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Intratympanic dexamethasone injection effects on transient-evoked otoacoustic emission.

PURPOSE: To investigate the effects of intratympanic dexamethasone injection, which is done because of tinnitus, on transient evoked otoacoustic emission (TEOAE) and so determine whether given dexamethasone cause any damage in the inner ear. PATIENTS AND METHODS: Twenty-six patients, aged between 32 and 75, with subjective tinnitus, were randomly selected. The selected patients were the ones whose improvement had not been achieved through minimum 6 months' medical therapy (eg, Ginkgo biloba extract EGb 761, betahistidine, and trimetazidin) and who were free of systemic or otolaryngologic disease (hypertension, diabetes mellitus, hypo/hypertyroidi, hypercholesterolemia, Meniere disease, and otosclerosis). Before and after the injections, audiometry including high-frequency tinnitus matching and TEOAE tests were done. The injections of 4 mg/mL dexamethasone were done 5 times in fixed protocols on days 0, 2, 4, 6, and 8. After each injection, the patients were kept supine for 60 minutes with the head turned 45 degrees to opposite ear. Paired t test was used to compare the beginning and final measurements. RESULTS: Temporary pain and vertigo attacks which lasted at most for 15 minutes occurred in some patients only during injections. Neither infection nor persistent perforation occurred in any patients. After the management, there was no significant difference on patient's pure tone averages ( P = .067) and high-frequency averages ( P = .592). When the obtained TEOAE results before and after management were compared, the only significant increase was detected in the reproducibility values ( P = .042). There was no significant difference in other TEOAE parameters which are stimulus stability, stimulus intensity, and overall signal-to-noise ratio ( P > .05). There is no fixed criteria for rejecting a response solely on the reproducibility. However, a high value of the reproducibility (or increase in reproducibility) is always meaningful. CONCLUSION: Intratympanic dexamethasone used for management in many indications, primarily in Meniere and tinnitus patients, was found to increase the reproducibility values of otoacoustic emission. Despite the fact that there was not a reasonable increase in the responses coming from the outer hair cells, the result was considered positive for the study as the responses did not decrease. It is found out that 4 mg/mL dexamethasone given intratympanically does not adversely affect the outer hair cell function as measured by otoacoustic emission. Within the limits of this study, dexamethasone appears to be safe when given intratympanically.

Adult↗
PubMed2006

Dexamethasone facilitates erythropoiesis in murine embryonic stem cells differentiating into hematopoietic cells in vitro.

Differentiating embryonic stem (ES) cells are increasingly emerging as an important source of hematopoietic progenitors with a potential to be useful for both basic and clinical research applications. It has been suggested that dexamethasone facilitates differentiation of ES cells towards erythrocytes but the mechanism responsible for sequential expression of genes regulating this process are not well-understood. Therefore, we in vitro induced differentiation of murine ES cells towards erythropoiesis and studied the sequential expression of a set of genes during the process. We hypothesized that dexamethasone-activates its cognate nuclear receptors inducing up-regulation of erythropoietic genes such as GATA-1, Flk-1, Epo-R, and direct ES cells towards erythropoietic differentiation. ES cells were cultured in primary hematopoietic differentiation media containing methyl-cellulose, IMDM, IL-3, IL-6, and SCF to promote embryoid body (EB) formation. Total RNA of day 3, 5, and 9-old EBs was isolated for gene expression studies using RT-PCR. Cells from day 9 EBs were subjected to secondary differentiation using three different cytokines and growth factors combinations: (1) SCF, EPO, dexamethasone, and IGF; (2) SCF, IL-3, IL-6, and TPO; and, (3) SCF IL-3, IL-6, TPO, and EPO. Total RNA from day 12 of secondary differentiated ES cells was isolated to study the gene expression pattern during this process. Our results demonstrate an up-regulation of GATA-1, Flk-1, HoxB-4, Epo-R, and globin genes (alpha-globin, betaH-1 globin, beta-major globin, epsilon -globin, and zeta-globin) in the 9-day-old EBs, whereas, RNA from 5-day-old EBs showed expression of HoxB-4, epsilon-globin, gamma-globin, betaH1-globin, and Flk-1. Three-day-old EBs showed only HoxB-4 and Flk-1 gene expression and lacked expression of all globin genes. These findings indicate that erythropoiesis-specific genes are activated later in the course of differentiation. Gene expression studies on the ES cells of secondary EB origin cultured in media containing dexamethasone showed a down-regulation of GATA-3 and an up-regulation of GATA-1, Flk-1, and Epo-R in comparison to the two other cytokines and growth factor combinations containing media. The secondary differentiation also showed an enhanced production of erythrocytic precursors in dexamethasone containing media in comparison to that in the control media. Our results indicate that dexamethasone can prove to be an effective agent which can be employed to enhance differentiation towards erythrocytic progenitors from ES cells.

