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PubMed1986

A comparison of adrenal cortical function in patients with depressive illness and Cushing's disease.

We measured total and free plasma cortisol, 24-hour urinary cortisol excretion, and corticosteroid-binding globulin in 21 normal subjects, 25 patients with depressive illness, and 6 patients with Cushing's disease. Patients with depression had mean 24-hour plasma (8.3 +/- 2.7 micrograms/dl) and urinary (36 +/- 33.55 micrograms/g creatinine) cortisol levels that did not differ from those of normal subjects (6.6 +/- 1.7 microgram/dl; 24.6 +/- 15.4 micrograms/g creatinine), but were significantly lower than those of patients with Cushing's disease (14.4 +/- 2.4 micrograms/dl; 215 +/- 101 micrograms/g creatinine). Not all patients with depression had hypercortisolemia, and the 1-mg dexamethasone suppression test identified some of those with adrenal hyperfunction. 17 of 25 patients had normal 8 a.m. and/or 4 p.m. plasma cortisol after dexamethasone (suppressors), while 8 patients had values greater than 5 micrograms/dl (nonsuppressor). Suppressors had normal total 24-hour plasma and urinary cortisol, while nonsuppressors had levels that were in the range seen in Cushing's disease. Patients with depression showed the expected circadian variation in total and free cortisol, but nonsuppressors had elevated levels in evening and early a.m. hours when levels in normal subjects were low. Patients with Cushing's disease had elevated levels throughout the day. The mean binding capacity of corticosteroid-binding globulin was not different in normal and depressed subjects (23.9 +/- 3.2 vs. 22.2 +/- 3.4 micrograms/dl), but was significantly decreased in patients with Cushing's disease (15.7 +/- 3.5 micrograms/dl). Although total cortisol levels were similar, nonsuppressors had significantly lower mean 24-hour plasma free cortisol (1.01 +/- 0.27 microgram/dl) than patients with Cushing's disease (2.4 +/- 0.54 microgram/dl).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex Function Tests↗
PubMed1990

Comparison of serum ethinyl estradiol, sex-hormone-binding globulin, corticoid-binding globulin and cortisol levels in women using two low-dose combined oral contraceptives.

The study included 69 women taking a desogestrel (n = 30)- or gestodene (n = 39)-containing low-dose combined oral contraceptive for at least 3 months. Group size was calculated to detect a difference in mean values of 80% of 1 standard deviation (alpha = 0.05, beta = 0.1). Seven serum samples were obtained up to 4 h, and 1 sample 24 h, after drug intake on 1 day between the 10th and the 21st day of the cycle. The concentrations of sex-hormone-binding globulin (SHBG), corticoid-binding globulin (CBG) and cortisol were measured in a 0- to 4-hour serum pool by radioimmunoassay. Ethinyl estradiol (EE2) levels were analyzed in single and pooled samples using anti-EE2-6 beta-carboxymethyloxime-bovine serum albumin antiserum. The area under the curves (AUC) up to 4 and 24 h and Cmax and tmax were evaluated. Statistical analysis (analysis of covariance) did not reveal a dependence of values on duration of treatment or day of cycle. Both treatments resulted in almost identical values for all parameters evaluated. The mean levels of SHBG, CBG and cortisol were in the range of 186-226 nmol/l, 89-93 mg/l and 280-281 micrograms/l, respectively. Mean maximum EE2 levels of 106-129 pg/ml were found 1.6-1.8 h after pill intake and AUC0-4 h accounted for 329-374 pg.h.ml-1. The recently reported differences in serum EE2 and CBG levels between two groups of 11 women each treated with desogestrel- and gestodene-containing pills, respectively, could not be confirmed.

Adult↗
PubMed1992

Serum concentrations of ethinylestradiol, 3-keto-desogestrel, SHBG, CBG and gonadotropins during treatment with a biphasic oral contraceptive containing desogestrel.

