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PubMed2003

Partial glucocorticoid resistance in obese children detected by very low dose dexamethasone suppression test.

The effects of glucocorticoids (GC) are mediated by the activation of specific receptors that can be quantified in vitro by several laboratory tests. In vivo, other tests to determine GC sensitivity have been described, but only employing pharmacological doses. In this study, we used a very low dose of dexamethasone, an in vivo model to assess individual GC sensitivity. Fifty-five obese children and adolescents and 17 controls were studied. The patients were submitted to four 12-h urine collections, starting at 22:00 h; dexamethasone was administered orally at the end of the second urine sample. Patients were divided in the following groups: group Ob75 (n = 29) and the control group (n = 17) received dexamethasone 75 microg/m2, and group Ob150 (n = 26) received dexamethasone 150 microg/m2. Urinary cortisol was determined by RIA and expressed as microg/m2/12 h. All patients and controls showed a circadian rhythm before GC, which was maintained after dexamethasone only in controls. In the obese patients the circadian rhythm was abolished following both doses of dexamethasone, but more prominently with the dose of 150 microg/m2. In the obese group given 75 microg/m2, urinary cortisol inhibition was only observed in the first 12 h after dexamethasone, suggesting a partial and shorter suppression of the hypothalamic-pituitary axis. In both control and obese patients, the very low dose of dexamethasone was able to create a gradient of cortisol suppression that could be useful to identify an individual's sensitivity to glucocorticoids.

Administration, Oral↗
PubMed1994

Interactions of insulin-like growth factor I with dexamethasone on trabecular bone density and mineral metabolism in rats.

Glucocorticoid treatment causes osteoporosis and growth retardation in humans. Insulin-like growth factor I (IGF-I) stimulates differentiation and replication of cultured osteoblast-like cells and induces longitudinal bone growth in IGF-I-deficient rats. We investigated the influence of subcutaneously infused IGF-I on bone and mineral metabolism of male rats treated with a high dose of dexamethasone. Dexamethasone was added to the drinking water in a concentration of 1 mg/l. After 30 days of dexamethasone treatment, recombinant human IGF-I (300 micrograms/day) or solvent was infused sc by osmotic minipumps for 21 days while dexamethasone was continued. Age-matched untreated male rats served as healthy controls. Dexamethasone-treated rats lost weight. Their IGF-I levels were decreased to 36% of healthy controls. Infusion of IGF-I resulted in an increase in IGF-I serum levels (582% compared to healthy controls) and allowed some weight gain. Osteocalcin and calcitriol levels were markedly decreased in dexamethasone-treated rats and were not influenced significantly by IGF-I infusion. In contrast, IGF-I treatment restored the free calcitriol concentration (molar ratio of calcitriol to vitamin D-binding protein) towards normal. Furthermore, infusion of IGF-I partially corrected the dexamethasone-induced hyperinsulinemia. Histomorphometric analysis revealed no difference in vertebral trabecular bone density (i.e. growth-independent bone remodeling) between the three groups. In contrast, mean trabecular bone density in tibial metaphyses was increased markedly by dexamethasone, presumably due to osteoclast inhibition. Insulin-like growth factor I infusion did not significantly influence these structural metaphyseal bone parameters.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗
PubMed2002

Early postnatal dexamethasone decreases hepatocyte growth factor in tracheal aspirate fluid from premature infants.

OBJECTIVE: To evaluate in preterm infants the effect of dexamethasone on hepatocyte growth factor (HGF), an epithelial cell mitogen, and on vascular endothelial growth factor (VEGF), an endothelial cell mitogen, in tracheal aspirate fluid (TAF). METHODS: Thirty preterm infants (birth weight: 1000-1500 g) with respiratory distress syndrome were randomized to receive dexamethasone or to serve as control subjects. Dexamethasone was started at the age of 12 to 24 hours at a dose of 0.5 mg/kg/d for 2 days and 0.25 mg/kg/d for the subsequent 2 days. HGF and VEGF levels were examined from TAF samples during the first postnatal week. For eliminating the effect of dilution, the concentration of the secretory component of immunoglobulin A was determined. Student t test, 1-way analysis of variance, chi2, and simple regression analysis were used for statistical analysis. RESULTS: Mean HGF concentrations were similar in the dexamethasone and control groups on days 1 to 2, but the dexamethasone group had a lower mean HGF concentration on days 3 to 4 and 5 to 7. In contrast, no differences existed in mean VEGF levels between the dexamethasone and control groups. CONCLUSIONS: In preterm infants who received early postnatal dexamethasone, reduced levels of HGF were seen in tracheal aspirates. This reduction may participate in the suppressive effects of dexamethasone on lung development.