Animals↗
PubMed2005

Insulin-like growth factor-I inhibits dexamethasone-induced proteolysis in cultured L6 myotubes through PI3K/Akt/GSK-3beta and PI3K/Akt/mTOR-dependent mechanisms.

We and others reported previously that IGF-I inhibits dexamethasone-induced proteolysis in cultured L6 myotubes. Recent evidence suggests that this effect of IGF-I at least in part reflects PI3K/Akt-mediated inhibition of Foxo transcription factors. The potential role of other mechanisms, downstream of PI3K/Akt, is not well understood. Here we tested the hypothesis that PI3K/Akt-mediated inactivation of GSK-3beta and activation of mTOR contribute to the anabolic effects of IGF-I in dexamethasone-treated myotubes. Cultured L6 myotubes were treated with 1 microM dexamethasone in the absence or presence of 0.1 microg/ml of IGF-I and inhibitors of GSK-3beta and mTOR. Protein degradation was measured by determining the release of trichloroacetic acid soluble radioactivity from myotubes that had been prelabeled with (3)H-tyrosine for 48 h. IGF-I reduced basal protein breakdown rates and completely abolished the dexamethasone-induced increase in myotube proteolysis. These effects of IGF-I were associated with increased phosphorylation of Akt, GSK-3beta, and the mTOR downstream targets p70(S6K) and 4E-BP1. The PI3K inhibitor LY294002 and the mTOR inhibitor rapamycin reversed the anabolic effect of IGF-I in dexamethasone-treated myotubes. In addition, the GSK-3beta inhibitors LiCl and TDZD-8 reduced protein degradation in a similar fashion as IGF-I. Our results suggest that PI3K/Akt-mediated inactivation of GSK-3beta and activation of mTOR contribute to the anabolic effects of IGF-I in dexamethasone-treated myotubes.

Animals↗
PubMed2004

Chronic antidepressant medication attenuates dexamethasone-induced neuronal death and sublethal neuronal damage in the hippocampus and striatum.

Dexamethasone, a synthetic corticosteroid, which can induce a range of mood disorders including depression and affective psychosis, is toxic to specific hippocampal and striatal neuronal populations. Chronic administration of antidepressants can induce neuroprotective effects, potentially by raising cellular levels of brain-derived neurotrophic factor (BDNF). We accordingly tested the hypothesis that chronic pretreatment of rats (Sprague-Dawley, male) with antidepressants would attenuate dexamethasone-induced neuronal damage as revealed by reductions in the level of neuronal death and in sublethal neuronal damage shown by the increase in the number of MAP-2 immunoreactive neurons. In support of this hypothesis, we demonstrate that chronic treatment with a range of antidepressants prior to dexamethasone administration (0.7 mg/kg, i.p.) attenuated the levels of neuronal death and loss of MAP-2 immunoreactivity in both the hippocampus and striatum. The antidepressants used were: desipramine (8 mg/kg, i.p., tricyclic), fluoxetine (8 mg/kg, i.p., selective serotonin reuptake inhibitor) and tranylcypromine (10 mg/kg, i.p., monoamine oxidase inhibitor) with each drug being injected once per day for 10 days. In contrast, acute injection of none of the antidepressants exerted a protective effect from dexamethasone-associated neuronal damage. Similarly, injection of neither cocaine nor chlordiazepoxide (benzodiazepine) exerted protective effects when injected either chronically or acutely. The observed protection from dexamethasone-induced neuronal damage is in keeping with the potential of chronic antidepressant medication to increase BDNF levels. The potential for dexamethasone to induce disorders of mood by damaging specific neuronal populations in the hippocampus and dorsomedial striatum is discussed.

