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PubMed2001

Antenatal dexamethasone and decreased birth weight.

OBJECTIVE: To test the hypothesis that antenatal dexamethasone treatment to promote fetal lung maturation results in decreased birth weight corrected for gestational age. METHODS: The birth weights of all dexamethasone-treated, singleton, live-born infants delivered at our hospital were compared with our overall obstetric population; a group of untreated infants frequency matched approximately 3:1 according to maternal race, infant sex, and gestational age at delivery; and an historical cohort of infants with an indication for dexamethasone but delivered in the 12 months before the introduction of corticosteroid therapy at our hospital. RESULTS: Dexamethasone-treated infants (n = 961), when compared with either the overall population (n = 122,629) or matched controls (n = 2808), had significantly lower birth weights after adjustment for week of gestation (P <.001). Compared with the historical cohort of infants, the average birth weight of dexamethasone-treated infants was smaller by 12 g at 24-26 weeks, 63 g at 27-29 weeks, 161 g at 30-32 weeks, and 80 g at 33-34 weeks' gestation. CONCLUSION: Antenatal dexamethasone administered to promote fetal maturation is associated with diminished birth weight.

Birth Weight↗
PubMed1986

The corticotropin-releasing-hormone test versus the high-dose dexamethasone test in the differential diagnosis of Cushing's syndrome.

The diagnostic accuracy of the corticotropin-releasing-hormone (CRH) test was compared with that of the oral high-dose dexamethasone suppression test in the differential diagnosis of Cushing's syndrome. A false-negative response to CRH was present in 9% (2 of 22) of patients with pituitary-dependent Cushing's disease and to high-dose dexamethasone in 11% (2 of 18). All 3 patients with Cushing's syndrome due to an adrenal adenoma were unresponsive to both CRH and dexamethasone. The only patient with ectopic corticotropin secretion had a false-positive response of corticotropin to dexamethasone and no response of corticotropin to CRH. Simultaneous failure of both tests to indicate the cause of Cushing's syndrome did not occur in this series, except in 1 patient with Cushing's disease and overt macronodular hyperplasia. It is concluded that the diagnostic accuracy of the CRH test in patients with Cushing's syndrome is comparable to that of the high-dose dexamethasone test and that the highest discriminatory score in the differential diagnosis of Cushing's syndrome is achieved by using both a CRH test and a high-dose dexamethasone test.

17-Hydroxycorticosteroids↗
PubMed1996

Dexamethasone in bronchiolitis: a randomised controlled trial.

BACKGROUND: Although corticosteroids are commonly prescribed in the treatment of bronchiolitis, there is no evidence on the efficacy of these drugs in this disorder. We designed a randomised, double-blind, prospective study to assess the efficacy of dexamethasone in infants with bronchiolitis who require hospital management. METHODS: Infants younger than 12 months who had been admitted to hospital for an initial episode of wheezing, were randomly allocated intramuscular dexamethasone (1 mg/kg daily) or placebo, every 24 h for three doses. We excluded infants who were younger than 4 weeks, who required admission to the intensive care unit, or who had a history of congenital heart disease, mechanical ventilation, or supplemental oxygen use. We assessed infants on admission and every 12 h thereafter--vital signs were taken, severity of accessory muscle use and wheezing were measured by a clinical severity score, and pulse oximetry in room air was done. Our primary endpoints were the time to resolution of symptoms--defined as the number of assessments needed to reach oxygen saturation of more than 95% while receiving no supplemental oxygen, an accessory muscle score of 0, a wheeze score of 0 or 1, and resumption of normal feeding--and duration of oxygen therapy. Follow-up assessments were made 10-14 days after discharge by telephone. We used a proportional-hazards model for our survival analysis. FINDINGS: 197 infants presented with bronchiolitis that required inpatient management. 75 were not enrolled (31 no consent, 28 no approach made, 16 transferred elsewhere). Of the 122 enrolled, four were excluded (clinical deterioration, diagnosis of cystic fibrosis, previous intubation, did not receive all study treatment). There were no differences between the dexamethasone (n = 65) and placebo-treated infants in demographic factors, exposure to tobacco smoke, duration of illness, presence of respiratory syncytial virus (RSV) antigen, respiratory rate, or severity score. More dexamethasone-treated patients had an initial oxygen saturation of 95% or less (51 [79%] dexamethasone vs 31 [59%] placebo, p = 0.02). There were no differences in duration of oxygen therapy (p = 0.74) or time to resolution of symptoms (p = 0.22). Stratification for presence of RSV antigen or family history of atopy did not affect the results. INTERPRETATION: Our findings do not support the use of dexamethasone in the treatment of bronchiolitis in infants.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2000

Efficacy of diclofenac versus dexamethasone for treatment after strabismus surgery.

