmunoassay and were used to calculate the fraction of unbound cortisol. Serum CBG and cortisol concentrations corrected for hemodilution were significantly higher than non-corrected values. Perioperatively, CBG measurements were significantly intercorrelated. Intraoperatively, total and unbound cortisol concentrations were not significantly increased compared to preoperative values. Postoperatively up to the end of the study period serum concentrations of total and unbound cortisol were significantly increased compared to baseline values. Our results suggest that hemodilution occurs in all patients during cardiac surgery and continues up to the second postoperative day. This may lead to an underestimation of serum cortisol and CBG concentrations in patients undergoing heart surgery with CPB. Intraoperatively, concentrations of total and unbound cortisol were not significantly elevated. The postoperative rise in serum total cortisol concentration was accompanied by an increase in unbound cortisol concentration. The postoperative increase of unbound cortisol concentrations in patients undergoing cardiac surgery with CPB was largely due to an increase in cortisol secretion.

Aged↗

PubMed1979

Plasma clearance of cortisol as a function of plasma cortisol levels in normal and obese persons and in patients with uraemia or cirrhosis of the liver.

Plasma cortisol levels in 2 normal persons, 2 obese persons, 2 uraemic patients, and 2 patients with cirrhosis of the liver were raised in 4 steps by a combination of iv priming doses and continuous infusions of cortisol. Plasma cortisol levels and transcortin binding were measured as well as plasma clearance rates of labelled and unlabelled cortisol during each of the 5 experimental periods. Plasma cortisol levels increased less and plasma clearance rates of labelled and unlabelled cortisol increased more in obese persons than in normal persons; in patients with disturbed metabolism of cortisol (uraemia, cirrhosis of the liver) the reverse is true. Plasma clearance rates of free cortisol were calculated and differed from an estimated hepatic plasma flow of 0.7 1/min under certain conditions. Since free cortisol is metabolized faster than transcortin-bound cortisol, increasing plasma clearance rates of cortisol are probably due to increasing ratios free/bound cortisol when total plasma cortisol levels are raised. Low plasma clearance rates of cortisol in uraemia and cirrhosis of the liver are thought to be due to endproduct inhibition, respectively reduced liver cell mass.

Adult↗

PubMed2005

Effects of high-intensity isokinetic exercise on salivary cortisol in athletes with different training schedules: relationships to serum cortisol and lactate.

Physical exercise is associated with increases of serum and salivary levels of cortisol. The concomitant increase in serum lactate has been implicated as one of the mechanisms responsible for adrenocortical activation. We evaluated the responses of serum lactate and serum and salivary cortisol to an acute bout of high-intensity isokinetic exercise in eleven non-competitive and twenty competitive athletes (NCA and CA, respectively). The latter group was composed of endurance- and power-trained athletes (EA and PA, respectively). Aims of the study were to determine interindividual differences in the lactate and cortisol responses as a function of type and intensity of training and to search for relationships both between lactate and cortisol production and between serum and salivary cortisol levels. The isokinetic exercise test elicited significant cortisol and lactate responses. No difference was evident in the lactate responses between NCA and CA, while the PA showed a higher response during and after the exercise in comparison to EA (peak levels immediately after the exercise: PA 15.0 +/- 1.5 mmol/l vs. EA 11.1 +/- 2.6 mmol/l, p < 0.01). Serum cortisol was higher in the CA in comparison to the NCA group at 30 and 120 minutes after the termination of the exercise, while no differential response was evident between EA and PA groups. Salivary cortisol response was higher in the CA group in comparison to NCA immediately after the exercise and at 90 and 120 minutes after the termination and was higher in PA in comparison to EA at 60, 90, and 120 minutes after the termination (peak levels at 60 minutes: PA 51.2 +/- 18.5 nmol/l vs. EA 27.5 +/- 20.8 nmol/l, p < 0.05). No significant correlations were found between serum or salivary cortisol and lactate levels. The relationship between serum and salivary cortisol was markedly non-linear, the slope of the serum-saliva regression line being lower for serum cortisol concentrations over 500 nmol/l than for concentrations below that value (0.019 and 0.037, respectively, p < 0.01). We have confirmed in this particular setting the existence of an important adrenocortical response that can be reliably and non invasively assessed by a serial saliva sampling and have supported the concept that cortisol and lactate responses to a high-intensity isokinetic exercise are independent. The interindividual differences in cortisol changes are likely to be related to the training status and mode as well as to the correspondence between the evaluation protocol and the discipline individually performed.

