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At least 451 records · Page 25Linked to original sources
PubMed1976

Glucocorticoid maintenance therapy following adrenalectomy: assessment of dosage and preparation.

Plasma cortisol was monitored repeatedly after oral administration of cortisol and cortisone (cortisone acetate) to seven adrenalectomized patients with pituitary-dependent Cushing's syndrome. The amount of glucocorticoid administered was 25 mg cortisol or 33 mg cortisone/g urine creatinine/24 h. Peak plasma cortisol levels were within recommended values in all patients after cortisone and in three of the patients after cortisol. The remaining four patients had elevated peak plasma cortisol levels after cortisol. Transcortin binding capacity in plasma was normal. It is concluded that cortisol as well as cortisone is suitable for oral glucocorticoid substitution therapy in patients with normal liver function, but that cortisone apparently gives a marginally smoother plasma cortisol curve. However, it is essential to monitor plasma cortisol after institution of glucocorticoid maintenance therapy, since different and unpredictable plasma cortisol levels may exist after a given amount of glucocorticoid, although the dose required correlates reasonably well with creatinine excretion in urine.

Administration, Oral↗
PubMed1991

[Combination of cyproterone acetate and natural estrogens in the treatment of hirsutism].

The effects of oral administration of cyproterone acetate (CPA) (50 mg) associated with natural estrogens, was investigated in two groups of hirsute women. One group received 17-beta estradiol valerianate (E2) (2 mg) (n = 22) and the other, micronized E2 (2 mg) plus estriol (E3) (1 mg) daily (n = 22) for 21 days every month. After a six month period of treatment, hirsutism improved in 70% of the patients. The more frequent adverse effect was amenorrhea. Except in one, weight gain was prevented by a low calorie diet in overweight patients. During treatment, the plasma concentration of E2 was within the normal range for the follicular phase, whereas estrone was higher, and significantly (p less than 0.001) higher under E2 + E3 than under E2 alone (43.5 +/- 29.1 vs 23.9 +/- 6.1 ng/dl). The binding capacity of sex-steroid binding-protein (SBP) was increased by E2 + E3, and was not affected by E2; transcortin levels were unchanged during treatment. The plasma levels of SBP-unbound testosterone and of delta 4-androstenedione were significantly suppressed by CPA, while DHEAS was not significantly reduced. We concluded that oral administration of CPA and natural estrogens, is a well tolerated and efficient treatment of hirsutism.

Adolescent↗
PubMedDate not supplied

[The activation of specific type-III glucocorticoid receptors by pyrazolone series preparations].

Experiments were conducted on intact and adrenalectomized male Wistar rats (weighing 180-200 g) with labelled corticosterone of high specific activity to study the effect of analgin and aminopyrine on the level of type-III glucocorticoid receptors in the liver. Analgin and aminopyrine in doses of 10(-2) and 10(-3) increase the specific binding of labelled corticosterone by type-III glucocorticoid receptors of the hepatic cytosol and by blood plasma transcortin in modelled experiments. The effect of the agents depends on the dose. Intravenous administration of 140 mg/100 g of analgin to intact rats and intraperitoneal injection of an equal dose of analgin to adrenalectomized rats also increases the specific binding of labelled corticosterone by type-III glucocorticoid receptors of the hepatic cytosol. The importance of the revealed effect of agents of the pyrazolone series in stress regulation is discussed.

Adrenalectomy↗
PubMed1988

[Functional activity of the adrenal glands and the hormone-protein interactions in patients with hypertension with a complicated course].

Patients with essential hypertension and hypertension complicated by coronary heart disease showed adrenal glucocorticoid activation along with reduced transcortin binding capacity (TBC). The addition of circulatory insufficiency (stage I and IIB) resulted in a decrease of the functional adrenal reserve and further diminution of TBC due to a reduction of protein binding sites concentration, and sometimes (stage IIB) also a decrease in the protein affinity of steroids. A correlation between TBC and plasma protein level was found. The absence of adrenal functional response to an abrupt drop in TBC is interpreted as a complete failure of the adaptation systems.

11-Hydroxycorticosteroids↗
PubMed1984

[Changes in the biochemical indices of patients with myocardial infarcts complicated by cardiogenic shock].