OBJECTIVE: To compare the efficacy of topical diclofenac sodium 0.1% versus dexamethasone 0.1% on the conjunctival healing process and on intraocular pressure (IOP) after strabismus surgery. DESIGN: A randomized clinical trial. PARTICIPANTS: Forty consecutive pediatric patients who underwent strabismus surgery. INTERVENTION: The patients were assigned before surgery to receive topical diclofenac 0.1% (study group, 20 patients) or dexamethasone 0.1% (control group, 20 patients) from immediately after surgery to up to 4 weeks after surgery (both combined with chloramphenicol 0.2%, polymyxin B sulfate 2500 U). MAIN OUTCOME MEASURES: Between-group comparison of five parameters: patient discomfort, conjunctival chemosis, inflammation, gap, and intraocular pressure (IOP) at 1, 2, and 4 weeks after surgery. RESULTS: At postoperative week 2, the diclofenac-treated group showed significantly less patient discomfort and less conjunctival inflammation, edema, and gap than the dexamethasone group (P: = 0.003, P: = 0.04, P: = 0.02, P: = 0. 001, respectively). At week 4, the study patients continued to show less discomfort and conjunctival gap (P: = 0.02). The dexamethasone group showed a significant change in IOP between the preoperative and the fourth postoperative week (P: = 0.001 in the right eye, P: = 0.0005 in the left eye) and an increased prevalence of higher IOP during the fourth postoperative week (P: = 0.01 in the right eye, P: = 0.02 in the left eye). Thirty-eight percent of the dexamethasone group showed an increase in IOP to more than 21 mmHg during the four postoperative weeks. No increase in IOP was noted in the diclofenac group. CONCLUSIONS: Topical diclofenac is superior to dexamethasone for each of the five postoperative parameters examined. Its maximal effect occurred at 2 weeks after surgery, without an increase in IOP or in local subconjunctival hemorrhage.

Adolescent↗
PubMed1998

Differential regulation by thalidomide and dexamethasone of cytokine expression in human peripheral blood mononuclear cells.

Immunosuppressive drugs are used routinely to reduce the inappropriate production of cytokines in an immune response. Recent attention has focused on drugs that selectively inhibit specific cytokines. Both thalidomide and dexamethasone have been reported to exhibit immunomodulatory effects on cytokines in vitro. We wished to examine the effects of thalidomide and dexamethasone on the production of cytokines by peripheral blood mononuclear cells (PBMC), following mitogenic stimulation, at the level of both secreted product and mRNA production. PBMC from healthy human volunteers were stimulated optimally with phytohaemagglutinin (PHA) in the presence of varying concentrations of thalidomide and dexamethasone using dimethyl sulphoxide (DMSO) as the solvent. Analysis of supernatants by enzyme-linked immunosorbent assay (ELISA) showed that thalidomide caused a dose-dependent inhibition of the pro-inflammatory cytokines interleukin 6 (IL-6) and tumour necrosis factor alpha (TNF-alpha), maximally reducing production by 20 (P < 0.05) and 30% (P < 0.01), respectively, compared with controls. However, thalidomide did not affect either proliferation or the production of interleukin 2 (IL-2), interleukin 4 (IL-4) or interleukin 10 (IL-10). A slight bell shaped inhibition of interferon gamma (IFN-gamma) was seen which was statistically significant (P < 0.05). In contrast, dexamethasone inhibited markedly the expression of all cytokines tested (IL-2, IL-4, IL-6, IL-10, IFN-gamma and TNF-alpha) in dose-dependent fashion, reducing levels to near to background. Reverse transcription-polymerase chain reaction (RT-PCR) analyses showed that thalidomide inhibited selectively the expression of TNF-alpha and IL-6 mRNA, whereas dexamethasone inhibited mRNA levels of all cytokines examined. The data indicate that dexamethasone is a broad range immunosuppressant inhibiting all cytokines tested in a dose-dependent manner at the level of both secreted product and mRNA. Conversely, thalidomide selectively inhibits the production of IL-6 and TNF-alpha. Due to their markedly different effects on cytokine production, and the fact that both drugs act at the level of transcription, we believe they influence separate pathways involved in cytokine gene regulation.

