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PubMed1979

Virilizing adrenal adenoma stimulated by dexamethasone in a middle-aged woman.

In a middle-aged woman with virilizing adenoma, 2 mg dexamethasone increased urinary excretion of 17-ketosteroids (17-KS) and 17-hydroxycorticosteroids, whereas 8 mg dexamethasone increased urinary excretion only of 17-KS. With discontinuation of dexamethasone, 17-KS excretion returned to the predexamethasone level. Dexamethasone depressed the basal level of cAMP synthesis and basal testosterone production by the normal adrenal tissue in vitro. Dexamethasone also depressed the increase of cAMP produced by ACTH in the normal tissue. In contrast, dexamethasone increased basal cAMP synthesis and stimulated testosterone secretion in the tumor tissue. ACTH and dexamethasone were additive in their effects on cAMP and testosterone in the tumor tissue. It is suggested that dexamethasone acted directly on the adrenal tumor to stimulate steroid secretion in this patients.

11-Hydroxycorticosteroids↗

PubMed1977

Development of Neutrophilia by serially increasing doses of dexamethasone.

Dexamethasone (4-8 mg/m2 body surface area) was given orally or intravenously to six normal volunteers. The maximum neutrophil count occurred 4-6 h after oral or intravenous administration of dexamethasone and was due almost entirely to an increase in mature neutrophils; concomitantly there was a lymphocytopenia. A second rise in the neutrophil count occurred 24 h after oral ingestion of dexamethasone, coinciding with a lymphocytosis. Neutrophil alkaline phosphatase (NAP) activity during development fell as the neutrophil count rose. Other haematological values were unchanged except for small increments in erythrocyte sedimentation rate (ESR). Sodium concentration in serum and urine remained normal but urinary potassium excretion and urine volume increased after the intravenous dose. There was a direct relationship between plasma concentration of dexamethasone and the rise in neutrophil count following intravenous but not oral administration. The concentration of dexamethasone in plasma fell to half its peak value in 2-6 h. Dexamethasone-induced neutrophilia was similar to that induced by other corticosteroids. Dexamethasone in a dose of 6 mg/m2 produced minimal discomfort while inducing an adequate neutrophilia in the volunteers.

Adult↗

PubMed1975

Differences in corticosterone and dexamethasone binding to rat brain and pituitary.

In an attempt to relate binding of 3H-corticosterone and 3H-dexamethasone to their respective potencies in blocking pituitary-adrenal activity, cytosol binding in vitro and cell nuclear binding both in vivo and in tissue slices in vitro were studied in hippocampus, hypothalamus, and anterior pituitary of adrenalectomized rats. It was found that the extremely potent glucocorticoid dexamethasone has a different pattern of binding than corticosterone in the brain and in the anterior pituitary. 1) In cytosol, differences in the estimated binding capacities in a particular tissue for 3H-corticosterone and 3H-dexamethasone and different rates of inactivation in the ability to bind the two steroids are observed. 2) For 3H-corticosterone, cytosol binding in hippocampus is higher than that in hypothalamus, and cell nuclear binding follows the same pattern. For 3H-dexamethasone, cytosol binding is again higher in the hippocampus than in hypothalamus but cell nuclear binding in the two structures is not significantly different. With respect to the anterior pituitary, binding to cell nuclei is higher for 3H-dexamethasone, while the binding to cytosol macromolecules is higher for 3H-corticosterone. 3) In vivo and in vitro cell nuclear binding for both steroids showed the same pattern among the three tissues, but in vivo data showed more distinctly the preference of 3H-dexamethasone for the anterior pituitary and the preference of 3H-corticosterone for the hippocampus. 4) When labeled in tissue slices, cell nuclear radioactivity appears to be bound to macromolecules. 5) Steroid metabolism does not occur in slices during 60 min in vitro at 25 C and cannot account for the observed tissue differences in binding. The existence of more than one population of corticosteroid-binding sites in brain and in anterior pituitary is suggested. The results are consistent with the view that the dexamethasone blockade of stress-induced ACTH release is mediated by the anterior pituitary, while the high specificity of cotricosterone binding in the hippocampus implies a specific but as yet undetermined effect of the hormone in this brain area, an effect which may not be directly related to regulation of ACTH secretion.

