cosyntropin and Obesity

Body fat mass and nutrition influence secretion of the adrenocortical hormones--aldosterone and cortisol--via several mechanisms. However, there are no data on adrenocortical function following widely prescribed mild diet-induced weight loss (10%) in obese subjects. In the present study, 25 healthy obese volunteers (BMI 32.9+/-4.3 kg/m (2)) followed a 30% calorie restricted diet over 12 weeks. Hypothalamic-pituitary-adrenal (HPA) axis function was assessed by 24-hour urine free cortisol/cortisone and a 1 mcg ACTH stimulation test with measurement of total and free cortisol and corticosteroid-binding globulin (CBG). The renin-angiotensin-aldosterone system (RAAS) was assessed by measurement of plasma aldosterone and renin under salt depleted (30 mmol/d) and loading (250 mmol/d) conditions. Volunteers' weight fell by 8.5+/-0.8 kg (8.9+/-0.7%) and seated systolic blood pressure fell by 8.7+/-2.7 mmHg and diastolic blood pressure by 7.0+/-1.4 mmHg (p<0.01). Plasma aldosterone and renin levels fell significantly with weight loss (aldosterone: 853+/-156-635+/-73 pmol/l; renin: 35.4+/-7-24+/-3 mU/l, both p<0.05). The volunteers were relatively salt insensitive (mean arterial pressure change with salt intake: 4 mmHg) and this was not affected by weight loss. Moderate weight loss had no effect on 24-hour urine free cortisol/cortisone, or on basal, or ACTH-stimulated free and total cortisol, or CBG. Hence this conventional weight loss program reduces blood pressure and activity of the RAAS via an effect on renin release. Despite various described influences of fat mass and energy restriction on HPA axis function, there were no changes in basal and stimulated HPA axis function with moderate weight loss. There may be a threshold effect of weight loss/energy restriction required to alter HPA axis function, or moderate weight loss may lead to a counterbalanced effect of stimulatory and inhibitory influences on HPA axis function.

Topics: Adult; Aged; Aldosterone; Blood Pressure; Body Weight; Caloric Restriction; Cosyntropin; Cross-Over Studies; Diet, Reducing; Female; Humans; Hydrocortisone; Male; Middle Aged; Obesity; Pituitary-Adrenal System; Renin; Renin-Angiotensin System; Sodium Chloride, Dietary; Transcortin; Weight Loss

Controversy persists regarding the use of the low-dose adrenocorticotropic hormone (ACTH) stimulation test (LDST) for the diagnosis of adrenal insufficiency (AI) and optimal test result interpretation. However, many centers are now using the LDST to assess cortisol secretion adequacy, and some only use a 30-minute cortisol level to determine adrenal sufficiency or AI. This study examined both 30- and 60-minute cortisol levels to assess whether the interpretation of the test was affected when both cortisol levels were taken into consideration.. Data were obtained by retrospective chart review from a single pediatric endocrinology unit over a 7-year period. We identified 82 patients who completed the LDST. Their mean age was 11.7 years, and 37% were female. Cortisol levels were evaluated at baseline and 30 and 60 minutes after cosyntropin administration. A cutoff value ≥18 μg/dL was used to define adrenal sufficiency.. We found that 54% of patients reached peak cortisol levels at 60 minutes, and 11 patients who did not pass the test at 30 minutes did so at 60 minutes. The only predictive characteristic was weight status; overweight and obese individuals tended to peak at 30 minutes, and normal and underweight individuals tended to peak at 60 minutes.. Although further studies are necessary to confirm our findings, it appears that measuring cortisol both 30 and 60 minutes following synthetic ACTH administration may be necessary to avoid overdiagnosing AI.

Topics: Adolescent; Adrenal Insufficiency; Body Weight; Child; Cosyntropin; Female; Humans; Hydrocortisone; Kinetics; Male; Obesity; Overweight; Retrospective Studies; Time Factors

Topics: Adolescent; Adrenal Insufficiency; Adult; Child; Cosyntropin; Humans; Hydrocortisone; Insulin; Obesity; Pituitary-Adrenal System; Prader-Willi Syndrome; Prevalence; Retrospective Studies; Scotland