Adult↗

PubMedDate not supplied

Urinary cortisol and cortisol metabolite excretion in chronic fatigue syndrome.

OBJECTIVES: Reduced basal hypothalamic-pituitary-adrenal (HPA) axis output in chronic fatigue syndrome (CFS) has been inferred from low cortisol levels in blood, saliva, and urine in some studies. Because > 95% of cortisol is metabolized before excretion, we assessed cortisol output by assay of both cortisol metabolites and free cortisol in 24-hour urine collections and also investigated sex differences in these between CFS and control groups. METHOD: We calculated total urinary cortisol metabolites (TCM) and cortisol metabolite ratios from individual steroid data in 40 patients (20 males and 20 females) with CFS who were free of medication or comorbid psychiatric disorder likely to influence the HPA axis. Results were compared with those of 40 healthy volunteers (20 males and 20 females) well matched for age and body mass index. Data for free cortisol was obtained on 28 of the patients and 27 of the controls. RESULTS: The mean of TCM and cortisol metabolite ratios was not significantly different between patients and controls for either sex (p > .05 for all parameters). Previously established sex differences were confirmed in our controls and were found to be similar in CFS for TCM and the ratios 11OH/11OXO, 5alpha/5beta THF, and 20OH/20OXO (see text) (p < .005, p < .05, p < .05, and p < .005, respectively). Urinary free cortisol values were numerically (but not statistically) lower in patients with CFS than controls, and correlated inversely with fatigue levels in patients. CONCLUSION: The finding of normal urinary cortisol metabolite excretion in patients with CFS is at variance with earlier reports that CFS is a hypocortisolemic state. If serum and saliva cortisol levels are lower in CFS, this would suggest that metabolic clearance of cortisol is faster in patients with CFS than controls. This study also demonstrates that sex differences must be taken into account when interpreting results in patients with CFS.

11-beta-Hydroxysteroid Dehydrogenases↗

PubMed2005

Stress responses at birth: determinants of cord arterial cortisol and links with cortisol response in infancy.

OBJECTIVE: To investigate (A) the determinants of infant stress response at delivery and (B) test the hypothesis that stress at birth, as reflected by cord arterial cortisol, influences cortisol response to vaccination at two months. DESIGN: Prospective observational study. SETTING: Tertiary referral maternity hospital. POPULATION: One hundred and seventy-two primiparous women with uncomplicated singleton pregnancies. METHODS: Women were recruited antenatally. At birth, cord arterial blood and obstetric data were collected. Saliva was collected from infants immediately before and after vaccination at two months. Cortisol was analysed from cord blood and saliva by radio-immunoassay. MAIN OUTCOME MEASURES: Stress response at birth, as demonstrated by cord arterial cortisol; association with saliva cortisol response to vaccination at two months. RESULTS: Cord arterial cortisol varied with mode of delivery, combined spinal/epidural use and pH. Salivary cortisol response at two months correlated with cord arterial cortisol (r= 0.24, P < 0.05). Infants with the highest and lowest cord arterial cortisol had markedly different cortisol responses at two months (P= 0.017). These groups had different modes of delivery with caesarean rates of <8% in the high cortisol response group and 83% in the low cortisol response group (P < 0.0001). CONCLUSION: Babies born vaginally mount greater cortisol responses at birth than those delivered by caesarean section. Stress at delivery may influence the infant HPA axis response for up to two months.

