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PubMed1986

Cushing's syndrome from the therapeutic use of intramuscular dexamethasone acetate.

We present, to our knowledge, the first case of Cushing's syndrome due to large doses of intramuscular dexamethasone acetate. Dexamethasone levels after intramuscular dexamethasone administration were measured in two patients. Serial determination of the dexamethasone levels demonstrated prolonged serum half-lives of seven and 33 days in the two patients, respectively. Furthermore, pharmacologic levels of dexamethasone were present as long as seven months after the initial injections. The present recommendation for the use of intramuscular dexamethasone acetate is as frequent as every one to three weeks. However, our patients demonstrate that supraphysiologic levels of dexamethasone may still be present well beyond the three-week period.

Addison Disease↗

PubMed1984

Effect of levamisole on lymphocyte blastogenesis and neutrophil function in dexamethasone-treated cattle.

Levamisole was evaluated at 6 dose levels for its ability to prevent the dexamethasone-induced suppression of in vitro lymphocyte blastogenesis or neutrophil function in cattle. Dexamethasone (0.4 mg/kg of body weight, IM) and levamisole hydrochloride (0.5, 1.0, 2.0, 4.0, or 8.0 mg/kg orally) were administered to groups of 4 cattle daily for 3 days. Another group of 4 cattle were given the 3-day dexamethasone treatment and 6.0 mg/kg of levamisole (the recommended anthelmintic dose) was given only once on the 1st day that dexamethasone was given. Results obtained from the dexamethasone-levamisole-treated cattle were compared with results obtained from cattle that were given only dexamethasone. Levamisole had no apparent consistent ability to enhance lymphocyte blastogenic responsiveness (to the mitogens phytohemagglutinin, concanavalin A, or pokeweed mitogen or in a 1-way mixed lymphocyte reaction) or to enhance neutrophil function (random migration, nitroblue tetrazolium reduction, iodination, or antibody-dependent cell-mediated cytotoxicity) in dexamethasone-treated cattle.

Adrenocorticotropic Hormone↗

PubMed1981

Maturation of sympathetic neurotransmission in the rat heart. VII. Suppression of sympathetic responses by dexamethasone.

Effects of dexamethasone on development of sympathetic nerve function in the heart were evaluated by giving 1 mg/kg of dexamethasone s.c. daily for several days beginning the day after birth. Dexamethasone interfered with tyramine- and isoproterenol-induced tachycardia in the neonates but did not cause alterations in development of a marker for presynaptic sympathetic nerve terminals (synaptic vesicle uptake of [3H] norepinephrine) nor of postsynaptic beta adrenoceptor binding of [3H]dihydroalprenolol; the deficit was also unrelated to general cellular effects of the hormone. These data suggest that the subnormal chronotropic responses of the heart to sympathetic stimulation in dexamethasone-treated neonatal rats result from uncoupling of receptors from the organ response. The effects of dexamethasone on cardiac responses were specific to the neonate, as mature rats given dexamethasone did not show suppression of cardiac sympathetic action. Neonatal dexamethasone treatment also produced a deficit of adrenomedullary development with deficiencies in catecholamine levels and in catecholamine biosynthetic enzymes; deficits in phenylethanolamine N-methyltransferase activity persisted into young adulthood.

Animals↗

PubMed1982

[ACTH in the dexamethasone suppression test].

Despite the great clinical importance of the low-dose dexamethasone suppression test (determination of cortisol after dexamethasone 2 mg p.o. at 11.00 p.m. in the evening before) and of the determination of ACTH in plasma, so far only little is known about the ACTH response to dexamethasone in normal subjects. In the present study cortisol and ACTH were determined by radioimmunoassay in normal subjects at 8.00 a.m., 10.00 a.m. and noon before and after dexamethasone. Additionally the cortisol response to ACTH was tested under both conditions. The ACTH concentrations in the morning show a periodicity quite similar to the well-known circadian rhythm of cortisol secretion. Dexamethasone blocks this periodicity without decreasing ACTH significantly. The cortisol response to ACTH after dexamethasone is normal. In the morning only a basal and presumably biologically inactive ACTH is secreted which can not further be suppressed by dexamethasone. Therefore it is advisable for the diagnosis of hypercortisolism to measure ACTH only in stimulation tests, e.g. insulin-induced hypoglycemia.