The aim of this study was to investigate the phenotypic parameters and associated factors characterizing the development of glucose intolerance in polycystic ovary syndrome (PCOS). Among the 121 PCOS female subjects from the Mediterranean region, 15.7 and 2.5% displayed impaired glucose tolerance and type 2 diabetes, respectively. These subjects were included in a single group of overweight or obese subjects presenting with glucose intolerance (GI) states. PCOS women with normal glucose tolerance (81.8%) were subdivided into two groups: those who were overweight or obese and those of normal weight. Metabolic and hormonal characteristics of the GI group included significantly higher fasting and glucose-stimulated insulin levels, more severe insulin resistance, hyperandrogenemia, and significantly higher cortisol and androstenedione responses to 1-24 ACTH stimulation. One important finding was that lower birth weight and earlier age of menarche were associated with GI in PCOS women. Frequency of hirsutism, oligomenorrhea, acne, and acanthosis nigricans did not characterize women with GI. Our findings indicate that PCOS patients with GI represent a subgroup with specific clinical and hormonal characteristics. Our observations may have an important impact in preventative and therapeutic strategies.

Topics: Adolescent; Adult; Androstenedione; Blood Glucose; Cohort Studies; Cosyntropin; Diabetes Mellitus; Diabetes Mellitus, Type 2; Family Health; Feeding Behavior; Female; Glucose Intolerance; Humans; Hydrocortisone; Insulin; Insulin Resistance; Mediterranean Region; Obesity; Phenotype; Physical Fitness; Polycystic Ovary Syndrome; Sex Hormone-Binding Globulin

Topics: Adrenal Glands; Adult; Aged; Aging; Anorexia Nervosa; Body Weight; Cosyntropin; Female; Humans; Male; Middle Aged; Obesity; Pituitary Gland

Obesity with abdominal body fat distribution (A-BFD) and hypothalamic-pituitary-adrenal (HPA) axis activity are somehow linked, but the exact interactions still need clarification. Obese subjects display normal circulating plasma cortisol concentrations with normal circadian rhythms. However, when the HPA axis is pharmacologically challenged, body fat distribution matters and then A-BFD obese women differ from those with subcutaneous body fat distribution (P-BFD). We hypothesized that lower dose provocative and suppressive tests than those used to diagnose hypercortisolism of tumour origin or adrenal insufficiency would shed some light on the characteristics of the HPA axis activity in relation with body fat distribution.. Fifty premenopausal obese women were grouped according to their body fat mass distribution. Their plasma cortisol responses to (i) two low doses of dexamethasone (0.25 and 0.5 mg) with (ii) low dose of the ACTH analogue tetracosactrin (1 microg) were assessed. Salivary cortisol was also determined during the ACTH test.. A-BFD differed from P-BFD women in terms of HPA axis responsiveness. They had comparatively: (i) increased nocturnal cortisol excretion (9.38 +/- 2.2 vs. 6.82 +/- 0.91 nmol/micromol creatinine, A-BFD vs. P-BFD, respectively, P = 0.03); (ii) increased salivary cortisol response to ACTH stimulation (1 microg) [salivary cortisol peak: 33.4 (14.1-129) vs. 28.5 (13.2-42.8) nmol/l; salivary AUC: 825 (235-44738) vs. 537 (69-1420) nmol/min/l; A-BFD vs. P-BFD, P = 0.04 for both]; and (iii) increased pituitary sensitivity to dexamethasone testing [postdexamethasone (0.25 mg) plasma cortisol levels: 163 (26-472) vs. 318 (26-652) nmol/l and postdexamethasone (0.5 mg) plasma cortisol levels: 26 (26-79) vs. 33 (26-402) nmol/l; A-BFD vs. P-BFD, P = 0.01 for both).. These data demonstrate differences in the HPA axis activity and sensitivity to glucocorticoids between obese women differing in their body fat distribution, with both enhanced negative and positive feedback in those with abdominal obesity. Several mechanisms may explain these differences: central vs. peripheral hypotheses. Thus, abdominal obesity does not appear to be linked solely to one pathophysiological hypothesis.

Topics: Adolescent; Adult; Analysis of Variance; Body Constitution; Cosyntropin; Dexamethasone; Female; Glucocorticoids; Humans; Hydrocortisone; Hypothalamo-Hypophyseal System; Middle Aged; Obesity; Pituitary-Adrenal System; Saliva