Serum catecholamine and glucocorticoid levels, kinin activity and major lipids were measured in 144 patients with acute myocardial infarction aggravated by cardiogenic shock. Sympatho-adrenal and kinin activity, and glucocorticoid levels were increased considerably, whereas transcortine reserve binding capacity and serum lipid content were decreased. These parameters underwent the greatest change in patients with the true cardiogenic shock as the condition deteriorated. The demonstrated neuro-humoral changes may be of diagnostic and predictive value.

11-Hydroxycorticosteroids↗
PubMed1981

[Glucocorticoid functional characteristics of the adrenals in the terminal complications of acute myocardial infarct].

A follow-up study in the blood of the total, free and bound 11-oxycorticosteroids (11-OCS) and reserve binding capability of transcortin (RBCT) in 246 patients with acute myocardial infarction, complicated in 127 with cardiogenic shock, in 62 by ventricular fibrillation and in 57 by cardiac rupture was undertaken. In patients with acute myocardial infarction there was statistically reliable increased activation of glucocorticoid function of the adrenals with simultaneous marked drop of RBCT as compared with patients who had uncomplicated myocardial infarction. The greatest changes were found in patients with true cardiogenic shock and shock with cardiac rupture. Enhanced level of 11-OCS is retained for a long time in cardiogenic shock and ventricular fibrillation with lethal outcome. When the result is favourable there is a gradual decrease of glucocorticoids in the blood and a rise of RBCT.

Adrenal Glands↗
PubMed1980

Sexual dimorphism in binding and metabolism of cortisol during puberty in the guinea pig.

Sexual difference in plasma cortisol levels appeared in basal conditions on day 30 post-partum and values remained significantly higher in female guinea-pigs until day 70, disappearing on days 90 and 120. After stress, plasma cortisol levels increased in both sexes and the dimorphism was conserved with lower values obtained in males. Between days 30 and 70, cortisol metabolic clearance rate was significantly higher and binding capacity of transcortin for cortisol was significantly lower in males than in female guinea-pigs.

Aging↗
PubMed1995

[A comparative assessment of the effect of different methods of glucocorticosteroid therapy on the hypophyseal-adrenal system in bronchial asthma patients].

As shown by morphofunctional examinations of hypophyseal-adrenal system in 137 BA patients and post mortem examinations of adrenal cortex in 72 BA cases, most pronounced defects in glucocorticosteroid (GCS) biosynthesis and metabolism were recorded in patients on long-term GCS regiments (5-10 years and more). They displayed low levels of 11-OCS and 17-OCS, enhanced transcortin binding capacity, diminished adrenocortical reserves. Beclometasone propionate, endobronchial liposomes with hydrocortisone had no negative adrenal effects.

11-Hydroxycorticosteroids↗
PubMed1977

The effect of ascorbic acid supplementation on some parameters of the human immunological defence system.

We have investigated the effect of ascorbic acid (vitamin C) supplementation on some parameters of the human immune defence system in a group of 25 healthy, male university students. The subjects ingested 1 g ascorbic acid per day for a period of 75 days. Serum levels of IgA, IgG, IgM, C-3 complement component, cortisol and transcortin were measured before and after the ascorbic acid course. Corresponding measurements were performed on a control group of 20 healthy, male university students receiving no extra-dietary vitamin C. Our results showed that ascorbic acid supplementation caused a statistically significant increase in the serum levels of IgA, IgM and C-3 complement. Our study does not permit of conclusions regarding the mechanisms of action of ascorbic acid.

Adolescent↗
PubMedDate not supplied

Biochemical basis for the selection of oral contraceptives.

Many specific plasma proteins show dose-related changes when oral estrogens are administered. Large increases in concentration are seen in many important binding proteins, such as the sex hormone-binding globulin, transcortin, the retinol-binding protein, ceruloplasmin, and transferrin. A smaller group of plasma proteins are reduced in amount. These changes are related to altered rates of hepatic synthesis and secretion. As the overall effect of estrogen is one of increased protein synthesis, there is a reduction in the amount of plasma-free amino acids and in the pattern of distribution. Oral contraceptive (OC) users frequently show significant alterations in biochemical tests of vitamin status, at least some of which are related to alterations in plasma proteins. Other biochemical changes associated with OC use include a fasting hyperlipidemia, due mainly to increases in triglycerides, although there is often also a small increase in cholesterol. These changes are due primarily to increases in several lipoprotein fractions and are related mainly to the estrogen component. A deterioration in glucose tolerance occurs in many OC users and is probably induced by both estrogens and progestogens. There is evidence that certain clinical side effects of OCs, such as depression, are associated with specific biochemical changes.