Adrenalectomy↗

PubMed1978

Effects of dexamethasone on fetal and maternal thyroxine, triiodothyronine, reverse triiodothyronine, and thyrotropin levels.

The concentrations of T4, T3, rT3, and TSH were measured at term pregnancy in maternal and umbilical plasma and in amniotic fluid of 11 normal patients who received 8-16 mg dexamethasone 3-48 h before elective cesarean section and of 10 control patients who received no dexamethasone. The mean (+/- SE) concentrations of T4 (micrograms per dl) in maternal and umbilical plasma of dexamethasone-treated patients (12.5 +/- 0.9 and 13.0 +/- 0.9) were not significantly different (P less than 0.05) from those of the control patients (13.9 +/- 1.5 and 10.4 +/- 0.6, respectively). The mean (+/- SE) maternal plasma concentrations of T3 and rT3 (nanograms per dl) of dexamethasone-treated patients (204 +/- 6 and 82 +/- 11) were not significantly different (P less than 0.05) from those of the control patients (201 +/- 26 and 72 +/- 6, respectively). However, the mean (+/- SE) concentrations of T3 and rT3 (nanograms per dl) in umbilical plasma of dexamethasone-treated patients (106 +/- 13 and 360 +/- 35) were 3- and 2-fold and significantly higher (P less than 0.05) than those of the control group (39 +/- 6 and 195 +/- 19, respectively). No significant differences (P less than 0.05) were observed between the mean concentrations of TSH (microunits per ml) in maternal and umbilical plasma of dexamethasone-treated patients (2.5 +/- 0.5 and 3.0 +/- 1.0) and those of the control group (2.8 +/- 0.5 and 6.9 +/- 2.7, respectively). Under the conditions studied, no differences in the mean concentrations of amniotic fluid T4, T3, rT3, or TSH were observed between the two groups of patients (P less than 0.05). The increase of T3 and rT3 levels in umbilical plasma after dexamethasone administration indicates alteration in fetal thyroid economy.

Dexamethasone↗

PubMed1976

The insulin tolerance test after pre-treatment with dexamethasone.

The plasma 11-hydroxycorticosteroid and serum GH responses to insulin-induced hypoglycaemia were studied in 25 healthy volunteers. The results of a control insulin tolerance test were compared with those of 2 similar tests which were performed after pre-treatment with dexamethasone 0.5 and 1.0 mg, respectively. The GH response to hypoglycaemia was significantly lower in women than in men in all 3 tests. In men, but not in women, the GH response was lower after pre-treatment with 1 mg dexamethasone than in the other 2 tests. The plasma 11-hydroxycorticosteroid response was significantly greater after pre-treatment with 0.5 mg dexamethasone than in the control test, and was at least as good after 1 mg dexamethasone. After pre-treatment with dexamethasone the subjects experienced less discomfort and a shorter duration of sweating than in the control insulin tolerance test. Pre-treatment with 1 mg dexamethasone also has other advantages. Thus, the basal plasma cortisol level is low and stable, which facilitates estimation of the magnitude of the cortisol response. Furthermore, information is obtained about the dexamethasone suppression response.

11-Hydroxycorticosteroids↗

PubMed1977

The effect of dexamethasone therapy in prolonged pregnancy.