Amniotic Fluid↗

PubMed2002

Abnormal cortisol metabolism and tissue sensitivity to cortisol in patients with glucose intolerance.

Recent evidence suggests that increased cortisol secretion, altered cortisol metabolism, and/or increased tissue sensitivity to cortisol may link insulin resistance, hypertension, and obesity. Whether these changes are important in type 2 diabetes mellitus (DM) is unknown. We performed an integrated assessment of glucocorticoid secretion, metabolism, and action in 25 unmedicated lean male patients with hyperglycemia (20 with type 2 diabetes and 5 with impaired glucose intolerance by World Health Organization criteria) and 25 healthy men, carefully matched for body mass index, age, and blood pressure. Data are mean +/- SE. Patients with hyperglycemia (DM) had higher HbA(1c) (6.9 +/- 0.2% vs. 6.0 +/- 0.1%, P < 0.0001) and triglycerides. Cortisol secretion was not different, as judged by 0900 h plasma cortisol and 24 h total urinary cortisol metabolites. However, the proportion of cortisol excreted as 5alpha- and 5beta-reduced metabolites was increased in DM patients. Following an oral dose of cortisone 25 mg, generation of plasma cortisol by hepatic 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD 1) was impaired in DM patients (area under the curve, 3617 +/- 281 nM.2 h vs. 4475 +/- 228; P < 0.005). In contrast, in sc gluteal fat biopsies from 17 subjects (5 DM and 12 controls) in vitro 11beta-HSD 1 activity was not different (area under the curve, 128 +/- 56% conversion.30 h DM vs. 119 +/- 21, P = 0.86). Sensitivity to glucocorticoids was increased in DM patients both centrally (0900 h plasma cortisol after overnight 250 micro g oral dexamethasone 172 +/- 16 nM vs. 238 +/- 20 nM, P < 0.01) and peripherally (more intense forearm dermal blanching following overnight topical beclomethasone; 0.56 +/- 0.92 ratio to vehicle vs. 0.82 +/- 0.69, P < 0.05). In summary, in patients with glucose intolerance, cortisol secretion, although normal, is inappropriately high given enhanced central and peripheral sensitivity to glucocorticoids. Normal 11beta-HSD 1 activity in adipose tissue with impaired hepatic conversion of cortisone to cortisol suggests that tissue-specific changes in 11beta-HSD 1 activity in hyperglycemia differ from those in primary obesity but may still be susceptible to pharmacological inhibition of the enzyme to reduce intracellular cortisol concentrations. Thus, altered cortisol action occurs not only in obesity and hypertension but also in glucose intolerance, and could therefore contribute to the link between these multiple cardiovascular risk factors.

Administration, Topical↗

PubMed2000

[Reactions of dairy cows to ACTH administration and ingestion of liquid feed at different age points before and in the course of rearing with automatic milk feeding--plasma cortisol, saliva cortisol, hematologic, metabolic variables and heart rate].