Animals↗
PubMed2006

Roles of p38 and ERK MAP kinases in IL-8 expression in TNF-alpha- and dexamethasone-stimulated human periodontal ligament cells.

Orthodontic tooth movement is recognized as a pro-inflammatory stressor of human periodontal ligament (hPDL) cells. However, the cell-signaling pathways linking interleukin-8 (IL-8), intercellular adhesion molecule-1 (ICAM-1), pro-inflammatory cytokines, and dexamethasone in hPDL cells have not been well elucidated. In this study, we investigated the role of mitogen-activated protein (MAP) kinases in dexamethasone- and TNF-alpha-induced IL-8 and ICAM-1 expression in hPDL cells. IL-8 production was measured by enzyme-linked immunosorbent assay (ELISA) and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. MAP kinase activation and IkappaB degradation were determined by Western blot analysis, and ICAM-1 expression was determined by RT-PCR and FACS analysis. TNF-alpha increased IL-8 mRNA expression and protein secretion in a dose- and time-dependent manner. Dexamethasone suppressed TNF-alpha-induced IL-8 production in a dose-dependent manner. In addition, dexamethasone inhibited TNF-alpha-induced phosphorylation of p38 MAP kinase and extracellular-regulated kinases (ERKs), IkappaB degradation, and NF-kappaB activation. Selective inhibitors for ERKs and p38 attenuated TNF-alpha-induced IL-8 and ICAM-1 expression in the presence and absence of dexamethasone, indicating that MAP kinases play a role in the response of hDPL cells to TNF-alpha. Furthermore, these results suggest that inflammatory cytokine- and dexamethasone-induced IL-8 and ICAM-1, produced via a MAP kinase pathway, may serve as an important mediator of PDL immunoregulation involved in bone remodeling during orthodontic tooth movement.

Anti-Inflammatory Agents↗
PubMed2004

Minor neurological dysfunction, cognitive development, and somatic development at the age of 3 to 7 years after dexamethasone treatment in very-low birth-weight infants.

The objective of this study was to assess minor neurological dysfunction, cognitive development, and somatic development after dexamethasone therapy in very-low-birthweight infants. Thirty-three children after dexamethasone treatment were matched to 33 children without dexamethasone treatment. Data were assessed at the age of 3-7 years. Dexamethasone was started between the 7th and the 28th day of life over 7 days with a total dose of 2.35 mg/kg/day. Exclusion criteria were asphyxia, malformations, major surgical interventions, small for gestational age, intraventricular haemorrhage grades III and IV, periventricular leukomalacia, and severe psychomotor retardation. Each child was examined by a neuropediatrician for minor neurological dysfunctions and tested by a psychologist for cognitive development with a Kaufman Assessment Battery for Children and a Draw-a-Man Test. There were no differences in demographic data, growth, and socio-economic status between the two groups. Fine motor skills and gross motor function were significantly better in the control group (p<0.01). In the Draw-a-Man Test, the control group showed better results (p<0.001). There were no differences in development of speech, social development, and the Kaufman Assessment Battery for Children. After dexamethasone treatment, children showed a higher rate of minor neurological dysfunctions. Neurological development was affected even without neurological diagnosis. Further long-term follow-up studies will be necessary to fully evaluate the impact of dexamethasone on neurological and cognitive development.