To investigate adrenal activity in visceral obesity in which adrenal hyperactivity has been hypothesized. This could reflect hypothalamus-pituitary alterations leading to slight hyperfunction of the adrenal. Primary adrenal hypersensitivity to ACTH drive in obesity has also been suggested. However, it has also been reported that dehydroepiondrosterone (DHEA) levels in obesity are reduced and it has been hypothesized that this could play a role in the increased cardiovascular risk in obese patients.. We have studied seven obese women with visceral adiposity (OB, age: 33.6+/-3.3 years, BMI: 33.8+/-1.3 kg/m2, WHR: 0.88+/-0.01). The results in OB were compared with those recorded in a group of age-matched normal women (NS, age: 30+/-1.3 years, BMI: 19.9+/-0.4 kg/m2, WHR: 0.76+/-0.02).. We have studied the cortisol (F), aldosterone (A) and DHEA responses to ACTH 1-24 administered at low (LD, 0.5 microg/m2) or very low (VLD, 0.125 microg/m2) dose followed by a second challenge with supramaximal dose (HD, 250 microg).. Basal F, A and DHEA levels in OB were similar to those in NS. The peak F responses to ACTH were dose-related in both groups. At each dose the F peaks in OB (VLD: 495.6+/-43.9 nmol/l, HD: 722.3+/-67.7 nmol/l; LD: 519.2+/-46.0 nmol/l, HD: 729.6+/-44.7 nmol/l) were similar to those in NS (VLD: 556.7+/-45.9 nmol/l, HD: 704.8+/-20.7 nmol/l; LD: 511.8+/-22.8 nmol/l, HD: 726.7+/-26.5 nmol/l). The peak A responses to ACTH were dose-related in both groups. At each dose, the A peaks in OB (VLD: 0.55+/-0.03 pmol/l, HD: 0.79+/-0.09 pmol/l; LD: 0.63+/-0.04 pmol/l, HD: 0.78+/-0.09 pmol/l) were similar to those in NS (VLD: 0.8+/-0.10 pmol/l, HD: 0.86+/-0.09 pmol/l; LD: 0.8+/-0.10 pmol/l, HD: 0.95+/-0.12 pmol/l). The peak DHEA responses to ACTH were dose-related in both groups. At each dose the DHEA peaks in OB (VLD: 58.6+/-13.3 nmol/l, HD: 61.9+/-13.1 nmol/l; LD: 55.18+/-6.4 nmol/l, HD: 72.3+/-9.8 nmol/l) were similar to those in NS (VLD: 54.3+/-8.2 nmol/l, HD: 57.8+/-8.2 nmol/l; LD: 42.2+/-3.7 nmol/l, HD: 56.9+/-4.3 nmol/l).. This study shows that the cortisol, aldosterone and dehydroepiondrosterone responses to high, low and very low ACTH doses in obese women overlap with those in age-matched lean controls; these findings suggest normal sensitivity of the different zones of the adrenal cortex to ACTH in obesity.

Topics: Adolescent; Adrenal Cortex; Adrenal Cortex Function Tests; Adult; Aldosterone; Case-Control Studies; Cosyntropin; Dehydroepiandrosterone; Dose-Response Relationship, Drug; Drug Administration Schedule; Female; Humans; Hydrocortisone; Obesity

Fifteen middle-aged to older, overweight cats attending a first-opinion clinic were investigated to rule out hyperadrenocorticism as a cause of their weight problem, using two different protocols for the adrenocorticotropic hormone (ACTH) stimulation test. The cats received intravenous synthetic ACTH (tetracosactrin) at an initial dose of 125 microg; a second test was performed between two and three weeks later, using a dose of 250 microg intravenously. The mean basal serum cortisol concentration was 203 nmol/litre (range 81 to 354 nmol/litre). The highest mean serum cortisol concentration occurred at 60 minutes following the 125 microg dose and at 120 minutes following the 250 microg dose. There was, however, no statistically significant difference between these peak cortisol concentrations attained using either dose of tetracosactrin. A significantly higher mean serum cortisol concentration was attained after the higher dose at the 180 minutes time point, indicating a more prolonged response when compared with the lower dose. The cats were followed up for one year after the initial investigations and none were found to develop hyperadrenocorticism during this time.

Topics: Adrenocorticotropic Hormone; Animals; Cat Diseases; Cats; Cosyntropin; Dose-Response Relationship, Drug; Female; Hydrocortisone; Infusions, Intravenous; Male; Obesity; Time Factors

Topics: 17-alpha-Hydroxypregnenolone; 17-alpha-Hydroxyprogesterone; Adrenal Glands; Adult; Aged; Aged, 80 and over; Androgens; Cosyntropin; Dexamethasone; Diabetes Mellitus; Diabetes Mellitus, Type 2; Estrogens; Female; Humans; Hydroxyprogesterones; Male; Middle Aged; Obesity; Premenopause