Anti-Inflammatory Agents↗
PubMed2002

Dexamethasone prevents long-lasting learning impairment following neonatal hypoxic-ischemic brain insult in rats.

We examined for 18 weeks the effect of dexamethasone treatment on learning and memory impairment produced by hypoxic-ischemic stress at postnatal day 7 in rat in addition to brain histological study. Dexamethasone of 0.5 mg/kg was injected i.p. 4 h before hypoxic-ischemic stress, in which the left carotid artery was ligated followed by 2 h hypoxia (8% oxygen). Dexamethasone treatment improved behavior in each learning task: in choice reaction time tasks relating to the attention process, in 8-arm radial maze task examining working and reference memory, and in water maze task relating to reference memory. Improvement to the extent of the sham-control level was observed. Dexamethasone treatment also completely prevented histological brain damage. No adverse effect in learning and memory tests was observed in the animals treated with dexamethasone without hypoxic-ischemic stress. It is concluded that dexamethasone treatment is significantly effective in prevention not only of histological brain damage but also of learning and memory impairment occasioned by subsequent hypoxic-ischemic insult, warranting further clinical investigation.

Animals↗
PubMed2000

Thymosin alpha1 is a time and dose-dependent antagonist of dexamethasone-induced apoptosis of murine thymocytes in vitro.

It is well established that glucocorticoid hormones induce apoptosis in immature developing thymocytes. Thymocyte apoptosis can be modulated by growth factors, anti-oxidants and adhesion receptors. We have previously demonstrated that thymosin alpha1 (Talpha1) antagonizes dexamethasone-induced apoptosis of CD4+CD8+ thymocytes. In the present study, we further characterize the dose and time dependence of Talpha1's antagonism of dexamethasone-induced thymocyte apoptosis. Talpha1 is effective at concentrations ranging from 2 to 100 microg/10(6) thymocytes. Talpha1 pre-treatment is necessary to achieve its anti-apoptotic activity. Talpha1 provides temporary protection to thymocytes by slowing dexamethasone's apoptotic activity up to 12 h post dexamethasone treatment. Additionally, Talpha1's activity is not sensitive to cycloheximide treatment, suggesting Talpha1's activity is independent of protein synthesis. Finally, Talpha1 is unable to antagonize apoptosis induced by the reactive oxygen species, H2O2, suggesting Talpha1's antagonism of dexamethasone occurs at the early stages of dexamethasone-induced apoptosis, prior to the production of reactive oxygen species. This evidence suggests that Talpha1 may provide a mechanism to transiently extend the life of a thymocyte during thymic selection.

Adjuvants, Immunologic↗
PubMed1993

Dexamethasone as adjuvant therapy for severe acute pharyngitis.