During a cross-over study, the pharmacokinetics of ethinylestradiol (EE) and 3-keto-desogestrel (KDG) were investigated on days 7 and 22 of one cycle of treatment with two biphasic formulations containing 50 micrograms EE (7 tablets) and 50 micrograms EE + 125 micrograms desogestrel (DG) (15 tablets) (50/50 EE) or 40 micrograms EE + 25 micrograms DG (7 tablets) and 30 micrograms EE + 125 micrograms DG (15 tablets) (40/30 EE). Peak serum levels and areas under the curve of EE increased significantly by 50% between days 7 and 22 of those taking 50/50 EE, while during treatment with 40/30 EE, no difference was found between days 7 and 22. Both formulations caused identical KDG levels on day 22. There were only slight differences in the effects of both preparations on sex-hormone-binding globulin (SHBG; +150 to +160%) and on corticosteroid-binding globulin (CBG; +130 to +150%) on day 7. On day 22, the changes were more pronounced with 50/50 EE (SHBG, +310%; CBG, +240%) than with 40/30 EE (SHBG, +250%; CBG, +180%). On day 22 after discontinuation of treatment, the SHBG and CBG levels were still significantly above the control values. Using both formulations, LH and FSH levels were significantly suppressed on day 22, while on day 7 no significant reduction was observed. The rise in the EE levels between days 7 and 22 of 50/50 EE intake and the time course of the EE concentrations during treatment with 40/30 EE appear to be due to an inhibition of hepatic metabolism by the contraceptive steroids, as EE is nearly exclusively bound to albumin which does not change.

Adult↗
PubMed1982

Altered prednisolone kinetics in patients with the nephrotic syndrome.

The impact of low plasma protein levels on the kinetics of prednisolone was investigated in patients with the nephrotic syndrome. Nephrotics exhibited higher unbound fractions of prednisolone, lower total plasma concentrations than normal volunteers, but normal unbound plasma concentrations and normal mean residence times. Thus altered prednisolone kinetics in patients with low plasma protein levels do not explain the higher frequency of prednisolone-related side-effects in these patients, compared to patients with normal plasma protein levels.

Adult↗
PubMed1984

Cortisol binding in uremic plasma. I. Absence of abnormal cortisol binding to cortisol binding to corticosteroid-binding globulin.

Increased morning plasma free cortisol levels have been reported previously in chronic renal failure (CRF) patients. To see whether binding abnormalities of plasma proteins contributed to the increase in morning free cortisol, binding characteristics of corticosteroid-binding globulin (CBG) were studied in pooled plasma from CRF patients and normal subjects. Using an isocolloidosmolar equilibrium dialysis method the unbound, albumin-bound, and CBG-bound fractions of plasma cortisol were measured within the physiologic range of plasma cortisol levels. Cortisol binding to CBG was equal in uremic and nonuremic plasma as determined by the affinity constants and the binding capacities of CBG for cortisol. In addition, the distribution of cortisol binding was identical in uremic and in nonuremic plasma samples at equal total cortisol concentrations. By confirming that cortisol binding properties of CBG are unaltered in CRF patients, these data support the assertion that elevated morning free cortisol levels in CRF patients are probably due to increases of plasma total cortisol.

Adult↗
PubMed1995

Corticosteroid-binding globulin in preterm infants in an intensive care unit.

Blood concentration of corticosteroid-binding globulin (CBG) was measured in 85 preterm (24-36 weeks of gestational age) infants over the first 6 weeks of postnatal life. CBG concentrations directly correlated to gestational age and postnatal age in the first week of life. There was a significant increase in CBG values over the first 6 weeks such that mean values at weeks 4 through 6 were significantly greater than values at weeks 1 and 2. Postnatal CBG values were significantly lower in infants who had pulmonary disease during week 1 (p = 0.001). In summary, CBG values were directly correlated to gestational and postnatal age, and negatively correlated to acute illness. We speculate that the lower CBG values with lung disease may reflect an ongoing inflammatory response.

Aging↗
PubMed1996

Regulation factors of corticosteroid-binding globulin: lesson from ontogenesis.