To determine whether delta 5-Androstene-3 beta,17 beta-diol or androstenediol secretion increases with body mass.. A prospective study.. University-based clinical research center.. Twenty healthy, nonhirsute, eumenorrheic women, 10 with a body mass index (BMI) < 31 kg/m2 and 10 with a BMI > 31 kg/m2 were studied.. All patients had blood sampled before (0 minute) and 60 minute after acute administration of 1 mg ACTH-(1-24) i.v. Body circumferences were obtained, and the BMI and waist-hip ratio was calculated.. Total T, androstenedione (A), E2, sex hormone binding globulin, DHEA, DHEAS, and androstenediol were measured at 0 minutes (steroid 0): and DHEA, A and androstenediol were also measured after stimulation (steroid 60). The net steroid increment (delta) from 0 to 60 minute was calculated.. Compared with thin women, obese subjects had higher levels of androstenediol 60 (95.8 +/- 20.3 versus 130.7 +/- 40.7 ng/dL, respectively [conversion factor to SI units, 0.03443]) and delta androstenediol (17.4 +/- 8.7 versus 37.8 +/- 29.0 ng/dL, respectively [conversion factor to SI units, 0.03443]). Neither the BMI, height, nor the body circumference measures correlated with any of the steroid levels or responses to adrenal stimulation, except for a weak positive correlation between BMI and estrone (E1) (r = 0.38) and a negative correlation between waist-hip ratio and delta androstenediol (r = -0.51). The basal level of T, E1, and DHEA0, but not A or DHEAS, correlated with androstenediol 0 (r = 0.65, 0.62, and 0.67, respectively) and delta androstenediol (r = 0.66, 0.63, and 0.63 to 0.005, respectively).. Although the unstimulated morning androstenediol level did not differ between obese and thin euandrogenic healthy women, the response of androstenediol to ACTH-(1-24) stimulation was greater in obese individuals. The present findings, together with our previous data demonstrating an increased adrenal secretion of the E1 precursor A in response to ACTH in obese women, suggests that the adrenal cortex in overweight women may further enhance the estrogenic milieu of these women.

Topics: Adrenal Glands; Adult; Androstane-3,17-diol; Body Mass Index; Cosyntropin; Female; Hormones; Humans; Menstrual Cycle; Obesity; Peptide Fragments; Reference Values

To investigate whether obese subjects with abdominal obesity may be characterized by hyperactivity of the hypothalamic-pituitary-adrenal axis, we examined two groups of obese women with a waist to hip ratio (WHR) lower than 0.80 (n = 13), therefore having peripheral body fat distribution (P-BFD), or a WHR higher than 0.85 (n = 12), thus having abdominal body fat distribution (A-BFD). A group of seven normal weight healthy women served as controls. All subjects underwent the following protocol study that included 1) measurement of daily urinary free cortisol excretion rate; 2) a CRF test (human CRF, 1 microgram/kg BW, as iv bolus), with blood samples taken at regular intervals for ACTH and cortisol determination; and 3) an ACTH test, performed by administering two boli of ACTH (Synacthen, 0.2 microgram/kg BW, iv), at 90-min intervals, with blood samples taken for cortisol determination. Each woman also had a control saline study. Basal levels of both ACTH and cortisol rose significantly after CRF administration in all groups, but this increase was significantly higher in A-BFD than in P-BFD and control women. A significant correlation was found between the incremental area of cortisol and that of ACTH during the CRF test (r = 0.502), but not between these parameters and WHR values. Although the cortisol increase after the ACTH test was higher in A-BFD than in the other groups, these differences were only significant at 60 min during the test and when the analysis for repeated measures was applied. On the contrary, the incremental cortisol area after the ACTH test was not significantly different in the three groups. Moreover, it was not significantly correlated with the incremental cortisol area after CRF test or WHR values. Daily urinary free cortisol excretion rates (per g creatinine), however, were significantly higher in A-BFD than in P-BFD and control women. These results, therefore, suggest that obese women with A-BFD may have hyperactivity of the hypothalamic-pituitary-adrenal axis. This abnormality could be central in origin, due to hypersecretion of CRF or ACTH; alternatively, it could represent an adaptive phenomenon secondary to a state of functional cortisol resistance.