Child↗
PubMed2004

Antiemetic effect of dexamethasone on cisplatin-induced early and delayed emesis in the pigeon.

We investigated the ability of dexamethasone to attenuate cisplatin (4 mg/kg, i.v.)-induced early and delayed emesis. These appear within the first 8-h period (early phase) and between 8 and 48 h (delayed phase), respectively, after cisplatin administration in the pigeon. Dexamethasone (0.1 and 1 mg/kg, i.m.) reduced significantly the number of emetic responses to cisplatin by 56% and 82% (P<0.05), respectively, in the early phase, and by 41% and 66% (P<0.05), respectively, in the delayed phase. Dexamethasone (1 and 10 microg/kg, i.c.v.) reduced the number of emetic responses by 66% and 91% (P<0.05), respectively, in the early phase, and by 56% and 87% (P<0.05), respectively, in the delayed phase. Indomethacin (10 mg/kg, i.m.) did not suppress cisplatin-induced early and delayed emesis. Dexamethasone (1 mg/kg, i.m.) did not affect the content of platinum in the medulla oblongata after cisplatin administration. The above results suggest that dexamethasone has antiemetic effects on both the early and delayed emetic responses to cisplatin in pigeons, partially via its central site of action, and that the antiemetic mechanism of dexamethasone is related to factors other than its inhibition of prostanoid synthesis or its membrane stabilizing effect which reduces influx of cisplatin into the medulla oblongata.

Animals↗
PubMed2004

Dexamethasone delays ulcer healing by inhibition of angiogenesis in rat stomachs.

Using the non-ulcerogenic doses of dexamethasone, we explored the action of glucocorticoids on ulcer healing and its relationship with angiogenic factors in the gastric mucosa. We applied dexamethasone (0.1 or 0.2 mg/kg/day) intragastrically in rats with acetic acid-induced gastric ulcer. The mucosal prostaglandin E(2) level and protein expressions of basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) at the ulcer margin were determined. Ulcer induction significantly increased protein expressions of bFGF, VEGF, and prostaglandin E(2) level at the ulcer margin together with angiogenesis at the ulcer margin and base. The non-ulcerogenic doses of dexamethasone inhibited angiogenesis at the ulcer margin and ulcer base and delayed ulcer healing. These were associated with a significant decrease of prostaglandin E(2) level and VEGF expression, but not the bFGF expression. Supplementation with prostaglandin E(2) attenuated the inhibitory action of dexamethasone on VEGF expression and reversed the adverse effects of dexamethasone on angiogenesis and ulcer healing, without influencing bFGF expression. We concluded that dexamethasone given at non-ulcerogenic doses could decrease angiogenesis and delay acetic acid-induced ulcer healing; these actions were at least, in part, due to depletion of prostaglandin E(2) level followed by down-regulation of VEGF at the ulcer margin of the stomach.

Angiogenesis Inhibitors↗
PubMed2006

Effectiveness of dexamethasone and low-power laser in minimizing oedema after third molar surgery: a clinical trial.

UNLABELLED: Postoperative oedema is common following removal of impacted lower third molars. Several types of drug therapy (corticosteroids, non-steroidal anti-inflammatory drugs, enzymes) have been tried. The aim of this study was to compare the effectiveness of low-power laser (LPL) and dexamethasone after surgical removal of impacted lower third molars under local anaesthesia (2% lidocaine/epinephrine). MATERIAL AND METHODS: There were 120 healthy patients divided into four groups of 30 each. Group 1 received LPL irradiation immediately after operation (energy output 4 J/cm2 with constant power density of 50 mW, wavelength 637 nm); group 2 also received i.m. injection of 4 mg dexamethasone (Dexason) into the internal pterygoid muscle; group 3 received LPL irradiation supplemented by systemic dexamethasone (Dexason), 4 mg i.m. in the deltoid region, followed by 4 mg of dexamethasone intraorally 6h postoperatively; and the fourth (control) group received only the usual postoperative recommendations (cold packs, soft diet, etc.). RESULTS: LPL irradiation with local use of dexamethasone (group 2) resulted in a statistically significant reduction of postoperative oedema in comparison to the other groups. No adverse effects of the procedure or medication were observed. CONCLUSION: LPL irradiation after lower third molar surgery can be recommended to minimize swelling. The effect is enhanced by simultaneous local intramuscular use of dexamethasone.