Bronchoalveolar Lavage Fluid↗
PubMed1994

Dexamethasone potentiates the stimulatory effect of insulin-like growth factor-I on collagen production in cultured human fibroblasts.

We examined the effects of insulin-like growth factor-I (IGF-I) and dexamethasone on the production of collagen by cultures of human infant foreskin fibroblasts, and the interaction between these two factors. IGF-I at 500 ng/ml maximally increased collagen accumulation fourfold. Collagen was increased twofold relative to total protein production. Dexamethasone at a concentration of 1 mumol/l reduced collagen production by between 25% and 40% in unstimulated cells and those cultured with up to 100 ng IGF-I/ml. However, dexamethasone did potentiate collagen production in cells stimulated with 250 ng IGF-I/ml. This potentiation was independent of any effects of IGF-I or dexamethasone on prostaglandin (PG)E2 production. Transforming growth factor-beta (TGF-beta) is also a potent stimulator of collagen formation. However, no potentiation of TGF-beta-stimulated collagen production by dexamethasone was apparent. The mechanism by which dexamethasone potentiates IGF-I-stimulated collagen production was investigated. Dexamethasone treatment increased IGF-I binding to the type 1 IGF receptor without altering the binding affinity. Dexamethasone also attenuated the secretion of IGF-binding proteins by IGF-I-maintained cells.

Carrier Proteins↗
PubMed2005

Dexamethasone prevents podocyte apoptosis induced by puromycin aminonucleoside: role of p53 and Bcl-2-related family proteins.

Nephrotic-range proteinuria is due to glomerular diseases characterized by podocyte injury. Glucocorticoids are the standard of care for most forms of nephrotic syndrome. However, the precise mechanisms underlying the beneficial effects of glucocorticoids on podocytes, beyond its general immunosuppressive and anti-inflammatory effects, are still unknown. This study tested the hypothesis that the synthetic glucocorticoid dexamethasone directly reduces podocyte apoptosis. Growth-restricted immortalized mouse podocytes in culture were exposed to puromycin aminonucleoside (PA) to induce apoptosis. Our results showed that dexamethasone significantly reduced PA-induced apoptosis by 2.81-fold. Dexamethasone also rescued podocyte viability when exposed to PA. PA-induced apoptosis was associated with increased p53 expression, which was completely blocked by dexamethasone. Furthermore, the inhibition of p53 by the p53 inhibitor pifithrin-alpha protected against PA-induced apoptosis. Dexamethasone also lowered the increase in the proapoptotic Bax, which was increased by PA, and increased expression of the antiapoptotic Bcl-xL protein. Moreover, the decrease in p53 by dexamethasone was associated with increased Bcl-xL levels. Podocyte apoptosis induced by PA was caspase-3 independent but was associated with the translocation of apoptosis-inducing factor (AIF) from the cytoplasm to nuclei. AIF translocation was inhibited by dexamethasone. These results show that PA-induced podocyte apoptosis is p53 dependent and associated with changes in Bcl-2-related proteins and AIF translocation. The protective effects of dexamethasone on PA-induced apoptosis were associated with decreasing p53, increasing Bcl-xL, and inhibition of AIF translocation. These novel findings provide new insights into the beneficial effects of corticosteroids on podocytes directly, independent of its immunosuppressive effects.

Active Transport, Cell Nucleus↗
PubMed2001

Effects of dexamethasone on emesis in cats sedated with xylazine hydrochloride.