Topics: Abdomen; Adipose Tissue; Adrenocorticotropic Hormone; Adult; Analysis of Variance; Body Height; Body Weight; Corticotropin-Releasing Hormone; Cosyntropin; Female; Hip; Humans; Hydrocortisone; Hypothalamo-Hypophyseal System; Obesity; Pituitary-Adrenal System; Regression Analysis; Time Factors

Alterations in adrenocortical biosynthesis, as measured by the steroid response to acute adrenocorticotropic hormone (ACTH) stimulation, have frequently been reported in female hyperandrogenism. These patients are also commonly obese, which may account for some of these abnormalities. The object of this study was to test the hypothesis that obesity alters the adrenal response to acute adrenal stimulation.. A prospective study of healthy premenopausal women of varying weights.. University-based clinical research center.. Fifty-seven healthy, eumenorrheic, nonhirsute female volunteers were studied, 30 weighing between 90% and 110% (normal-weight) and 27 weighing greater than 120% (obese) their ideal body weight.. All subjects underwent a 60-minute acute intravenous ACTH-(1-24) stimulation test in the follicular phase (days 3 to 8) of the menstrual cycle.. The basal levels of dehydroepiandrosterone sulfate (DHEAS), total and free testosterone (T), sex hormone-binding globulin (SHBG), estrone, estradiol, prolactin, and the luteinizing and follicle-stimulating hormone ratio were measured. Basal and poststimulation levels of androstenedione (A), dehydroepiandrosterone (DHEA), 17 alpha-hydroxyprogesterone (17 alpha-OHP), 17-hydroxypregnenolone (17-PREG), 11-deoxycortisol (S), and cortisol (F) were also obtained, and the net increments after stimulation were calculated.. Normal-weight and obese women did not differ in age, height, or waist-hip ratio. Obese volunteers demonstrated lower circulating SHBG, 17-PREG, and S levels, and S/F ratio, but a higher free T and DHEAS/DHEA levels. No other differences were observed in either basal or adrenal response measures, with the exception of the net increment in A, which was almost twofold higher in obese volunteers (P less than 0.001).. Obesity in eumenorrheic nonhirsute women is associated with lower circulating SHBG activity and higher free T and DHEAS/DHEA levels. No significant difference in adrenocortical response to acute ACTH-(1-24) stimulation was observed between obese and normal-weight women, with the exception of a higher net adrenal output of A. It does not appear that the abnormal adrenal stimulation results frequently observed in hyperandrogenic women are a consequence of their obesity.

Topics: Adult; Body Constitution; Body Mass Index; Cosyntropin; Female; Gonadal Steroid Hormones; Hip; Hormones; Humans; Menstruation; Obesity; Reference Values

Morning plasma corticosterone concentrations have been reported to be elevated in obese Zucker rats compared with lean rats. The aim of this study was to determine if differences in adrenal sensitivity or maximal responsiveness to adrenocorticotropic hormone (ACTH)-(1-24) could account for this disparity. Serum and adrenal glands were collected from lean and obese, male and female Zucker rats (10-13 wk old) between 10:00 and 11:00 A.M. Adrenocortical cells were isolated and challenged with ACTH-(1-24). The serum corticosterone and ACTH concentrations were significantly greater in obese males compared with lean males (45.3 +/- 10.3 vs. 23.2 +/- 1.45 ng/ml and 156.6 +/- 15.3 vs. 113.3 +/- 9.4 pg/ml, respectively). Although serum corticosterone concentrations were similar in female rats, serum ACTH concentrations tended (P = 0.07) to be lower in obese female rats than in lean female rats (67.6 +/- 9.3 vs. 103.5 +/- 15.1 pg/ml, respectively). The median effective concentration (EC50) and the maximal corticosterone response per microgram of DNA of dose-response curves derived from lean and obese rats were not significantly different. Additionally, a morphometric evaluation of adrenal tissue from lean and obese rats suggested that cells of the zona glomerulosa were smaller in obese rats than in lean rats. Our data confirm that morning serum corticosterone concentrations are elevated in 10- to 13-wk-old male Zucker rats. This difference does not appear to be due to differences in the sensitivity or maximal secreting capacity of adrenocortical cells to ACTH.

Topics: Adrenal Cortex; Animals; Corticosterone; Cosyntropin; DNA; Dose-Response Relationship, Drug; Female; Kinetics; Male; Obesity; Proteins; Rats; Rats, Mutant Strains; Rats, Zucker; Sex Factors; Species Specificity