Fifty-six patients, chosen by random sampling from a total group of 120 post-term women, received dexamethasone (Decadron, "MSD" 2 mg 3 times a day for 4 days, the other 64 patients acting as controls. The evolution of uterine activity was evaluated using pelvic score (PS) and a modified low dosage oxytocin sensitivyt test (OST) before (T1) and after (T2) the treatment. During the interval from the second to the 6th day inclusive after T1 35 women of the dexamethasone group and 15 of the control group had a spontaneous onset of labour (SO) (0.001 less than P less than 0.01). Five patients in the dexamethasone group with primary rupture of membranes started labour spontaneously within 12 hours after membrane rupture, 7 patients in the control group with primary rupture of membranes received oxytocin as labour did not start within 24 hours. Excluding patients artifically induced, the mean interval from T1 to SO was 6.8 days in the control group and 5.2 days in the dexamethasone group (P less than 0.001). In both groups PS and the sum of Montevideo units (MU) during OST increased from T1 to T2, the increase was significantly greater in the dexamethasone group than in the control group. We found no correlation between the results of OST and the T1--SO interval. Dexamethasone, as used in this study, may promote labour in prolonged human pregnancy. Due to its low potency, it is not a substitute for oxytocin in the induction of labour. The lowered placento-fetal quotient in the dexamethasone group warrants further study of the effects of steroid hormone on placental function.

Administration, Oral↗

PubMed1979

Effects of dexamethasone on tumor-induced brain edema and its distribution in the brain of monkeys.

A human choriocarcinoma was successfully adapted to grow in the brain of monkeys (Macaca mulatta), thus providing a model of tumor-induced brain edema. Four animals were given dexamethasone (3 mg/kg/day) during 3 to 5 days after the onset of clinical signs, and the other five received no treatment for the same period. Tissue water and electrolyte content of treated and untreated animals were compared in cortex and white matter at various distances from the edge of the tumor. In untreated animals, 67.9% and 23.6% swelling was detected in adjacent and remote white matter, respectively, but only 11.8% swelling was noted in adjacent cortex. In animals treated with dexamethasone these percentages of swelling were improved to 32.4% and 11.9% in the corresponding white matter, and to 4.9% in adjacent cortex. The electrolyte changes shown in edematous brain of control animals also demonstrated significant improvement in the dexamethasone-treated group. Tissue radioactivity of 3H-dexamethasone at 60 minutes after intravenous injection was high in the periphery of tumor, adjacent cortex, and white matter, but low in the center of tumor, remote cortex, and white matter. The sites with high concentrations of dexamethasone also showed significant improvement of brain edema after dexamethasone treatment, suggesting that dexamethasone may act directly at these loci.

Animals↗

PubMed1979

The response of focal ischemic cerebral edema to dexamethasone.

Twenty-four h after permanent occlusion of the middle cerebral artery (MCA) in the cat, the hemispheric swelling due to edema is markedly reduced under treatment with large doses of dexamethasone than is the case with the untreated group. The increase of regional water and sodium content in the MCA territory is less in the dexamethasone treated group, whereas the potassium changes in the ischemic tissue showed only small differences between the two groups. The potassium content of the non-ischemic tissue is slightly increased in the dexamethasone treated animals when comparing with the untreated group. RISA activity in the tissue is increased in the grey and the white matter of both groups. The less marked RISA-131 activity in the cortical grey matter of the treated animals indicates blood-brain barrier damage of a smaller degree due to dexamethasone. These findings indicate a beneficial effect of dexamethasone on local ischemic edema. Regarding our results and the pharmacokinetics of this steroid the dexamethasone loading of a patient has to be in the range of about 100 mg per day for the adult, and has to be started immediately after the onset of a stroke.

Animals↗

PubMed1976

The effects of dexamethasone on plasma free androgens during the normal menstrual cycle.