STUDY OBJECTIVE: To determine the efficacy of dexamethasone as adjuvant therapy to improve pain relief in patients with severe, acute exudative pharyngitis. DESIGN: Prospective, randomized, double-blinded, placebo-controlled clinical trial. SETTING: Large, urban community hospital emergency department with an emergency medicine residency program. TYPE OF PARTICIPANTS: Patients aged 12 to 65 years old with exudative pharyngitis and severe dysphagia/odynophagia. Patients with cancer, AIDS, diabetes mellitus, recent steroid use, pregnancy, or suspicion of peritonsillar abscess were excluded. INTERVENTIONS: All patients received oral penicillin (500 mg Pen VK) or erythromycin (333 mg base) three times daily for ten days in addition to either 10 mg single-dose dexamethasone or saline placebo IM injection. MEASUREMENTS AND RESULTS: Fifty-eight patients graded their initial degree of throat pain on a visual-analog scale that was 15 cm long and scored from 0 to 3.0 in 0.5-cm increments. Follow-up was obtained on 51 patients to determine their condition at 24 hours. At entry, there was no difference in age, weight, antibiotic assignment, or initial pain score between groups. Improvement in pain score (initial versus 24 hours) was 1.8 +/- 0.8 in the 26 patients of the dexamethasone group and 1.2 +/- 0.9 in the 25 patients of the placebo group (P < .05). Time to onset of pain relief was also faster in steroid-treated patients who demonstrated relief beginning at 6.3 +/- 5.3 hours, compared with 12.4 +/- 8.5 hours in the placebo group (P < .01). Of the 26 patients evaluated at seven days (13 in each group), time to complete lack of pain averaged 15.0 +/- 11.4 hours in the dexamethasone group and 35.4 +/- 17.9 hours in the placebo group (P < .02). Complications attributable to dexamethasone were not observed. CONCLUSION: In patients with severe, acute exudative pharyngitis, single-injection dexamethasone adjuvant compared with placebo resulted in statistically and clinically significant improvement, as evidenced by more rapid onset and greater degree of pain relief.

Acute Disease↗
PubMed2001

The effect of betamethasone versus dexamethasone on fetal biophysical parameters.

BACKGROUND: Clinical observations suggest that betamethasone reduces maternal perception of fetal movements and short term variability, but that this dose not occur after treatment with dexamethasone. OBJECTIVES: To compare the effect of betamethasone and dexamethasone on fetal biophysical parameters. METHODS: In a randomized, prospective, double blind study, 20 courses of betamethasone and 20 courses of dexamethasone were given in random sequence to patients with imminent preterm labor. During the first 32h after initiation of treatment, fetal movements were counted by the mothers and recorded by ultrasound, and a nonstress test was performed. RESULTS: Betamethasone induced a significant decrease in fetal movements as perceived by the mother and observed by ultrasound. Fetal breathing movements also decreased. Dexamethasone did not change fetal body movements. Neither drug changed the short term variability. CONCLUSIONS: Unlike betamethasone, dexamethasone does not induce a decrease in fetal movements. Dexamethasone might, therefore, be preferred for enhancement of lung maturation in imminent preterm labor.

Adult↗
PubMed2001

Immunoconversion against Sarcocystis neurona in normal and dexamethasone-treated horses challenged with S. neurona sporocysts.

Equine protozoal myeloencephalitis is a common neurologic disease of horses in the Americas usually caused by Sarcocystis neurona. To date, the disease has not been induced in horses using characterized sporocysts from Didelphis virginiana, the definitive host. S. neurona sporocysts from 15 naturally infected opossums were fed to horses seronegative for antibodies against S. neurona. Eight horses were given 5x10(5) sporocysts daily for 7 days. Horses were examined for abnormal clinical signs, and blood and cerebrospinal fluid were harvested at intervals for 90 days after the first day of challenge and analyzed both qualitatively (western blot) and quantitatively (anti-17kDa) for anti-S. neurona IgG. Four of the challenged horses were given dexamethasone (0.1mg/kg orally once daily) for the duration of the experiment. All challenged horses immunoconverted against S. neurona in blood within 32 days of challenge and in CSF within 61 days. There was a trend (P = 0.057) for horses given dexamethasone to immunoconvert earlier than horses that were not immunosuppressed. Anti-17kDa was detected in the CSF of all challenged horses by day 61. This response was statistically greater at day 32 in horses given dexamethasone. Control horses remained seronegative throughout the period in which all challenged horses converted. One control horse immunoconverted in blood at day 75 and in CSF at day 89. Signs of neurologic disease were mild to equivocal in challenged horses. Horses given dexamethasone had more severe signs of limb weakness than did horses not given dexamethasone; however, we could not determine whether these signs were due to spinal cord disease or to effects of systemic illness. At necropsy, mild-moderate multifocal gliosis and neurophagia were found histologically in the spinal cords of 7/8 challenged horses. No organisms were seen either in routinely processed sections or by immunohistochemistry. Although neurologic disease comparable to naturally occurring equine protozoal myeloencephalitis (EPM) was not produced, we had clear evidence of an immune response to challenge both systemically and in the CNS. Broad immunosuppression with dexamethasone did not increase the severity of histologic changes in the CNS of challenged horses. Future work must focus on defining the factors that govern progression of inapparent S. neurona infection to EPM.