Administration, Oral↗
PubMed2007

A randomized comparison of dexamethasone 0.15 mg/kg versus 0.6 mg/kg for the treatment of moderate to severe croup.

BACKGROUND: Although previous studies have shown that dexamethasone is useful in croup, the optimal dosage has not been clarified yet. The aim of this study was to investigate the effectiveness of dexamethasone 0.15 mg/kg single dose compared with the recommended dose of 0.6 mg/kg for treatment of hospitalized children with moderate to severe croup. METHOD: Forty-one children aged 6 months to 5 years admitted from March 2001 to October 2003 at the pediatric ward of Hatyai Hospital with moderate to severe croup were recruited for the study. After random allocation, each child received a single intravenous injection of either dexamethasone 0.6 mg/kg (maximum dose 12 mg) or 0.15 mg/kg (maximum dose 3 mg). All children were given a single dose of epinephrine nebulization at the beginning of the study. The croup scores were measured at 0, 1, 2, 3, 4, 6, 8, 10 and 12 h after the dexamethasone injection. RESULTS: One hour following the injection, the mean croup scores were significantly reduced from baseline values in both groups (p<0.01). There was no difference in the mean croup scores between the two groups at any time. Median times to croup scores equal or less than two in both high- and low-dose groups were 8 and 7.9 h, respectively. No patient required intubation or was removed from the study because of a rising croup score after enrollment. There was no significant adverse reaction from dexamethasone treatment in either group. CONCLUSION: Dexamethasone 0.15 and 0.6 mg/kg are equally effective in the treatment of moderate to severe croup.

Anti-Inflammatory Agents↗
PubMed2004

Dexamethasone protects against dopaminergic neurons damage in a mouse model of Parkinson's disease.

The pathological process of neurodegeneration, which is observed in Alzheimer's (AD) and Parkinson's (PD) diseases and that follows any insult to the central nervous system, is accompanied by an inflammatory reaction, which is believed to contribute to the pathogenesis of the diseases. In accordance to this, the anti-inflammatory agents are suggested to be effective in slowing or inhibiting the degenerative process. In this study, we investigated the influence of dexamethasone (DXM) on the nigrostriatal dopaminergic neurons damage following administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropiridine (MPTP). Mice C57BL received pre-treatment of the various doses of dexamethasone followed by MPTP administration (40 mg/kg). We found that dexamethasone 1 mg/kg diminished a dopamine content depletion in striatum by about 20%, when the doses of 0.1 mg/kg was ineffective and 10 mg/kg even aggravate the dopamine content decrease. In the second step of the experiment, we chose the effective doses, 1 mg/kg, and started the treatment before and 24 h after MPTP administration. We observed the same protection in both situations: less dopamine depletion and less decrease in the number of dopaminergic cells in the substantia nigra (SN). Dexamethasone also similarly decreased the inflammatory reaction (glial activation, lymphocytic infiltration) in the injured areas. Our study showed that dexamethasone may exert a neuroprotective effect towards neurons injured by MPTP, but only when used in a proper dose. The mechanism of dexamethasone protective properties may be an inhibition of inflammatory process; however, direct interactions with neurons are also possible.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2006

High throughput HPLC-ESI-MS method for the quantitation of dexamethasone in blood plasma.