OBJECTIVE: To determine antiemetic efficacy of prophylactic administration of dexamethasone and its influence on sedation in cats sedated with xylazine hydrochloride. ANIMALS: 6 healthy adult cats (3 males and 3 females). PROCEDURE: The prophylactic antiemetic effect of 4 doses of dexamethasone (1, 2, 4, and 8 mg/kg of body weight, IM) or saline (0.9% NaCl) solution (0.066 ml/kg, IM) administered 1 hour before administration of xylazine (0.66 mg/kg, IM) was evaluated. Cats initially were given saline treatment (day 0) and were given sequentially increasing doses of xylazine on days 7, 14, 21, and 28. After xylazine injection, all cats were observed for 30 minutes to allow assessment of frequency of emesis and time until onset of the first emetic episode. The influence of dexamethasone on xylazine-induced sedation in these cats also was evaluated. RESULTS: Prior treatment with 4 or 8 mg/kg of dexamethasone significantly reduced the frequency of emetic episodes and also significantly prolonged the time until onset of the first emetic episode after xylazine injection. Time until onset of the first emetic episode also was significantly prolonged for dexamethasone at a dose of 2 mg/kg. Time until onset of sedation after administration of xylazine was not altered by administration of dexamethasone. CONCLUSIONS AND CLINICAL RELEVANCE: Dexamethasone (4 or 8 mg/kg, IM) significantly decreased the frequency of emetic episodes induced by xylazine without compromising sedative effects in cats. Dexamethasone may be used prophylactically as an antiemetic in cats treated with xylazine.

Adrenergic alpha-Agonists↗
PubMed2000

Differential effects of dexamethasone and clenbuterol on rat growth and on beta2-adrenoceptors in lung and skeletal muscle.

Beta-adrenergic agonists increase growth rate, but their efficacy is reduced over time as the number of beta2-adrenoceptors in muscle decreases. Dexamethasone increases beta2-adrenoceptor density in many tissues, but this effect has not been reported in skeletal muscle. In this study, male rats were treated daily for 10 d with either clenbuterol (4 mg/kg of feed), dexamethasone (.2 mg/kg BW, s.c.), or clenbuterol plus dexamethasone. Untreated rats served as controls. Dexamethasone caused a marked suppression of growth rate, which resulted in decreased (P < .001) body weight (-29%), carcass weight (-30%), hind-limb muscles (-22%), omental fat (-22%), and heart weight (-10%). Feed intake was reduced (-26%), but feed conversion efficiency was also impaired (P < .001). Clenbuterol caused a small increase in growth rate (+6%; P < .05), with an increase in leg muscle (+7%; P < .01) and heart mass (+8%; P < .05). Feed efficiency was improved (P < .001) by clenbuterol. Rats given the combined treatment still showed a reduction in growth rate (-81%). Clenbuterol caused only a mild attenuation of the effects of dexamethasone on feed intake, BW, and carcass weight, but reduced the catabolic effect of dexamethasone on hind-limb muscle to only -8%. Clenbuterol caused a slight increase in the affinity beta2-adrenoceptors in lung for binding to the radioligand (-)[125I]iodocyanopindolol. Relative to control values, the density of beta2-adrenoceptors in lung was +31% with dexamethasone treatment, -45% with clenbuterol, and -23% with the combined treatment. Clenbuterol also decreased beta2-adrenoceptors in skeletal muscle (-35%), but so did dexamethasone (-13%), so the effects of the beta-adrenergic agonist were not attenuated through use of the combined treatment (-40%). The results show that the inductive effect of glucocorticoids on beta2-adrenoceptors is tissue-specific and that glucocorticoid treatment is not a useful adjunct to beta-adrenergic agonist treatment in animal production.

Adrenergic beta-Agonists↗
PubMed2000

Effects of triglyceride accumulation on induction of urea synthesis by glucagon and dexamethasone in monolayer cultures of bovine hepatocytes.