On dairy calves (totally 35 animals; 14 male; 21 female) measurements of rectal temperature, heart rate and blood values (acid-base balance, Hb, Hk, MCHC, gas content and gas pressure, hemoglobin derivatives, cortisol, total protein, albumin, blood urea, creatinine, glucose, lactate, Ca, Mg, P, Fe) and of salivary cortisol were done before and after i.v. ACTH application and liquid feed intake at 5, 15, 40 and 60 days of life age. Mean values of P-cortisol, S-cortisol, heart rate and COHb were elevated and those of total protein, albumin, Mg, Hb, Hk, O2CAP were decreased after i.v. ACTH and feed intake. Mean glucose and P concentration changed differently in younger and older calves after ACTH and liquid feed intake. Changes of Ca and Fe concentration were not significant at all age points. Effects of gender could be found for cortisol, O2CONT, MCHC, total protein, creatinine, lactate, Mg, and Ca at some age points. Initial P-cortisol levels were higher at 5 and 15 days than at 40 and 60 days of life, the levels after stimulation were higher at 5 days than at 15, 40 and 60 days. Initial levels of S-cortisol were significantly different between all age points, the levels after stimulation were not different. Female calves had significantly greater P-cortisol values at 40 and 60 days as male calves and at 40 days greater S-cortisol values too. Significant correlations between P-cortisol and S-cortisol could be found before stimulation (5 days: r = 0.626; 15 days: r = 0.366; 60 days: r = 0.357) not thereafter. All measures except P-cortisol, S-cortisol, O2SAT, and HHb had significant correlations before and after ACTH and liquid feed intake indicating great interindividual variation and individual specificity of reaction within this growth period. Results were discussed under the viewpoint of reactivity of adrenocortex and steroid distribution concerning organ specific effects of steroids in calves.

Adrenocorticotropic Hormone↗

PubMed1992

Simultaneous measurement of cortisol in serum and saliva after different forms of cortisol administration.

To prove the clinical usefulness of cortisol measurements in saliva for the exact assessment of a patient's corticoid status under therapeutic hormone substitution, we measured simultaneously total cortisol in serum and non-protein-bound cortisol in saliva after administration of different forms of hydrocortisone (cortisol) in eight cortisol-suppressed, healthy male volunteers. The intravenous and oral administration of 20 mg of cortisol exceeds the binding capacity of the corticosteroid-binding globulin (CBG), leading to an increase of the ratio between salivary and serum cortisol at the higher cortisol concentrations in blood. After rectal administration of 100 mg of cortisol acetate, the serum cortisol concentration does not exceed the binding capacity of CBG, so the ratio between salivary and serum cortisol remains nearly constant. However, this ratio was higher after rectal administration than after intravenous and oral administration, probably because of weaker binding of the acetate form of cortisol to CBG. Thus, the salivary measurement of the non-protein-bound (i.e., biologically active) cortisol offers a convenient way to monitor the effectiveness of various forms of systemic corticoid substitution.

Administration, Oral↗

PubMed1996

The use of saliva cortisol, urinary cortisol, and catecholamine measurements for a noninvasive assessment of stress responses in dogs.

A problem in assessing animal welfare is that collecting data in itself may be stressful to the animals. Therefore, noninvasive methods for collecting data have to be devised and tested. A first step in investigating saliva cortisol, urinary cortisol, and urinary catecholamine as noninvasive indicators of canine well-being is the validation of these hormonal measures as alternatives for those in plasma. Using a model of insulin (0.2 U/kg)-induced hypoglycemia, we report on stress-induced responses in saliva cortisol, urinary cortisol, and urinary catacholamines relative to cortisol and catecholamine responses in plasma. Hypoglycemia in six dogs induced significant (P < 0.05) increases in plasma cortisol and adrenaline but not noradrenaline. Saliva cortisol responses expressed as net area under the response curve correlated significantly with plasma cortisol responses (r > 0.92). Saliva cortisol levels measured 7 to 12% of plasma cortisol concentrations. Cortisol/creatinine rations in urine were significantly higher when voided after insulin administeration, compared to when voided after saline treatment. Insulin-induced increments in cortisol/ creatinine ratios were nonsignificant when urine samples were assayed after dichloromethane extraction. Although urinary adrenaline/creatinine (A/C) ratios were significantly correlated with maximum plasma adrenaline values after insulin administration, A/C ratios did not differ significantly between insulin and saline treatment. The present experiment provides strong support for using saliva sampling and urine collection as noninvasive methods to establish stress-induced cortisol responses. For measuring acute plasma adrenaline responses, measuring A/C ratios may not be a valid alternative.

Animals↗

PubMed1987

Clinical use of unbound plasma cortisol as calculated from total cortisol and corticosteroid-binding globulin.