In order to evaluate the ovarian and adrenal contribution to peripheral plasma concentrations of total testosterone (TTe), indixes of the plasma concentrations of free testosterone (FTeI), free 17 beta-hydroxysteroid androgens (FHSI), and testosterone-binding globulin (TeBG) during the menstrual cycle, women were examined during three normal cycles and three other cycles under dexamethasone (0.5 mg., four times a day) suppression. All study cycles were apparently ovulatory. The mean TTe and FTeI during the midcycle period were significantly higher than during the early follicular (P less than 0.005) and the midluteal periods (P less than 0.01 and P less than 0.001, respectively). During the menstrual cycles under dexamethasone suppression only the difference in TTe and FTeI between the midcycle (37 +/- 12.4 (S.D.) ng. per 100 ml. and 10.5 +/- 4.0 (S.D.), respectively) and the midluteal (26.0 +/- 10.1 (S.D.) ng. per 100 ml and 7.2 +/- 3.2 (S.D.), respectively) periods was significant statistically (P less than 0.05). No significant differences in the mean levels of FHSI and TeBG between three periods within the cycle were noted in either the control or the dexamethasone-treated cycle. When each phase was compared, the mean levels of TTe, FTel, and FSHI were significantly lower in the dexamethasone-treated cycles than in the normal cycles. The data suggest that the level of TeBG is not perceptibly affected by physiologic fluctuation of estrogen levels during the menstrual cycle, and the FHSI levels are stable throughout the ovulatory cycle. Decrease in levels of TTe, FTeI, and FHSI during dexamethasone suppression seems to be due to reduction of androgen production as TeBG, a major determinant of the metabolic clearance rate of androgens, was not affected by dexamethasone.

Adult↗

PubMed1976

Effect of endogenous corticosterone on the determination of dexamethasone receptor levels in rat liver cytosol.

The effect of endogenous corticosterone on the quantitative measurement of dexamethasone receptors in liver cytosols from developing rats has been studied. Liver cytosols from adrenalectomized rats were preincubated with increasing concentrations of nonlabeled corticosterone and the levels of detectable dexamethasone receptors were subsequently determined either directly or after removal of unbound corticosterone. Corticosterone concentrations of 50 nM or lower had no significant effect on the specific binding of labeled dexamethasone. Higher concentrations of corticosterone resulted in under-estimation of dexamethasone receptor levels. The mean levels of endogenous corticosterone in liver cytosols from 19.5- to 21.5- day fetuses, 22-day fetuses, 6-day-old immature rats and adult rats were 27.40, 11.91, 0.81 and 4.05 nM, respectively. It is concluded that variations in the levels of circulating corticosterone in the rat under normal physiological conditions have no significant effect on the quantitative measurement of total (occupied and unoccupied) receptor sites for dexamethasone in liver cytosol. This is supported by the finding that prior treatment of liver cytosols, from rats at different stages of development, with charcoal to remove unbound steroids has no effect on the amount of detectable dexamethasone receptors.

Animals↗

PubMed1979

Dexamethasone suppressibility of plasma pregnenolone or dehydroepiandrosterone in gonadectomized patients.

The 9 AM dexamethasone suppression test was carried out in gonadectomized patients, and plasma pregnenolone or dehydroepiandrosterone (DHA) was radioimmunoassayed following various amounts of dexamethasone administration. Pregnenolone, as well as the plasma ACTH level, was completely suppressed with 1 mg dexamethasone, whereas 4 mg or 8 mg of dexamethasone was needed to induce a complete DHA suppression. These findings suggest that the gonads alone contribute to the poor dexamethasone suppressibility of pregnenolone in normal subjects, and that adrenal DHA secretion might be also regulated by an unidentified factor other than ACTH, which would be suppressed with large doses of dexamethasone.

Adrenocorticotropic Hormone↗

PubMed1978

Enhanced dexamethasone resistance in cystic fibrosis cells: potential use for heterozygote detection and prenatal diagnosis.

Cultured skin fibroblasts from patients with cystic fibrosis (CF) are more resistant to dexamethasone toxicity than are normal cells. We now report that, when fibroblasts cultured from obligate CF heterozygotes are exposed to dexamethasone, they have an intermediate survival compared to normal and homozygous CF cells. When dexamethasone survival was tested on cells from four patients undergoing amniocentesis, cells from a woman at risk of producing a child with CF showed significant dexamethasone resistance, similar to that of fibroblasts derived from lnown CF homozygotes; the other amniotic cell specimens showed dexamethasone sensitivity similar to that of normal skin fibroblasts. These data suggest that the dexamethasone resistance previously observed in skin fibroblasts may also be useful in the prenatal diagnosis of CF.

Amniotic Fluid↗

PubMed1978

Effects of dexamethasone on the morphogenesis of two mutants of Rous sarcoma virus.