Animals↗
PubMed1999

Dexamethasone selectively suppresses microglial trophic responses to hippocampal deafferentation.

Hippocampal deafferentation increases the expression of insulin-like growth factor-1 by microglia, and of ciliary neurotrophic factor and basic fibroblast growth factor by astroglia in fields and periods of reactive axonal growth. Glucocorticoids attenuate lesion-induced hippocampal sprouting, possibly by reducing trophic signals that stimulate growth. With an interest in this hypothesis, the present studies evaluated the influence of systemic treatment with the synthetic glucocorticoid dexamethasone on entorhinal lesion-induced increases in neurotrophic factor expression in young adult rat hippocampus. Daily dexamethasone injections almost completely blocked increases in insulin-like growth factor-1 messenger RNA content, but did not perturb increases in ciliary neurotrophic factor or basic fibroblast growth factor messenger RNA content, in the deafferented dentate gyrus molecular layer. To determine if the suppression of insulin-like growth factor-1 expression was secondary to a general inhibition of microglial responses, and to identify the time period of glucocorticoid sensitivity, additional rats were prepared to evaluate the effects of semi-chronic (i.e. daily) and single dexamethasone injections on microglial proliferation, ED-1 immunoreactivity (a marker of microglial reactivity) and insulin-like growth factor-1 messenger RNA expression. Semi-chronic dexamethasone treatment attenuated all three measures of deafferentation-induced microglial reactivity. However, a single dexamethasone injection given two (but not one or three) days postlesion inhibited deafferentation-induced increases in insulin-like growth factor-1 messenger RNA content, without having significant effects on other measures. These results demonstrate that dexamethasone treatment preferentially suppresses microglial, as opposed to astroglial, trophic responses to deafferentation, and suggest that glucocorticoids attenuate reactive axonal sprouting by inhibiting the microglial production of insulin-like growth factor-1.

Animals↗
PubMed1998

Differential effects of hydrocortisone and dexamethasone on cortisol suppression in a child psychiatric population.

The suppressive effect of hydrocortisone and dexamethasone on salivary cortisol was investigated in a 2-year study of pituitary-adrenal function in a variety of child psychiatric patients and healthy controls. Symptomatology was assessed using the Child Behavioral Checklist (CBCL). Cortisol day profiles were assessed at 2-h intervals from 0800 to 2000 h on three occasions. Dexamethasone and hydrocortisone were administered orally twice at 2000 h, the doses being adjusted for bodyweight according to the standard dexamethasone suppression test. Fifty-one patients, including patients with dysthymia, oppositional defiant disorder, pervasive developmental disorder, and attention deficit hyperactivity disorder, and ten age and sex matched controls participated. Basal cortisol levels in patients were generally lower than in controls. Both dexamethasone and hydrocortisone were effective in suppressing salivary cortisol, although dexamethasone was somewhat more potent and its effect lasted longer. Hyporesponsiveness to hydrocortisone, but not to dexamethasone, distinguished patients with dysthymia and oppositional defiant disorder from controls. Responsiveness to hydrocortisone was correlated with the symptom clusters social problems and anxious/depressed. The data support the idea that there exist syndrome aspecific disturbances in feedback activity beyond the level of the pituitary, i.e. at the hypothalamic level, at an early age. From this perspective, hydrocortisone suppression is a useful tool for studying pituitary-adrenal function in children. Behavioral correlates of these disturbances of pituitary-adrenal function should be determined.

Arousal↗
PubMed2001

Effect of adrenalectomy and dexamethasone treatment on prolactin secretion of lactating rats.