Amino Acids↗
PubMed1981

Blood collection technique: no effect on in vitro protein binding of prednisolone.

The effect of the blood collection vessel and systemic heparin administration on in vitro protein binding of prednisolone was examined in blood collected from human subjects. No differences in the fractional binding of prednisolone were found in plasma from plain glass culture tubes, heparinized culture tubes, and two types of red- and green-top commercial vacuum tubes. Thus, these blood collection techniques do not alter serum or plasma albumin and transcortin binding of prednisolone.

Blood Proteins↗
PubMed1981

Dose-dependent protein binding and disposition of prednisolone in rabbits.

An animal model was sought that would mimic humans with regard to the dose-dependent pharmacokinetics of prednisolone. Four rabbits were each given 0.5 and 10 mg iv of prednisolone, and timed blood samples were obtained. Plasma prednisolone and prednisone concentrations were assayed by high-performance liquid chromatography, and protein binding was assessed using equilibrium dialysis at 37 degrees. Increases in the systemic clearance, volume of distribution at steady state, mean residence time (in three of four rabbits), and variance of residence time occurred as dose was increased. As in humans, prednisolone was partly converted to prednisone in the rabbit. Transcortin and albumin concentrations and their affinity constants for binding prednisolone were also similar to humans.

Animals↗
PubMed1984

Determination and prediction of tissue binding of prednisolone in the rabbit.

Binding of prednisolone to rabbit tissue was determined experimentally and by computation to assess factors and proteins responsible for tissue distribution of this corticosteroid. Binding in tissue slices ranged from 36% in the lung to 83% in the liver. The results obtained were compared with steady-state tissue distribution data generated in vivo in the rabbit. Linear uptake with good agreement between the two sets of data was observed for the skeletal muscle and kidney, but not for the liver and lung. In vivo uptake of prednisolone in the liver is severely affected by metabolism and biliary excretion, while in vitro distribution into liver slices showed a pattern typical of saturation of a low-capacity site followed by linear nonspecific binding at higher concentrations. Specific saturable binding (K1 = 1.95 X 10(7) M-1) accounted for 74% of drug bound at a steroid concentration in the liver of 0.3 X 10(-6) M, but its contribution decreased to 5% at a concentration of 20 X 10(-6) M. Expected prednisolone binding in rabbit tissue was calculated based on various effective protein concentrations in tissues and binding parameters of prednisolone to rabbit plasma. The use of total Lowry protein concentrations markedly overestimates, while albumin (and transcortin) concentrations severely underestimate the tissue binding of prednisolone. The thiopental effective protein fraction best approximates the in vivo and tissue slice binding of prednisolone. Metabolism and saturable binding in liver complicate the otherwise relatively linear uptake of prednisolone into various tissues where macromolecules other than albumin dominate in tissue binding of the steroid.

Animals↗
PubMed1984

Fluid shifts and other factors affecting plasma protein binding of prednisolone by equilibrium dialysis.

The effects of drug stability, radioactive tracer purity, buffer composition, protein concentration, and fluid shifts on the nonlinear plasma protein binding of prednisolone were examined by equilibrium dialysis. Prednisolone exhibits a concentration-dependent degradation; however, the limited extent of this does not affect protein binding. Impure tritiated prednisolone used as a tracer produces incorrect, low fractional binding values with the binding parameters generated for transcortin affected more than those for albumin. Isotonic sodium phosphate and Krebs original Ringer phosphate buffers yield similar fractional binding of prednisolone and identical protein binding parameters. Fractional binding of the steroid decreases with total plasma protein concentration, but the association constants remain constant over a twofold dilution of plasma proteins. Further dilution increases these parameters. A time-dependent colloidal osmotic fluid shift during dialysis causes dilution of plasma protein concentrations and diminished drug binding. Theoretical simulations show that the osmotic fluid shifts produce the largest changes in fractional binding for compounds that are bound by low-capacity proteins with low association constants (K less than 10(6) M-1). A mathematical equation was developed to correct bound drug concentrations and fraction bound for protein dilution caused by this effect. The fluid shifts can be prevented by the addition of dextran (mol. wt. 70,000) to the dialysis buffer in a concentration of 55% of the total protein concentration. Multiple factors can diminish the nonlinear prednisolone binding as artifacts during equilibrium dialysis, but the changes are relatively modest.