Dexamethasone is a synthetic glucocorticoid with potent anti-inflammatory properties. However, its administration causes significant side effects, specially in long-term therapy. A new approach for limiting adverse effects consists in the slow and constant deliver of this drug, using dexamethasone-21-phosphate-loaded erythrocytes (RBC) as circulating bioreactors converting the non-diffusible dexamethasone-21-phosphate into the diffusible dexamethasone. In order to evaluate the real possibility to use this new method of administration, a simple, cheap and rapid assay was set to manage a large number of samples originating from clinical studies. Due to the sample complexity and analite polarity, electrospray mass spectrometry (MS) is the most powerful technique to achieve qualitative and quantitative data. In order to overcome the complex, time-consuming and expensive LC-MS/MS methods reported in the literature in the present work a standard fluxes HPLC-ESI-MS method was set up for quantitative evaluation of dexamethasone. Thanks to the extraction ion chromatogram (XIC) feature of the software, it was possible to obtain sharp profiles for dexamethasone (DXM) and for the employed internal standard (IS) flumethasone (FM), in spite of the extremely complicated chromatogram obtained after HPLC separation of acetonitrile extracted plasma sample, thus avoiding the use of the expensive deuterated internal standard. This enabled us to obtain a linear response curve, allowing the quantification of DXM from blood samples at the picomoles level.

Anti-Inflammatory Agents↗
PubMed2004

Effects of dexamethasone and sulfasalazine on prostaglandin E2 output by human placental cells in vitro.

OBJECTIVE: Prostaglandins (PG) are key mediators of the labor process. We investigated effects of dexamethasone on PGE2 output in term human placental cells in the presence of indomethacin, an inhibitor of PGH synthase enzymes PGHS1 and PGHS2 activity; meloxicam, a relatively specific inhibitor of PGHS2; and sulfasalazine, an inhibitor of 15-OH PG dehydrogenase (PGDH), a PG-metabolizing enzyme. METHODS: Cells were treated for 24 hours with indomethacin (1 microM), meloxicam (1 microM), sulfasalazine (1 microM), or combinations of these three compounds in the presence or absence of glucocorticoids. RESULTS: Meloxicam alone had no effect on basal output of PGE2. Dexamethasone produced a significant, almost doubling of PGE2 output, but this was not altered further by meloxicam. Sulfasalazine alone doubled the output of PGE2, and this increased further in the presence of dexamethasone. That increase was reduced by addition of meloxicam. Indomethacin significantly reduced stimulation of PGE2 output measured after dexamethasone treatment. In addition, indomethacin significantly attenuated the stimulation of PGE2 output seen with the addition of sulfasalazine or the further increase seen with sulfasalazine plus dexamethasone. CONCLUSION: Basal PGE2 output by placental cells likely depends on the activity of PGHS1, not PGHS2. The effects of sulfasalazine suggest the importance of endogenous PGDH in regulating PGE2 output, and interactions with sulfasalazine, dexamethasone, and meloxicam suggest that glucocorticoid-stimulated output of PGE2 by placental cells may be attributable to both up-regulation of PGHS and down-regulation of PGDH.

Animals↗
PubMed2005

Dexamethasone reduces gut permeability in pediatric cardiac surgery.

OBJECTIVES: Little attention has been paid to the effect of the systemic inflammatory response syndrome on intestinal dysfunction in the postoperative period. Several proinflammatory cytokines have been reported to increase the permeability of intestinal mucosa in vitro. We investigated the effect of dexamethasone on gut permeability in pediatric patients undergoing cardiac surgery by using the dual sugar permeability test and absorption of 2 other saccharides. METHODS: Thirty-four patients scheduled for cardiac surgery with cardiopulmonary bypass were prospectively randomized to either act as control subjects or to receive dexamethasone (1 mg . kg -1) during induction of anesthesia. Intestinal permeability was measured with 3-O-methyl-D-glucose, D-xylose, L-rhamnose, and lactulose administered orally after induction of anesthesia and 12 and 24 hours later. RESULTS: Lactulose/rhamnose ratios were increased from the outset in both groups (mean 0.57 [95% confidence interval, 0.24-0.91] for the control group and 0.76 [95% confidence interval, 0.35-1.17] for patients receiving dexamethasone). Although the ratios decreased 12 hours (0.29 [95% confidence interval, 0.17-0.42]) and 24 hours later (0.17 [95% confidence interval, 0.08-0.15]) in the dexamethasone group, in the control group there was a rise at 12 hours (0.77 [95% confidence interval, 0-1.64]), with a slight reduction 24 hours later (0.46 [95% confidence interval, 0.06-0.85]). CONCLUSIONS: Infants and children undergoing cardiac surgery with cardiopulmonary bypass show a significant reduction in gut permeability when dexamethasone is used during induction of anesthesia. Dexamethasone does not affect the intestinal barrier at the functional level, as assessed on the basis of 3-O-methyl-D-glucose and D-xylose absorption.