Adrenocorticotropic Hormone↗

PubMed1982

[ACTH response in the dexamethasone suppression test].

Adrenocorticotropic Hormone↗

PubMed1984

Effects of single intravenous doses of dexamethasone on baseline plasma cortisol concentrations and responses to synthetic ACTH in healthy dogs.

The duration of adrenocortical suppression resulting from a single IV dose of dexamethasone or dexamethasone sodium phosphate was determined in dogs. At 0800 hours, 5 groups of dogs (n = 4/group) were treated with 0.01 or 0.1 mg of either agent/kg of body weight or saline solution (controls). Plasma cortisol concentrations were significantly (P less than 0.01) depressed in dogs given either dose of dexamethasone or dexamethasone sodium phosphate by posttreatment hour (PTH) 2 and concentrations remained suppressed for at least 16 hours. However, by PTH 24, plasma cortisol concentrations in all dogs, except those given 0.1 mg of dexamethasone/kg, returned to control values. Adrenocortical suppression was evident in dogs given 0.1 mg of dexamethasone/kg for up to 32 hours. The effect of dexamethasone pretreatment on the adrenocortical response to ACTH was studied in the same dogs 2 weeks later. Two groups of dogs (n = 10/group) were tested with 1 microgram of synthetic ACTH/kg given at 1000 hours or 1400 hours. One week later, half of the dogs in each group were given 0.01 mg of dexamethasone/kg at 0600 hours, whereas the remaining dogs were given 0.1 mg of dexamethasone/kg. The ACTH response test was then repeated so that the interval between dexamethasone treatment and ACTH injection was 4 hours (ACTH given at 1000 hours) or 8 hours (ACTH given at 1400 hours). Base-line plasma cortisol concentrations were reduced in all dogs given dexamethasone 4 or 8 hours previously.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex↗

PubMed1984

Dexamethasone induction of an inhibitor of plasminogen activator in HTC hepatoma cells.

Incubation of HTC rat hepatoma cells with dexamethasone causes a rapid decrease in cellular plasminogen activator (PA) activity. Mixing experiments show the presence of an inhibitor of PA in dexamethasone-treated cells. This study investigates whether the decrease in PA activity is secondary to the induction of an inhibitor by glucocorticoids, to a decrease in the amount of PA, or to a combination of both mechanisms. PA and its inhibitor are dissociated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis under non-reducing conditions, and both activities are then recovered and quantitated. HTC cells have two major forms of PA with Mr values of 110,000 and 64,000. Although PA activity in the unfractionated extracts from dexamethasone-treated cells is inhibited by 90% relative to control, there is no decrease in the total activity of sodium dodecyl sulfate-dissociated PA activity, suggesting that dexamethasone causes no decrease in the amount of the enzyme. PA inhibitor activity migrates as a single band of Mr = 50,000. The total activity of inhibitor increases in a time-dependent fashion, reaching a maximum of greater than 10 times control after a 4-6-h incubation with 0.1 microM dexamethasone. The induction of inhibitor requires both RNA and protein synthesis and shows a dependence on dexamethasone concentration identical to that for responses known to be mediated by glucocorticoid receptors. We conclude that dexamethasone inhibits PA activity by inducing the synthesis of an inhibitor rather than by decreasing the amount of PA.

Animals↗

PubMed1981

Dexamethasone suppression test in the management of hyperandrogenized patients.