This short review summarizes recent data on corticosteroid-binding globulin (CBG), especially enlightening results on regulation factors of CBG gene expression during ontogenesis. The role of CBG as a specific steroid carrier, a structurally conserved glycoprotein of 50-60 kD in vertebrate species, is well documented, but this knowledge has often been limited to the young or adult life since CBG levels are low in the neonate. However, CBG and CBG mRNA have been recently detected, sometimes, in relatively high amounts, in various fetal tissues of mammals including liver, lung, pancreas, adrenal and kidney. CBG can thus participate in glucocorticoid-inducible events crucial for maturation. Moreover, its original molecular cloning, followed by its chromosomal localization, has shed a new light on the CBG role, as a member of the serine protease inhibitors and substrates (SERPINS) superfamily. This evidenced a special and unexpected way of steroid hormones delivery to their sites of action. Additionally, two classes of CBG receptors have been characterized, and an adenylate cyclase activity has been measured when the CBG-glucocorticoid complex binds to cell membranes.

Aging↗
PubMed1996

Corticosteroid-binding globulin during inflammation and burn injury: nutritional modulation and clinical implications.

Corticosteroid-binding globulin (CBG) is the main carrier of glucocorticoids in mammals. Serum CBG shows little physiological variation with the exception of pregnancy. Experimental inflammation and burn injury decrease serum CBG in rats and while the mechanism of this effect is unknown, in vitro experiments suggest that interleukin-6 may be involved. In severely burned patients, we have found that CBG was markedly decreased within a few hours postinjury. This decrease lasted about 2 weeks and was accompanied by an increase in the free fraction of serum cortisol. In addition, serum CBG responded to dietary manipulation in these patients, with low fat feeding resulting in higher serum CBG concentrations and lower serum-free cortisol values. This feeding suggests that during severe stress, CBG may be important in regulating the amount of cortisol reaching target tissues such as the immune system and wounds.

Animals↗
PubMed1997

Expression of sex hormone-binding globulin and corticosteroid-binding globulin mRNAs in corpus luteum of human subjects.

To understand the biology of sex steroids in human ovarian corpus luteum, the expression of intracellular sex hormone-binding globulin (SHBG) and corticosteroid-binding globulin (CBG) mRNAs as a manifestation of intracellular SHBG and CBG expression was determined. The expression of SHBG and CBG mRNAs was detected in all samples analyzed. Luteal SHBG mRNA level showed no significant change during the endometrial secretory phase of the menstrual cycle. On the other hand, luteal CBG mRNA level was significantly higher (p < 0.05) at the mid-secretory phase than that at the early and late secretory phases of the endometrium. These findings suggest that human ovarian corpus luteum synthesizes SHBG and CBG intracellularly, CBG being plausibly involved in the functional life span of corpus luteum.

Adult↗
PubMed1983

Transfer of 3H-cortisone and 3H-cortisol between the amniotic, allantoic, and fetal blood compartments in the rabbit at day 25 of gestation.

We have examined the rate of disappearance and the form of the radiolabel following the injection of either [1,2-3H]-cortisone (3H-E) or [1,2,6,7,n-3H]-cortisol (3H-F) into the amniotic sac of rabbits at day 25 of gestation. The half-life of 3H-E was approximately 35 min and was very much shorter than that of 3H-F. Concurrent with the disappearance of 3H-E was an increase in the amount of tritium in both the allantoic and the fetal blood compartments. Whereas following injection of 3H-E there was a rapid conversion of E to F that was reflected in all three compartments, following injection of 3H-F the vast majority of the tritium label remained as F. We conclude that amniotic E may act as a ready source of fetal F.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1990

Plasma cortisol distribution in the pig from birth to six weeks of age.

Plasma levels of cortisol and percent distribution of cortisol among protein-bound (corticosteroid-binding globulin (CBG) and albumin) and unbound forms were measured in naturally born/conventionally reared pigs from birth to 6 weeks of age. Total cortisol and percent unbound cortisol were highest in pigs at birth and decreased (p less than 0.01) in a linear fashion over the sampling period. Percent CBG-bound cortisol was lowest on days 3-21 relative to the peak value seen on day 42. However, actual CBG-bound cortisol was not different after day 1. Percent albumin-bound cortisol was highly correlated with percent CBG-bound cortisol (r = -0.90; p less than 0.001). These results suggest that a rapid shift in cortisol distribution from unbound and albumin-bound forms to that which is bound to CBG occurs by approximately day 28 of age in the neonatal pig.