A method to calculate unbound cortisol from total cortisol (measured by competitive protein binding) and CBG (measured by radial immunodiffusion) based on the binding equilibrium has been evaluated. The calculated results (y) correlate well with those (x) obtained by centrifugal ultrafiltration at 37 degrees C (y = 1.04 x - 2.11 ng/ml; r = 0.975; n = 150). The concentration of CBG is similar in normal men (37.7 +/- 3.5 (SD) micrograms/ml; n = 12) and women (39.5 +/- 3.7 (SD) micrograms/ml; n = 7) and shows no diurnal variation, but marked diurnal variation is observed for total cortisol (193.7 +/- 35.0 (SD) ng/ml at 08.00 h vs 43.2 +/- 23.3 (SD) ng/ml at 22.00 h; n = 19) and particularly for unbound cortisol (16.5 +/- 5.6 (SD) ng/ml at 08.00 h vs 2.3 +/- 1.8 (SD) ng/ml at 22.00 h; n = 19). The concentration of CBG (89.1 +/- 11.2 (SD) micrograms/ml) and of total cortisol (395.6 +/- 103.3 (SD) ng/ml at 08.00 h; 110.3 +/- 16.6 (SD) ng/ml at 22.00 h) are clearly elevated in estrogen treated women (n = 11) but unbound cortisol levels (17.2 +/- 7.7 (SD) ng/ml at 08.00 h; 2.5 +/- 0.5 (SD) ng/ml at 22.00 h) are similar to the control group. The concentration of CBG is significantly decreased in patients with Cushing's syndrome (33.2 +/- 5.6 micrograms/ml; n = 17) and unbound cortisol is relatively more elevated than total cortisol in these patients. In adrenal insufficiently CBG is normal, but total and unbound cortisol are markedly decreased. There is a significant decrease of CBG in hyperthyroidism (35.7 +/- 5.5 micrograms/ml; n = 22), in cirrhosis (32.0 +/- 8.0 micrograms/ml; n = 14) and in renal disease and a significant increase in patients treated with antiepileptic drugs (47.5 +/- 6.3 micrograms/ml; n = 14), but total and unbound cortisol are normal in all these conditions. We conclude that unbound cortisol can be calculated in a simple and reliable way from total cortisol and CBG and permits a better evaluation of adrenal function, particularly in patients with altered CBG concentrations.

Circadian Rhythm↗

PubMed1990

Cortisol production rate in children by gas chromatography/mass spectrometry using [1,2,3,4-13C]cortisol.

A urinary method of determining the cortisol production rate (CPR) in children was studied under physiologic conditions by administration of low amounts of [1,2,3,4-13C]cortisol. The CPR in three patients with multiple pituitary deficiency ranged from 7 to 16 mumoles d-1 m-2, and the CPR in three patients with congenital adrenal hyperplasia (CAH) due to 11 beta-hydroxylase deficiency (11 beta OHD) and 17 alpha-hydroxylase deficiency (17 alpha OHD) from 0.1 to 2.11 mumoles d-1 m-2. Results showed that with this method, very low CPRs can be reliably measured. The metabolism of [13C4]cortisol or [9,12,12-2H]cortisol was compared with that of native cortisol in adrenalectomized piglets. For the urinary cortisol metabolites, small to substantial differences in isotope dilution were noted relative to that in the original cortisol mixture. With [13C4]cortisol, the so-called secondary isotope effects were approximately 2% to 3% for tetrahydrocortisone (THE) and tetrahydrocortisol (THF), and about 10% for the cortolones, relative to the cortisol mixture. When [2H3]cortisol was used, the cortisol metabolites THE and THF contained only two deuterium atoms. Together with this apparent loss of one deuterium atom, the secondary isotope effects in these steroids amounted to 5% to 10%. It was concluded that [13C4]cortisol was the better tracer to use for the measurement of urinary CPR.

Adolescent↗