The authors evaluated 86 hyperandrogenized women with measurements of serum cortisol, dehydroepiandrosterone sulfate, testosterone, and dihydrotestosterone in pooled sera before and after a dexamethasone suppression test. According to strict criteria, 70 (81%) of 86 women demonstrated a major glucocorticoid-suppressible component to their hyperandrogenism. Endocrine therapy was dictated by the results of the dexamethasone suppression test. To assess the predictive value of this test, we evaluated the clinical responses of the subgroup of 55 women who received appropriate endocrine suppression therapy for 6 to 15 months. Of this subgroup, 38 were identified as having adrenal hyperandrogenism; 3 had ovarian hyperandrogenism; and 14 had mixed hyperandrogenism. Of the 55 patients, 49 received dexamethasone alone; 3 received dexamethasone plus Ovral (an oral contraceptive containing the synthetic progestogen norgestrel 0.5 mg and ethinyl estradiol 0.05 mg); and 3, all with ovarian hyperandrogenism, received depomedroxyprogesterone acetate (Depo-Provera). Clinical response was assessed in terms of improvement or no improvement in menstrual status, acne, and hirsutism. Of 29 patients with adrenal or mixed hyperandrogenism associated with abnormal menses, the menstrual status of 17 (59%) improved after dexamethasone therapy. Acne improved in 39 (100%) of 39 subjects. Hirsutism showed moderate to marked improvement in 40 (73%) of 55 women after 6 to 15 months of endocrine suppression therapy. These results indicate the endocrine suppression therapy, particularly with repeated low-dose dexamethasone, prescribed on the basis of a dexamethasone suppression test, is an effective means of managing hyperandrogenism.

Adolescent↗

PubMed1984

Inhibition of sodium-independent amino acid transport by dexamethasone in rat hepatoma cells.

We studied the uptake of leucine, phenylalanine, and the amino acid analog, 2-aminonorborane-2-carboxylic acid, by rat hepatoma cells in tissue culture. The uptake of these amino acids was partially mediated by a plasma membrane transport system similar to the L agency described in other cell types in that it does not require extracellular sodium and is subject to trans-stimulation. Initial rates of sodium-independent transport of these amino acids were calculated using mathematical transformations of the uptake time course curves. The glucocorticoid dexamethasone inhibits the activity of this transport system; the initial rates of sodium-independent uptake of leucine, phenylalanine, and 2-aminonorborane-2-carboxylic acid are decreased by approximately one-third (average = 30%, n = 19) after incubation of HTC cells with 0.1 microM dexamethasone. This inhibition requires at least 15 h, reaching a maximum at 24 h of exposure of the cells to the hormone. Dexamethasone has an asymmetrical effect on sodium-independent amino acid transport in that exposure of the cells to the hormone does not inhibit the rates of outflow of leucine or phenylalanine from preloaded cells into medium without sodium. Inhibition of uptake is blocked by 0.1 mM cycloheximide and 4 microM actinomycin D, indicating the need for continuous protein synthesis for dexamethasone action. Insulin, which is known to partially reverse the inhibitory effect of dexamethasone on the A amino acid transport system in HTC cells, does not alter the action of dexamethasone on the L system. Previous investigations have demonstrated inhibition by dexamethasone of at least two distinct sodium-dependent amino acid transport activities in HTC cells. The data presented here, showing inhibition by the glucocorticoid of a sodium-independent transport activity, indicate that the effect of the hormone is independent of the energy source of the amino acid transport systems affected.

Amino Acids↗

PubMed1982

Effects of adrenalectomy and dexamethasone on hepatic lipid metabolism.

The influence of adrenalectomy and dexamethasone on hepatic free fatty acid metabolism was studied in isolated perfused livers from male rats. Adrenalectomy 1 week prior to perfusion did not affect uptake of oleate, output of triglyceride, or rate of ketogenesis compared to sham-operated match-fed controls. Livers from dexamethasone-treated rats (0-2 mg/kg per day for 7 days) removed less oleate from the perfusate, esterified more to total and very low density lipoprotein (VLDL) triglyceride, and oxidized less to ketone bodies, compared to match fed controls; additional studies with [1-(14)C]oleate confirmed these findings. The output of glucose by livers from dexamethasone-treated rats was also stimulated. The output of VLDL triglyceride was correlated with output of total perfusate triglyceride (r = 0.77, P < 0.001). Prior to perfusion, dexamethasone livers accumulated more triglyceride than did control livers. Adrenalectomy did not affect the concentration of plasma free fatty acid or blood ketones and glucose; however, the plasma concentration of triglyceride was elevated. Dexamethasone increased the concentration of plasma free fatty acid, total triglyceride, and VLDL protein, triglyceride, phospholipid, and free cholesterol. No changes were observed in the concentration or composition of plasma low density lipoprotein (LDL) lipids. The concentration of plasma high density lipoprotein (HDL) protein and lipid, and plasma apoA-I, tended to increase; the ratio of total HDL cholesterol to LDL cholesterol was elevated with dexamethasone treatment. These observations suggest that augmented synthesis and secretion of VLDL triglyceride contribute to glucocorticoid-induced hyper-triglyceridemia.-Cole, T. G., H. G. Wilcox, and M. Heimberg. Effects of adrenalectomy and dexamethasone on hepatic lipid metabolism.