Analysis of Variance↗
PubMed1997

Distribution between protein-bound and free forms of plasma cortisol in the gilt and fetal pig near term.

Thirty-five time-dated pregnant gilts were used to document plasma levels of total and free cortisol, corticosteroid-binding globulin (CBG) binding capacity, and percent distribution of cortisol among protein-bound (CBG and albumin) and free forms in the fetal pig during the last 24 days of gestation. Plasma from fetal pigs on days 110-114 of gestation (gestation length 114 days) had significantly higher levels of total cortisol (p < 0.01), percent albumin-bound and free cortisol (p < 0.10), and free cortisol concentration (p < 0.05) compared to samples on days 90, 100 and 105. Fetal plasma CBG binding capacity increased (p < 0.05) linearly from day 100 to 114. Fetal pigs located in the cervical region of the uterus had lower (p < 0.05) total and free cortisol and higher (p < 0.05) albumin and total protein concentrations compared to fetuses in the middle and oviductal regions. Total, percent free and free cortisol concentrations in maternal plasma on days 105-114 were greater (p < 0.10) than that measured on days 12-100 of gestation. These results suggest that the developmental patterns of plasma cortisol and CBG in the prenatal pig are directly related and highly similar to those of another precocious species, the sheep.

Animals↗
PubMed2006

Diagnosis of adrenal insufficiency in severe sepsis and septic shock.

RATIONALE: Diagnosis of adrenal insufficiency in critically ill patients has relied on random or cosyntropin-stimulated cortisol levels, and has not been corroborated by a more accurate diagnostic standard. OBJECTIVE: We used the overnight metyrapone stimulation test to investigate the diagnostic value of the standard cosyntropin stimulation test, and the prevalence of sepsis-associated adrenal insufficiency. METHODS: This was an inception cohort study. MEASUREMENTS AND RESULTS: In two consecutive septic cohorts (n = 61 and n = 40), in 44 patients without sepsis and in 32 healthy volunteers, we measured (1) serum cortisol before and after cosyntropin stimulation, albumin, and corticosteroid-binding globulin levels, and (2) serum corticotropin, cortisol, and 11beta-deoxycortisol levels before and after an overnight metyrapone stimulation. Adrenal insufficiency was defined by postmetyrapone serum 11beta-deoxycortisol levels below 7 microg/dl. More patients with sepsis (31/61 [59% of original cohort with sepsis] and 24/40 [60% of validation cohort with sepsis]) met criteria for adrenal insufficiency than patients without sepsis (3/44; 7%) (p < 0.001 for both comparisons). Baseline cortisol (< 10 microg/dl), Delta cortisol (< 9 microg/dl), and free cortisol (< 2 microg/dl) had a positive likelihood ratio equal to infinity, 8.46 (95% confidence interval, 1.19-60.25), and 9.50 (95% confidence interval, 1.05-9.54), respectively. The best predictor of adrenal insufficiency (as defined by metyrapone testing) was baseline cortisol of 10 microg/dl or less or Delta cortisol of less than 9 microg/dl. The best predictors of normal adrenal response were cosyntropin-stimulated cortisol of 44 microg/dl or greater and Delta cortisol of 16.8 microg/dl or greater. CONCLUSIONS: In sepsis, adrenal insufficiency is likely when baseline cortisol levels are less than 10 microg/dl or delta cortisol is less than 9 microg/dl, and unlikely when cosyntropin-stimulated cortisol level is 44 microg/dl or greater or Delta cortisol is 16.8 microg/dl or greater.

Adrenal Insufficiency↗
PubMed1979

Synthesis and secretion of corticosteroid-binding globulin by rat liver. A source of heterogeneity of hepatic corticosteroid-binders.