The contribution of corticosteroids to the control of prolactin secretion in lactating rats was investigated. The prolactin response to domperidone (20 microg/kg b.w., i.v.), a dopamine receptor antagonist and to domperidone plus formalin stress was tested in adrenalectomized and/or dexamethasone-treated continuously nursing rats. Animals were adrenalectomized on the 3rd day of lactation and tested on the 7th day of lactation. Dexamethasone was injected s.c. 24 h before testing (400 microg/kg b.w.) and on the day of testing (200 microg/kg b.w.). Domperidone caused a significant rise in plasma prolactin levels. The prolactin response to domperidone was twice as high in solely adrenalectomized dams and in solely dexamethasone-treated rats compared to controls. In adrenalectomized animals treated with dexamethasone, the prolactin response to domperidone was like in controls. Formalin injection to either adrenalectomized plus domperidone-treated animals or to animals injected with dexamethasone plus domperidone, resulted in a statistically significant depletion of plasma prolactin. In controls and in adrenalectomized animals receiving dexamethasone and domperidone, the prolactin response to formalin was very similar, i.e., plasma prolactin levels did not change after the administration of formalin. The present findings suggest that in lactating rats, corticosteroids are involved in the prolactin response to domperidone and to formalin stress.

Adrenalectomy↗
PubMed1997

Longitudinal assessment of growth and bone mineral accretion in prematurely born infants treated for chronic lung disease with dexamethasone.

The objective of this study in premature infants was to assess the relationship between dexamethasone, growth and bone mineral accretion. Nine appropriate size for gestational age premature infants treated for chronic lung disease with tapering doses of dexamethasone (0.5-0.1 mg/kg/day over 37 +/- 7 days) were individually matched to a comparison infant by sex, gestational age, birth-weight, and type of feed. Infant growth and bone mineral accretion were measured at equivalent gestational ages from recruitment until 6 months corrected age. During hospitalization, mean rate of weight, length and head circumference growth and bone mineral accretion in the distal radius were significantly lower in the dexamethasone-treated infants in spite of similar nutrient intakes. Dexamethasone infants had significantly lower plasma phosphorus, and urinary calcium, pyridinoline and N-telopeptide excretion. Dexamethasone affected absolute length, but not weight, throughout the study. No significant differences were observed in body composition or absolute radial and whole body bone mineral content. The results indicate that dexamethasone therapy compromises growth and bone mineral accretion in small premature infants. 'Catch-up' linear growth was not evident at 6 months of age and reflects the importance of early nutrition interventions.

Amino Acids↗
PubMed2003

Transcriptional induction of connective tissue growth factor/hypertrophic chondrocyte-specific 24 gene by dexamethasone in human chondrocytic cells.

Connective tissue growth factor (CTGF/Hcs24) is a critical growth factor for chondrocytic growth and differentiation. In this report, we describe for the first time glucocorticoid-mediated induction of the CTGF/Hcs24 gene in a chondrocytic cell line, HCS-2/8. Steady-state mRNA levels of CTGF/Hcs24 were remarkably increased after treatment with 50 nM dexamethasone, as confirmed by Northern blotting and quantitative real-time polymerase chain reaction (PCR) analysis. Corresponding to the increase in mRNA, production of CTGF/Hcs24 protein was remarkably enhanced, following a time course of up to 6 h. The observed increase in mRNA can be ascribed to transcriptional enhancement, since the stability of CTGF/Hcs24 mRNA was not affected by the same concentration of dexamethasone, which was indicated by the results of an mRNA degradation assay. However, unexpectedly, the prototypic ctgf/hcs24 promoter was not responsible for the dexamethasone stimulation, suggesting the glucocorticoid receptor binding site(s) to be elsewhere in the CTGF/Hcs24 gene. Enhancement of the prototypic promoter activity by dexamethasone was observed in murine fibroblastic cells, demonstrating the complexity of the regulatory mechanism of ctgf/hcs24 gene expression. Of importance, dexamethasone at the same concentration significantly stimulated proteoglycan synthesis in HCS-2/8 cells up to the same levels as exogenously added CTGF/Hcs24. These findings represent a novel effect of glucocorticoid on the production of CTGF/Hcs24 by chondrocytic cells, and indicate that CTGF/Hcs24 may mediate the stimulative effect of dexamethasone on chondrocytic phenotypes. Also, our results shed light on the complex mechanism of CTGF/Hcs24 induction by glucocorticoids.

3' Untranslated Regions↗
PubMed1998

The dexamethasone suppression test in schizophrenia.