Adolescent↗
PubMed2005

Repeated maternal dexamethasone treatments in late gestation increases 11beta-hydroxysteroid dehydrogenase type 1 expression in the hippocampus of the newborn rat.

This study was designed to investigate the effect of repeated maternal injections of dexamethasone in late gestation on the expression of newborn hippocampal 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1), the enzyme amplifying glucocorticoids' action by converting biologically inactive 11-ketone metabolites into active glucocorticoids. Daily dexamethasone treatments (0.10 mg/kg body weight) in the last week of gestation were carried out in the pregnant rat. The expression of 11beta-HSD1 in the newborn hippocampal tissue was analyzed with Western blot and real-time polymerase chain reaction (PCR). The effect of corticosterone on the expression of 11beta-HSD1 was studied in cultured hippocampal neurons derived from newborn offspring received prenatal dexamethasone treatments. Both body and brain weights of the offspring were reduced significantly by repeated dexamethasone treatments in the last week of gestation. Western blot and real-time PCR analysis showed that both 11beta-HSD1 protein and mRNA expressions were increased significantly in the hippocampus of the newborn offspring on the first and seventh days after birth. Corticosterone could induce 11beta-HSD1 expression in cultured hippocampal neurons prepared from newborns received prenatal dexamethasone treatments, which was blocked by glucocorticoid receptor antagonist RU38486. The above findings suggest that repeated prenatal dexamethasone treatments at the end of gestation increase 11beta-HSD1 expression in the hippocampal tissue of the offspring, which may trigger a positive feedback pathway for the generation of biologically active glucocorticoids in the hippocampal tissue of the newborns.

11-beta-Hydroxysteroid Dehydrogenase Type 1↗
PubMed2005

Dexamethasone inner ear perfusion by intratympanic injection in unilateral Ménière's disease: a two-year prospective, placebo-controlled, double-blind, randomized trial.

OBJECTIVE: To investigate the efficacy of dexamethasone inner ear perfusion by intratympanic injection in hearing loss, tinnitus, aural fullness, and vertigo in the treatment of unilateral Ménière's disease and compare it with the control group. STUDY DESIGN AND SETTING: A prospective, randomized, double-blind study with 2-year follow-up comparing changes secondary to dexamethasone inner ear perfusion versus placebo consisting of saline solution. PATIENTS: Twenty-two patients having definite Ménière's disease as outlined by the 1995 American Academy of Otolaryngology-Head and Neck Surgery Committee on Hearing and Equilibrium. All the patients were older than 18 years of age and were not receiving any other form of treatment with steroids for their Ménière's disease. METHOD: Five consecutive daily intratympanic injections of dexamethasone or placebo to the involved ear. RESULTS: In the dexamethasone group at 2-year follow-up, complete control of vertigo (class A) was achieved in 9 of 11 patients (82%) and substantial control of vertigo (class B) in the remaining 2 patients (18%.) In the control group only 7 of 11 patients (64%) finished the 2-year follow-up because in the other 4 patients (36%) we had to give another treatment for the continuing vertigo and thus they were classified as failure (class F.) From the 7 patients who have finished the follow-up of 2 years in the control group, 4 patients (57%) achieved class A, 2 patients (29%) achieved class C, and 1 patient (14%) class F. CONCLUSIONS: Dexamethasone (4 mg/mL) inner ear perfusion in a group of patients with unilateral Ménière's disease (Shea's stage III) showed 82% of complete control of vertigo over placebo (57%). There was also a subjective improvement in tinnitus (48%), hearing loss (35%), and aural fullness (48%) in the dexamethasone group compared with 20%, 10%, and 20% respectively in the control group.