An excessive insulin releasing effect of adrenocorticotropic hormone (ACTH) and ACTH fragments has been considered as a possible factor contributing to the hyperinsulinaemia of genetically obese hyperglycaemic (ob/ob) mice. To investigate this possibility, plasma glucose and insulin responses of 11- to 14-week-old fed lean and ob/ob mice were examined after intraperitoneal administration of ACTH 1-39, ACTH 1-24 and ACTH 18-39, each at a dose of 25 nmol/mouse (50-115 micrograms/mouse). ACTH 1-39 produced a marked and rapid increase of plasma insulin in both lean and ob/ob mice, the effect being much greater in the ob/ob mutant (maximum increases of 5.5 +/- 1.5 and 46.1 +/- 4.1 ng/ml at 10 min in lean and ob/ob mice respectively, P less than 0.001). In lean mice plasma glucose concentrations showed a protracted decreased (maximum decrease of 3.7 +/- 0.5 mmol/l at 120 min), whereas glucose concentrations were increased (maximum increase of 4.2 +/- 1.3 mmol/l at 60 min) in ob/ob mice. ACTH 1-24 produced qualitatively similar but generally smaller effects than ACTH 1-39, while ACTH 18-39 did not significantly affect glucose and insulin concentrations. In 24 h fasted mice, ACTH 1-39 produced similar but generally smaller effects than in fed mice. The results suggest that the effects of ACTH on glucose and insulin homoeostasis are conferred by the N-terminal 1-24 sequence, and ACTH may exert acute effects which contribute to the hyperinsulinaemia and hyperglycaemia of ob/ob mice.

Topics: Adrenocorticotropic Hormone; Animals; Blood Glucose; Body Weight; Corticotropin-Like Intermediate Lobe Peptide; Cosyntropin; Drug Evaluation; Hyperglycemia; Insulin; Male; Mice; Mice, Inbred Strains; Mice, Obese; Obesity; Peptide Fragments

The alpha ACTH-(1-24) threshold dose and the response slope were determined for cortisol (F), delta 4-androstenedione (A), and dehydroepiandrosterone (DHEA) in 10 normal and 16 obese eumenorrheic nonhirsute women matched for age. Each woman received 1 mg dexamethasone at 2300 h and again at 0700 h the next morning. At 0700 h, a continuous alpha ACTH-(1-24) infusion was begun at an initial dose of 30 ng/1.5 m2 body surface area X hr. The ACTH infusion rate was doubled every hour for 5 consecutive h to a maximum dose of 480 ng/1.5 m2 X h. Blood samples were collected for steroid assays before the infusion and at the end of each hour. The ACTH threshold dose was defined as the dose that produced a steroid response significantly above the basal level. The ACTH threshold dose for serum F and DHEA stimulation was not different between the groups, but the threshold dose for A was significantly lower in the obese women. Basal and stimulated serum DHEA to F ratios were significantly higher in the obese women. In both groups, the mean F response slope was significantly higher than that for DHEA, which in turn, was significantly higher than that for A. The mean DHEA response slope was significantly greater in the obese women. The F and A response slopes were not different between the groups. We conclude that the relative responsivity of the steroids to ACTH was the same in both groups: F greater than DHEA greater than A; in the obese women, the ACTH threshold dose for F stimulation was lower (greater sensitivity) than for DHEA or A stimulation; and in the obese women, the ACTH threshold dose for A was significantly lower (increased sensitivity) and the slope of the DHEA response to ACTH was steeper (greater responsivity) than in normal women.

Topics: Adrenal Cortex Function Tests; Adrenocorticotropic Hormone; Adult; Androstenedione; Cosyntropin; Dehydroepiandrosterone; Dexamethasone; Female; Humans; Hydrocortisone; Obesity

Cortisol concentrations were measured in matched plasma and salivary samples from 8 healthy controls, 8 patients with Cushing's syndrome and 4 patients suspected of having spontaneous hypercortisolism. In healthy subjects, the circadian rhythm in salivary cortisol paralleled that in plasma. Absence of the diurnal rhythm in Cushing's syndrome was seen in saliva as well as in plasma. After ACTH stimulation, mean peak cortisol in saliva showed a 3-fold increase while in plasma there was a 2.5-fold increment above baseline. Cushing's syndrome, due to pituitary or adrenal adenoma was diagnosed equally well by measuring the cortisol response to cosyntropin in either plasma or saliva. Finally, the low- and high-dose dexamethasone suppression test was reflected equally well in both plasma and saliva. In patients suspected of having Cushing's syndrome dynamic tests can be performed in both plasma and saliva. However, in some samples, the salivary cortisol measurement appears advantageous over plasma cortisol determination.

Topics: Adolescent; Adult; Circadian Rhythm; Cosyntropin; Cushing Syndrome; Dexamethasone; Female; Humans; Hydrocortisone; Kinetics; Male; Middle Aged; Obesity; Saliva