BACKGROUND: Cortisol non-suppression following the dexamethasone suppression test (DST) has been found to a variable extent in schizophrenia. The aetiology is unclear but may be related to depression or negative symptoms. METHODS: The DST was administered to 64 patients with DSM-IV schizophrenia. All patients were screened for DSM-IV major depression and rated on the Hamilton Rating Scale for Depression (HRSD), Scale for Assessment of Negative Symptoms (SANS) and the Brief Psychiatric Rating Scale (BPRS). RESULTS: DSM-IV criteria for major depression was fulfilled by 36% of the patients and 42% of patients had a history of parasuicide. Four patients had undetectable levels of dexamethasone and were excluded from the endocrine analyses. Only one remaining patient had a cortisol level above the cut-off point (> 138 nmol/l), indicating escape from dexamethasone suppression. The post-dexamethasone cortisol level correlated significantly with HRSD and BPRS scores but not with the SANS. The SANS and HRSD scores were not correlated, but they were independently correlated with the BPRS score. CONCLUSIONS: In contrast to some other work, rates of dexamethasone non-suppression were very low; together with the high rates of depression, this suggests that depression in schizophrenia may have a different neuroendocrine profile from major depressive disorders. Failure to measure dexamethasone levels can be misleading.

Adult↗
PubMed1990

The dexamethasone suppression test in Alzheimer's disease and major depression: relationship to dementia severity, depression, and CSF monoamines.

Patients with Alzheimer's disease (AD) have been reported to have a rate of nonsuppression on the dexamethasone suppression test (DST) comparable to that of patients with major depression. With symptoms of depression being increasingly recognized in patients with AD, studying their DST response may provide clues to the etiology of the abnormal response in both diagnostic groups. A correlation between dementia severity and post-dexamethasone cortisol was found within the group of male, but not female AD patients. Within the group of elderly depressives, a correlation between post-dexamethasone cortisol and ratings of depression was found. Serum dexamethasone levels were not significantly lower in the nonsuppressors as compared with suppressors in either diagnostic group. Within the AD group, dexamethasone levels themselves correlated significantly with ratings of dementia severity and with the Wechsler Memory Scale score. Cerebrospinal fluid (CSF) 3-methoxy-4-hydroxyphenylglycol (MHPG) correlated positively with 4:00 pm post-dexamethasone cortisol level and with ratings of dementia severity in the AD patients. Findings are discussed in light of the known clinical and other biological similarities between AD and major depression, followed by a review of theories regarding the etiology of the hypothalamic-pituitary-adrenal abnormalities in these two illnesses.

Aged↗
PubMed2006

Intravenous dexamethasone to prevent the recurrence of benign headache after discharge from the emergency department: a randomized, double-blind, placebo-controlled clinical trial.

OBJECTIVE: To evaluate whether the addition of intravenous (i.v.) dexamethasone to standard emergency department (ED) benign headache therapy would reduce the incidence of headache recurrence at 48-72 hours. METHODS: This randomized, double-blind, placebo-controlled clinical trial of adult patients presenting with the chief complaint of headache was conducted in the ED of 2 academic, urban Level 1 hospitals. Headache evaluation and therapy were determined by the treating physician, and, before discharge, patients were administered either 10 mg of IV dexamethasone or placebo. The treatment groups had similar baseline characteristics, abortive therapy, IV fluids and degree of pain relief achieved before discharge. Patients were contacted 48-72 hours following discharge and asked whether their headache was "better," "worse" or "remained unchanged" when compared with their symptoms at discharge. Those whose headaches were "worse" or "unchanged," and those who reported a return of headache after being pain free at discharge were considered to be treatment failures and classified as having had a recurrence. The patient's headache at follow-up was further categorized as severe (i.e., provoking another physician visit or interfering with daily activity) or mild (i.e., requiring self-medication or no treatment). RESULTS: Fifty-seven patients met the inclusion criteria and 2 were lost to follow-up, leaving 55 for analysis. At follow-up, 9.7% (3/31) of those receiving dexamethasone had headache recurrence, versus 58.3% (14/24) of those receiving placebo (p < 0.001). Four dexamethasone recipients (12.9%) had severe headaches at follow-up compared with 8 (33.3%) in the placebo group (p = 0.14). CONCLUSIONS: In this study, IV dexamethasone reduced headache recurrence at 48-72-hour follow-up. Given its excellent safety profile and likely benefit, IV dexamethasone should be considered for ED headache patients after standard evaluation and therapy.

Adult↗