Adult↗
PubMed2006

Dexamethasone treatment attenuates early seawater instillation-induced acute lung injury in rabbits.

There is very little evidence on the value of giving corticoids in cases of seawater drowning induced acute lung injury/acute respiratory distress syndrome (ALI/ARDS). Therefore, this study aimed to investigate whether dexamethasone treatment can attenuate seawater instillation-induced acute lung injury in rabbits. Seawater (4 ml/kg body weight) was instilled into the lower trachea of ventilated, anesthetized rabbits. Then these rabbits were assigned randomly 20 min later to receive intravenous injection of 1mg/kg body weight of dexamethasone (dissolving in 2 ml of normal saline) or 2 ml of normal saline. All animals demonstrated immediate drops in arterial oxygen tension (PaO2) and the total thoracic compliance, which were significantly improved after 2 h of dexamethasone treatment. Histopathological study also indicated that dexamethasone treatment markedly attenuated lung histopathological changes, alveolar hemorrhage and inflammatory cells infiltration with evidence of decreasing of myeloperoxidase (MPO) activity and tumor necrosis factor-alpha (TNF-alpha) concentration in lung tissue. In addition, dexamethasone treatment reduced extravascular lung water and lung epithelial-endothelial barrier permeability, up-regulated the expression of surfactant protein-A (SP-A) and alpha-epithelial Na+ channel, and increased Na+/K+-adenosine triphosphatase (Na+/K+-ATPase) activity and Na+/K+-ATPase-alpha1 protein abundance. Thus, these data indicate that dexamethasone treatment might be of benefit in patients with seawater aspiration-induced ALI.

Animals↗
PubMed1998

Comparison between oral and intramuscular dexamethasone in suppressing unconjugated estriol levels during the third trimester.

OBJECTIVES: Unconjugated estriol production depends on fetal adrenal androgen precursors. Fetal exposure to exogenous glucocorticoids results in adrenal suppression with a subsequent decrease in maternal serum unconjugated estriol levels. We compared the efficacy between oral and intramuscular dexamethasone in maternal serum unconjugated estriol suppression at 48 hours after the initial dose among women at risk for preterm delivery. STUDY DESIGN: Twenty-four gravidas at risk for preterm delivery were randomized to receive either 6 mg intramuscular or 8 mg oral dexamethasone every 12 hours for a total of 4 doses. Blood samples (9 mL) were obtained before the initial dexamethasone administration and again after the fourth dose. Serum was separated and frozen at -70 degreesC and subsequently underwent batch analysis. Unconjugated estriol levels were determined by radioimmunoassay with intra-assay and interassay coefficients of variation of 7.9% and 5.5%, respectively. All values are reported as mean +/- SD. The primary statistical analysis was a t test, with P <.05 considered significant. RESULTS: At the time of dexamethasone administration, gestational ages in both groups were similar. Predexamethasone and postdexamethasone unconjugated estriol levels were also similar between the intramuscular and oral groups (5.39 +/- 3.99 vs 1.80 +/- 2.49 ng/mL and 6.05 +/- 3.00 vs 1.61 +/- 1.03 ng/mL, respectively, P >.05). No difference in percent decrease in unconjugated estriol levels was found between the intramuscular (0.67 +/- 0.24) and oral (0.65 +/- 0.39) groups. CONCLUSION: Oral dexamethasone (8 mg) produces similar maternal serum unconjugated estriol suppression compared with intramuscular dexamethasone (6 mg) when evaluated 48 hours after administration.

Administration, Oral↗