Japanese quail cells transformed by the replication-defective, Bryan high-titer strain of Rous sarcoma virus, BH RSV(-)Q, clone 3, revealed intracytoplasmic A-type particles after dexamethasone treatment. In the absence of dexamethasone, or when superinfected with a helper virus in the presence or absence of dexamethasone, no such particles were observed. Chick embryo cells (CEC) infected with a temperature-sensitive sarcoma virus mutant, LA 334, coordinately defective for transformation and viral replication, showed abnormal accumulation of viral core substances and aberrant budding at the non-permissive temperature (41 degrees). CEC infected with LA 334 and treated with dexamethasone at 41 degrees resulted in more extensive accumulation of abnormal budding without increased release of viral particles. Dexamethasone, however, did not lead to abnormal morphogenesis of virus under permissive conditions. The selective effects of dexamethasone on the morphogenesis of these two mutants of avian sarcoma virus are discussed.

Animals↗

PubMed1978

Regulation of glutamine synthetase by dexamethasone in hepatoma tissue culture cells.

In certain lines of hepatoma tissue culture (HTC) cells, glutamine synthetase (EC 6.3.1.2) specific activity is increased 2.5- to 3-fold by the addition of glucocorticoids to the growth media. Actinomycin D blocks both the induction and deinduction of glutamine synthetase by glucocorticoids, suggesting a requirement of RNA synthesis for both processes. Using an antiserum raised against purified rat liver glutamine synthetase, we have precipitated radiolabeled glutamine synthetase from HTC cells. Electrophoresis of the immunoprecipitates on sodium didecyl sulfate-acrylamide gels isolates the subunit of glutamine synthetase and permits the radioactivity in the glutamine synthetase band to be quantitated. Using this technique, we have investigated the effect of dexamethasone, a synthetic glucocorticoid, on the rates of synthesis and degradation of glutamine synthetase. Dexamethasone (10(-7) M) increases the rate of synthesis of glutamine synthetase 2- to 3-fold but has no effect on the rate of glutamine synthetase degradation. The rates of total cell protein synthesis and degradation are not significantly affected by dexamethasone. The presence of actinomycin D at the time of removal of dexamethasone from induced cells prevents the fall in the induced rate of synthesis of glutamine synthetase normally seen when the inhibitor is removed from the culture medium. The regulation of glutamine synthetase by dexamethasone has been compared to the regulation of another dexamethasone-inducible enzyme in HTC cells, tyrosine aminotransferase, and been found to be similar in all parameters studied.

Carcinoma, Hepatocellular↗

PubMed1979

Experimentally induced synovitis of chickens with Mycoplasma synoviae: effects of dexamethasone treatment.

Specific - pathogen - free chickens were inoculated in the right tibiometatarsal joint with a synovitis-derived Mycoplasma synoviae strain before or during dexamethasone treatment. Development of synovitis in chickens inoculated during the drug treatment was apparently delayed in comparison with development of synovitis in non-treated chickens. Severity of clinical synovitis in chickens inoculated before the drug was given was apparently less than that in chickens not treated or in chickens treated with dexamethasone. Histopathologic changes in the early stage of the infection (1 to 2 weeks) were not modified by dexamethasone treatment, although those changes in the succeeding stage (6 to 7 weeks) were greatly lessened. A relationship was observed between the dosage of dexamethasone and the severity of synovitis, as well as the kinds of cells that infiltrated into the joint lesions. Although serum antibody titers in chickens treated with an excessive dose of dexamethasone were markedly lower, clinical, bacteriologic, and histopathologic observations in chickens treated with dexamethasone were similar to those previously found in surgically thymectomized chickens. These results may support the theory that multiple synovitis of chickens caused by M synoviae infection develops mainly because of an immune response, especially by thymus-dependent functions.

Animals↗

PubMed1979

Comparative study of anti-endotoxic potency of dexamethasone based on its different ester types.