Adrenalectomy↗

PubMed1982

Effects of dexamethasone on endotoxin shock in the anesthetized pony: hematologic, blood gas, and coagulation changes.

The effects of dexamethasone (1 mg/kg of body weight) on hematologic, blood gas, and blood coagulation values in anesthetized ponies during endotoxin-induced shock were evaluated. Fifteen ponies were assigned to 3 groups of 5 ponies each: group 1, anesthetized nontreated and dexamethasone-treated controls; group 2, endotoxin, nontreated; group 3, endotoxin, dexamethasone treated. The hematologic changes in this endotoxin shock model included leukopenia and hemoconcentration. Significant hematologic effects were not seen in ponies after administration of dexamethasone. However, dexamethasone treatment resulted in an increased trend in total WBC counts and neutrophils. The blood gas changes reflected a respiratory component resulting from anesthesia and a greater metabolic component from the endotoxemia. The plasma lactate increase was significantly (P less than 0.05) less in ponies treated with dexamethasone, compared with plasma lactate in non-treated ponies. During endotoxin shock, the changes observed in the blood coagulation values included a significant (P less than 0.05) prolongation of the activated partial thromboplastin time and thrombin time and an insignificant prolongation of the prothrombin time. Dexamethasone treatment prevented prolongation of thrombin time and permitted only a mild prolongation of activated partial thromboplastin time. Seemingly, corticosteroids are useful in the treatment of clinical endotoxin shock in horses as indicated by their desirable effects on total WBC, neutrophils, cellular metabolism, and blood coagulation.

Acidosis↗

PubMed1982

Treatment of persistent eustachian tube dysfunction in children with aerosolized nasal dexamethasone phosphate versus placebo.

Forty-five children aged two to 10 years with persistent eustachian tube dysfunction received a three-week course of aerosolized nasal dexamethasone phosphate or placebo. Patients were randomly assigned to the drug or placebo group and received one spray in each nostril three times a day for three weeks. Middle ear pressure and gradient were assessed with tympanometry. Tympanic membrane mobility, position and presence of middle ear fluid were assessed by the investigators initially and at weekly intervals during the study. Fasting morning plasma cortisol levels were obtained prior to starting the study and at its conclusion. The dexamethasone-treated group showed a significant increase in patients with normal middle ear pressure compared to placebo after one week and a significant increase in the number of patients with normal middle ear gradient at the second week. By the conclusion of the study there were no significant differences between the groups. Within the dexamethasone group, however, there were statistically significant increases in patients achieving normal middle ear pressure, tympanic membrane mobility and position in one or both ears. Plasma cortisol levels fluctuated widely from one determination to another and did not show an over-all declining trend for the dexamethasone group. However, two dexamethasone patients had a transient fall in cortisol level to below the normal range. These results support some therapeutic efficacy for nasal aerosolized dexamethasone but also point out the therapeutic value of time alone. The observation that most improvement occurred in the first two weeks and that some worrisome cortisol changes occurred suggests that dexamethasone therapy should be limited to two weeks and be undertaken with caution.

Administration, Intranasal↗

PubMed1981

Termination of pregnancy with cloprostenol and dexamethasone in intact or ovariectomized cows.