Classical glucocorticoid receptors (type II) have a high affinity for synthetic and natural glucocorticoids. We have previously demonstrated an additional binding site in kidney cytosol (type III) which has a high affinity for corticosterone but a low affinity for dexamethasone. In many ways, this binder resembles plasma corticosteroid-binding globulin (CBG). The first goal of this study was to determine the organ distribution of the type III binding sites. Cytosol was prepared from isolated cells to avoid plasma contamination. Of the tissues examined, type III sites were found only in liver and kidney; sites were absent from thymocytes, IM-9 lymphocytes, adipocytes, and bone cells. The second goal of this study was to ascertain whether CBG is synthesized in liver and kidney. Liver and kidney slices were incubated in vitro and the concentration of type III sites was seen to rise in hepatic cytosol and incubating medium but not kidney. To verify the impression that liver was synthesizing and secreting CBG, the following experiments were performed: (a) To demonstrate that type III sites were CBG, steroid-binding profiles and migration on polyacrylamide gel electrophoresis were shown to be identical for hepatic type III sites and serum. (b) To indicate that the rise in type III sites was dependent on protein synthesis, it was shown that cycloheximide blocked the appearance of new type III sites. (c) To establish that the type III sites were being secreted, in situ liver perfusion experiments showed time-dependent release of new sites into the perfusate. In conclusion, liver synthesizes and secretes type III sites, a finding previously suspected but never proved. The presence of type III sites in kidney remains to be explained.

Animals↗
PubMed1991

Scintillation proximity assay: determination of steroid hormones without separation of antibody-bound and free ligand.

Scintillation proximity assay (SPA), which does not require the physical separation of bound and free hormone, was applied to the determination of cortisol in plasma. Results showed excellent agreement with a conventional radioimmunoassay using dextran-coated charcoal to separate bound and free cortisol, with similar precision and sensitivity. When the SPA was applied to the measurement of plasma aldosterone, it was evident from the SPA and radioimmunoassay results that the blocking of aldosterone binding to corticosteroid-binding globulin by 8-amino-1-naphthalene-sulphonic acid was not completely effective, and that a different sample preparation technique should be used. SPA may become the method of choice for the determination of hormones in blood.

Aldosterone↗
PubMed1998

Effects of sex steroid hormones on corticosteroid-binding globulin gene expression in human endometrial cancer cell line Ishikawa.

The effect of progestins on intracellular corticosteroid-binding globulin (CBG) mRNA expression in an endometrial cancer cell line (Ishikawa) was examined in an attempt to understand the biological effects of high-dose progestins in the treatment of well-differentiated uterine endometrial cancers. Oestradiol-17 beta (E2) significantly increased CBG mRNA expression in a dose-dependent manner, while a high dose of progesterone with or without E2 suppressed it significantly. Furthermore, a high dose of progesterone or medroxyprogesterone acetate (MPA) suppressed CBG mRNA expression to a greater degree than did chlormadinone acetate or 17 alpha-hydroxyprogesterone caproate with or without E2. These findings suggest that the effects of high-dose progestins on cancer cells may be mediated via suppression of intracellular CBG.

Endometrial Neoplasms↗
PubMed1986

Fetal and maternal corticosterone and corticosteroid binding globulin in the diabetic rat gestation.

Delayed fetal lung development is a feature of the diabetic pregnancy. Since fetal glucocorticoids are important in the regulation of lung maturation, we measured corticosterone and corticosteroid-binding globulin binding capacity in streptozotocin-diabetic pregnant rats and their fetuses. Previous studies have demonstrated delayed fetal lung maturation in this animal model. In control fetuses, total corticosterone concentration increased through day 20 of gestation, then declined until day 22 (term). The unbound steroid, which accounted for 5-10% of the total, increased approximately 3-fold from day 18 to term. Corticosteroid-binding globulin binding capacity peaked on day 19 after which it decreased. Maternal total and unbound corticosterone levels and corticosteroid-binding globulin binding capacity remained relatively constant throughout the final week of normal gestation. When compared to controls, fetuses from diabetic pregnancies had significantly lower total corticosterone from day 19 through 22. Corticosteroid-binding globulin binding capacity was also significantly decreased in these fetuses for the last 4 days of gestation. Similar differences were noted in maternal samples. However, no significant differences in unbound, biologically active, corticosterone were seen when diabetic and control groups were compared. Thus, delayed fetal lung maturation observed in fetuses of streptozotocin-diabetic rats is associated with a decrease in total circulating corticosteroid levels late in gestation. However, since unbound corticosteroid levels were similar in fetuses of control and diabetic animals, it is likely that other mechanisms may be responsible for the observed delay in lung development in fetuses of diabetic pregnancies.

Animals↗