Difference in the anti-endotoxic potency in mice between dexamethasone 21-disodium phosphate (DM-P) and 21-sodium sulfate (DM-S) was investigated. Changes in the plasma levels of free 17-hydroxycorticoids (17-OHCS), further, were defined after intravenous administration of 2 mg/kg dexamethasone in elective surgical patients for elucidation of the metabolic basis of the different anti-endotoxic potencies of the two ester types of dexamethasone. Young male mice of DDN strain were pretreated with 0.2 mg DM-P or DM-S. Following the pretreatment, 0.5 mg of the endotoxin was administered at varying intervals of 0--24 hours, and survival rates were determined after 72 hours. In the DM-P group the mice exhibited a significant resistance to the endotoxin within two hours after the pretreatment, but in the DM-S group, the mice exhibited no anti-endotoxic potency. When different doses of dexamethasone (from 3.2 to 0.00625 mg) were administered with 0.5 mg of the endotoxin simultaneously, the mice in the DM-P group showed improvements in survival rates that tended to be dose related, but the mice in DM-S group showed no improvement in survival rates. Plasma levels of free 17-OHCS in elective surgical patients, further, were remarkably elevated after administration of DM-P, 2 mg/kg, but they showed no elevation after administration of DM-S, 2 mg/kg. Thus, it is clear that the in vivo metabolism of the two esters is different. DM-P easily liberates its free form, whereas DM-S does not. From this evidence, it was concluded that there is a close correlation between the anti-endotoxic potency of dexamethasone and its plasma level of free form, and that glucocorticoids can demonstrate their anti-endotoxic action when they are present at pharmacologically high levels in the bloodstream. There is considerable difference in biological action, moreover, between the two water-soluble esters of dexamethasone. More attention should be paid to this difference when investigating the treatment of shock with glucocorticoids.

17-Hydroxycorticosteroids↗

PubMed1979

Thymic regeneration after dexamethasone treatment as a model for subpopulation development.

Three mouse thymocyte subpopulations with differing sensitivity to dexamethasone were characterized by size and density. Distribution patterns were determined for thymocytes during normal development and during regeneration after treatment with dexamethasone. From these, the subpopulation proportions were calculated and cell population kinetics were evaluated. Medium-sized low density cells (type III) were least sensitive to dexamethasone and showed a relatively slow regeneration rate. The small cells of intermediate density, "early cortical" cells (type II), exhibited the most rapid regeneration rate, while the growth rate of the small cells of high density (type I) was intermediate. Cells of intermediate and high density were relatively sensitive to dexamethasone. The ratio of the phytohemagglutinin to concanavalin A (Con A) response increased after dexamethasone treatment with the increase in the proportion of type III cells. Con A responses were attributed to type II and type III cells. A tentative multipathway model for intra-thymic T cell development is presented. Large cells, not confined to a certain trajectory in the density gradient, may represent a pool of proliferating cells of the other three types.

Animals↗

PubMedDate not supplied

The effects of ephedrine and theophylline on dexamethasone metabolism in bronchial asthma.

The effect of ephedrine (nine patients) and theophylline (seven patients) on dexamethasone metabolism was studied before and after three weeks of drug therapy in 16 asthmatics. Five patients were studied similarily but treated with placebo. After treatment with ephedrine, there was a mean decrease in plasma dexamethasone half-life (t1/2) of 132 minutes, or 36 per cent (P less than 0.025), and mean increase in metabolic clearance rate (MCR) of 148 liters/day, or 42 per cent (P less than 0.001). Increase in the excretion of urinary radioactivity, predominantly in the conjugated fractions, was noted. In contrast, theophylline and placebo therapy resulted in no significant changes in dexamethasone t1/2 or MCR. The rate of urinary excretion of radioactivity was reduced after theophylline treatment. Since ephedrine accelerates labeled dexamethasone clearance while theophylline does not, caution is necessary when prescribing ephedrine for asthmatics requiring long-term therapy with dexamethasone and probably other corticosteroids. It would appear from the present investigation that theophylline is a more appropriate bronchodilator for these patients.

Adult↗