Termination of pregnancy in cows was investigated using sham-operated (SH) or ovariectomized (OV) cows treated with either a saline vehicle (V), cloprostenol (PG), dexamethasone (DEX) or dexamethasone and cloprostenol (DEX+PG). Surgery was done at 210 days of pregnancy and treatment was administered 72 hours later. Days (mean+/-S.E.) from treatment to termination of pregnancy for the treatment groups were: sham-operated +vehicle (SH+V): 61.5+/-11.3; ovariectomized+vehicle (OV+V): 53.4+/-15.7; sham-operated+cloprostenol (SH+PG): 61.8+/-1.7; ovariectomized+cloprostenol (OV+PG): 54.5+/-13.1; shamoperated+dexamethasone (SH+DEX): 74.8+/-4.8; ovariectomized+dexamethasone (OV+DEX): 2.8+/-0.4; shamoperated+dexamethasone+cloprostenol (SH+DEX+PG) 26.0+/-23.0; ovariectomized+dexamethasone+cloprostenol (OV+DEX+PG): 7.2+/-4.9. Pregnancies in the OV+DEX and OV+DEX+PG groups were terminated significantly earlier than in all other groups (P<0.05) except the SH+DEX+PG group. These findings suggest that dexamethasone will terminate pregnancy in cows near seven months of gestation after the ovarian source of progesterone has been removed by either an injection of prostaglandin or by ovariectomy.

Abortion, Induced↗

PubMed1980

Clinical, chemical, and CT evaluation of short-term and long-term antiedema therapy with dexamethasone and diuretics.

Three independent methods were used to quantify the therapeutic effect on peritumoral brain edema with respect to different forms of treatment (dexamethasone, furosemide, and their combination with different dosages and different periods of treatment). 1. The neurological deficit evaluated by frequency distribution analysis showed an improvement in nearly all cases. In a few cases the initial improvement was followed by a secondary deterioration. The various symptoms showed significant differences in regression with regard to the extent of the reduced deficit as well as the time dependence. 2. With a certain delay (compared to item 1), diminution of brain edema was detected by CT follow-up. The effect of dexamethasone and the combination with furosemide differed depending on the nature of the brain tumor. 3. Compared to the untreated patients, the water content was reduced by nearly 3% following dexamethasone treatment 4 x 4 mg for 4 to 6 days. Following dexamethasone/furosemide therapy for 4 to 6 days, it was reduced by about 4.5%. The result of long-term therapy with dexamethasone alone was similar. The sodium content changed parallel to the water content. Dexamethasone and dexamethasone/furosemide was most effective in patients with glioblastoma, where the water content decreased by nearly 6%. The data presented suggest that preoperative antiedema treatment with dexamethasone is necessary for several days or a few weeks in some cases. The period of treatment can be reduced significantly by dexamethasone/furosemide or extremely high doses of dexamethasone. On the other hand, the results of follow-up scoring of the neurological situation show that the optimal time of pretreatment must be limited with respect to the individual case. The therapeutic results presented allow inferences to be made concerning pathophysiology of the resolution of brain edema.

Brain Chemistry↗

PubMed1994

Dexamethasone down-regulation of insulin receptor substrate-1 in 3T3-L1 adipocytes.

Insulin resistance resulting from prolonged exposure of intact animals or cultured cells to glucocorticoids is often attributed to postreceptor signaling defects. To better understand the specific effects of glucocorticoids on insulin signaling, we have characterized the effect of dexamethasone on the expression of an insulin signaling intermediate, the insulin receptor substrate-1 (IRS-1) in 3T3-L1 adipocytes. Addition of dexamethasone resulted in a 40-70% decline in steady-state IRS-1 protein over 24-48 h of treatment. Dexamethasone did not significantly change the degradation rate of IRS-1 protein but decreased the net rate of amino acid incorporation into IRS-1 by 87%. Between 1 and 2.5 h of treatment with dexamethasone, actinomycin D, or both drugs given simultaneously, the concentration of IRS-1 mRNA declined with a half-life of 0.7-1.0 h. However, after 4 h of dexamethasone treatment, IRS-1 mRNA concentrations stabilized at approximately 35% of the control level. The dexamethasone-induced decline in IRS-1 protein could be prevented by simultaneous administration of the glucocorticoid antagonist mifepristone, RU38486. These results suggest that in 3T3-L1 adipocytes the loss of IRS-1 protein after dexamethasone treatment can be accounted for chiefly by inhibition of the synthesis of IRS-1 mRNA.

3T3 Cells↗

PubMed1993

[Value of dexamethasone in purulent meningitis in children. Apropos of a comparative study of 85 children].