Blood Proteins↗
PubMed1988

Prednisolone binding to plasma proteins in domestic species.

The binding of prednisolone to total plasma proteins of dogs, horses, cows, and sheep was characterized using equilibrium dialysis. Prednisolone was bound to a first protein with high affinity but low capacity (transcortin) and to a second protein according to a nonsaturable mechanism (albumin). Interspecies differences were observed, with cows and dogs exhibiting the lowest, and sheep and horses the highest specific binding capacities. The results are in good agreement with known pharmacokinetic properties of prednisolone in domestic species.

Animals↗
PubMed1990

Central action of adrenal steroids during stress and adaptation.

Corticosteroids interact with receptors in the central nervous system. These receptors display heterogeneity and can be distinguished as corticosterone- and aldosterone-binding mineralocorticoid receptors and dexamethasone-binding glucocorticoid receptors. Ligand specificity of mineralocorticoid receptors for either corticosterone or aldosterone seems to be determined by co-localized transcortin and the enzyme, 11 beta-hydroxysteroid dehydrogenase. Aldosterone-selective mineralocorticoid receptors appear to be present in the circumventricular organs and the AV3V region of the hypothalamus and mediate behavior that is driven by salt appetite. Highest concentrations of mineralocorticoid receptors are found in neurons of the hippocampus. These limbic mineralocorticoid receptor sites mediate tonic influences of corticosterone on brain processes. Glucocorticoid receptors bind corticosterone with a tenfold lower affinity than do mineralocorticoid receptors, and are widely distributed in neuronal and glial cells of the brain. Glucocorticoid receptors are involved in the termination of the stress response (negative feedback). Studies involving measurement of glucocorticoid receptor mRNA and binding sites have revealed that glucocorticoid receptors are subject to autoregulation. After ADX, glucocorticoid receptor concentration increases, but is reduced after chronic stress, chronic administration of glucocorticoids, and at senescence. A diminished glucocorticoid receptor concentration may compromise the negative feedback action exerted by glucocorticoids after stress. After ADX, mineralocorticoid receptor binding is acutely up-regulated and reaches its maximum between 7 and 24 hours post-ADX. Mineralocorticoid receptor mRNA level shows a transient increase following ADX. Long-term ADX has no effect on the mineralocorticoid receptor concentration, but, interestingly, chronic dexamethasone treatment results in an up-regulation of mineralocorticoid receptors. Mineralocorticoid receptor level is decreased at senescence, but this age-related decrement can be reversed by chronic treatment with the ACTH4-9 analog, ORG 2766. Functionally, mineralocorticoid receptors and glucocorticoid receptors are involved in different aspects of the organization of the stress response, and in conjunction they control the stress responsiveness of the animal.

Adaptation, Psychological↗
PubMed1986

The effect of prednisone and hydrocortisone on the plasma protein binding of prednisolone in man.

The protein binding of prednisolone was studied in plasma obtained from healthy volunteers in the presence of added amounts of prednisone and hydrocortisone. The plasma protein binding was determined using in vitro equilibrium dialysis for 16 h at 37 degrees C against isotonic Krebs-Ringer buffer using radioactive prednisolone. Prednisone appeared to have no effect on prednisolone binding. This surprising result was observed even when prednisone concentrations were more than 35 fold greater than prednisolone concentrations. In contrast, a marked competition between hydrocortisone and prednisolone was observed. These binding data were fit using a nonlinear least squares regression computer program and the capacity and affinity constants for the binding of prednisolone to transcortin and albumin were estimated including the competition for binding sites between prednisolone and hydrocortisone. The results from these studies compare favorably with recent parameter calculations, and our previous work where differences in binding were noted between cushingoid and noncushingoid patients.

Blood Proteins↗