BACKGROUND: The beneficial effect of dexamethasone plus antibiotic therapy in bacterial meningitis is still controversial. PATIENTS AND METHODS: Eighty-five children, aged 1 month to 14 years, were admitted between 1987 and 1990 for bacterial meningitis. They received the same antibiotic therapy for 10 days (7 days in meningococcal meningitis). The 44 children admitted since March 1989 were also given dexamethasone (0.15 mg/kg/6 hours for 4 days); the first injection was given before antibiotic therapy. Clinical (fever, neurological findings, audition) and laboratory data [CSF proteins, glucose, lactate, cell and bacterial counts; blood C-reactive protein (CRP), hemoglobin, leukocytes and platelets] were analyzed statistically. RESULTS: The group treated with antibiotics plus dexamethasone showed decreases significantly greater in CSF protein and lactate levels after 48 hours than the children given antibiotics alone and an early (6 hours after the start of treatment) increase in CSF glucose. The blood CRP level of the dexamethasone plus antibiotics group decreased significantly within 48 hours. The numbers of neurological sequelae and deaths in this group were clearly lower than for the antibiotic group, but the risk of deafness did not appear to be altered. CONCLUSIONS: These results confirm the beneficial effect of dexamethasone reported earlier. The relatively frequent transient recurrences of fever and increased CRP when dexamethasone was interrupted suggest that the dose and/or duration of dexamethasone treatment should be modified.

Adolescent↗

PubMed1996

Use of enzyme-linked immunosorbent assay and radioimmunoassay to determine serum and urine dexamethasone concentrations in thoroughbreds after intravenous administration of the steroid.

OBJECTIVE: To develop a simple and sensitive ELISA for detection of dexamethasone in horse serum and urine. SAMPLE POPULATION: Blood and urine samples from 3 thoroughbred mares. PROCEDURE: A dexamethasone oxime was prepared and conjugated to hemocyanin, bovine serum albumin and to horseradish peroxidase. One- and two-step double-antibody ELISA methods, as well as a radioimmunoassay method, were performed. The one-step ELISA was used to test urine from 3 Thoroughbred mares injected with 5 mg of dexamethasone, IV. RESULTS: The ELISA could detect dexamethasone in the range of 0.01 to 50 ng/ml, with intra- and interassay variations of 8.92 and 9.42%, respectively. Serum dexamethasone concentration reached a peak of 20 to 35 ng/ml 15 minutes after steroid administration and decreased to 1 ng/ml in 2.5 hours. Urine dexamethasone concentration 18 to 50 ng/ml 1 to 2 hours after drug administration and decreased to 1 ng/ml at 10 hours. CONCLUSION: The developed assay is sensitive as well as simple for detecting dexamethasone in horse serum and urine, and is comparable to radioimmunoassay. CLINICAL RELEVANCE: This method can be useful for screening samples from racehorses, because it is sensitive and does not require sample preparation or sophisticated equipment.

Animals↗

PubMed1996

Dexamethasone inhibits the early steps of antigen receptor signaling in activated T lymphocytes.

Glucocorticoids are very effective in inhibiting inflammatory and immune responses. In particular, the synthetic analogue dexamethasone has been shown to inhibit T cell proliferation and IL-2 production by interfering with the transcriptional activation of the IL-2 gene. The experiments described in this report were performed to determine whether dexamethasone treatment affects the early steps of TCR signal transduction in T cell hybrids. Incubation of murine T cell hybrids in the presence of dexamethasone prevents the intracellular calcium increase that normally follows TCR/CD3 aggregation. Accordingly, dexamethasone treatment decreases inositol phosphates production and phospholipase-Cgamma1 tyrosine phosphorylation induced after TCR/CD3 stimulation. Dexamethasone has no effect on cell surface expression of TCR-associated structures nor does it inhibit calcium responses induced by a heterologous G protein-coupled muscarinic receptor, suggesting that this hormone analogue specifically inhibits the TCR signaling pathway at a postreceptor stage. We also show that inhibition of membrane proximal events by dexamethasone requires binding to the intracellular glucocorticoid receptor and de novo protein synthesis. When splenic T cells were assayed, only activated but not resting T cells were found to be sensitive to this new immunomodulatory effect of dexamethasone. These findings indicate that in addition to their previously described inhibitory effects on cytokine gene transcription, glucocorticoids block IL-2 production in activated T cells by interfering with an early step of the signal transduction cascade initiated by TCR/CD3 cross-linking.

Animals↗