Hepatocyte monolayer cultures from two preruminating and two ruminating calves were used to study the effects of triglyceride accumulation on induction of ureagenesis by glucagon plus dexamethasone. Whether hepatocytes from preruminating and ruminating calves respond similarly to triglyceride accumulation and hormonal treatment was also determined. Hepatocyte monolayer cultures were incubated from 24 to 48 h with a physiological mixture of nonesterified fatty acids (NEFA, 0 or 1.5 mM) and a hormone mixture containing glucagon plus dexamethasone (0 or 100 nM of both) added as a 2 x 2 factorial (NEFA x hormones). Ureagenesis was measured at 0, .25, and 5 mM NH4Cl from 48 to 51 h and activities of ornithine transcarbamylase (OTC) and arginase were measured at 48 h. There was no significant age-related interaction for any of the measurements. Therefore, monolayer culture of hepatocytes from preruminating calves provides a reasonable model for studying the effects of glucagon, dexamethasone, and triglyceride accumulation on ureagenesis in the ruminating bovine. Intracellular triglyceride was increased by NEFA (2.3 vs 15.6 +/- 1.9 microg TG/microg DNA, P < .001). Triglyceride-engorged cells exhibited decreased ureagenesis (1.04 vs .87 +/- .135 nmol/(microg DNA x h), P < .05) but had unaltered OTC and arginase activity. Hormone addition did not affect triglyceride accumulation but increased ureagenesis (.70 vs 1.21 +/- .135 nmol/(microg DNA x h), P < .0001). There was no interaction between hormone addition and triglyceride accumulation on ureagenesis. To separate the effects of dexamethasone from that of glucagon on ureagenesis, hepatocyte monolayer cultures from one ruminating and three preruminating calves were used. Hepatocyte monolayer cultures were incubated from 24 to 48 h with glucagon (0 or 100 nM) and dexamethasone (0 or 100 nM) added as a 2 x 2 factorial. Ureagenesis was measured at 0, .25, and 5 mM NH4Cl from 48 to 51 h. Glucagon increased ureagenesis (.77 vs 1.24 +/- .11 nmol/(microg DNA x h), P < .0001). Dexamethasone did not affect ureagenesis, nor was there any interaction between glucagon and dexamethasone. Therefore, glucagon alone was responsible for the induction observed with the mixture of glucagon and dexamethasone. In conclusion, glucagon is able to increase ureagenesis in bovine hepatocytes, and triglyceride accumulation does not interfere with the induction.

Aging↗
PubMed2004

Decreasing incidence of chronic lung disease despite the gradual reduction of postnatal dexamethasone use in very low birth weight infants.

Dexamethasone has been widely used in very low birth weight infants (VLBWI) weighing less than 1,500 g at birth for the prevention or treatment of chronic lung disease (CLD). Recently, however the use of dexamethasone is being reduced, as its association with abnormal neurodevelopmental outcome is known. On the other hand, there have been persistent concerns about the increased risk of CLD according to the reduction of postnatal dexamethasone use. Hence, we did a retrospective cohort study to delineate the change in the incidence of CLD according to the reduction of dexamethasone use in VLBWI. The medical records of 559 VLBWI admitted to neonatal intensive care unit at Samsung Medical Center between November 1994 and December 2002 were reviewed with a focus on the use of postnatal dexamethasone and the incidence of CLD. The use of postnatal dexamethasone has significantly decreased over the study period. Especially, the use of high-dose regimen has markedly decreased. The day when postnatal dexamethasone therapy was begun has also been significantly delayed. The incidence of CLD has significantly decreased over the same period. In conclusion, the incidence of CLD has not increased despite the decreased use of postnatal dexamethasone.

Chronic Disease↗
PubMed1996

The dexamethasone suppression test in patients with mood disorders.

BACKGROUND: This study was undertaken to (1) determine whether the endogenous/nonendogenous mood disorder dichotomy is validated by the dexamethasone suppression test (DST); (2) determine whether other subtyping schemes (unipolar/bipolar, DSM-III melancholic/nonmelancholic, Winokur's family history subtypes) relate to the DST; (3) evaluate the relative contributions of symptom severity, weight loss, and other factors to DST status; and (4) assess the relative sensitivity of various post-dexamethasone cortisol determinations in the detection of dexamethasone nonsuppression. METHOD: 487 consecutive adult inpatients (N = 131) and outpatients (N = 356) with unipolar (N = 422) or bipolar disorder (N = 65) underwent the 1.0-mg DST. Nonsuppression was defined as at least one post-dexamethasone cortisol measurement > 4.0 micrograms/dL. RESULTS: Nonsuppression occurred in 27% of all patients with major depression and 43% of all bipolar depressed phase patients. For outpatients, dexamethasone nonsuppression occurred in 35.2% of subjects with endogenous (unipolar + bipolar; N = 145) and 9.0% of those with nonendogenous (unipolar only; N = 211) depressions (single 4 p.m. post-dexamethasone cortisol). For inpatients, dexamethasone nonsuppression was found in 61.5% of subjects with endogenous (N = 104) and 18.5% of those with nonendogenous (N = 27) depressions (three post-dexamethasone cortisol determinations). For the inpatient and outpatient sample together, the DST had a sensitivity of 46.2% and a specificity of 89.9% in differentiating endogenous from nonendogenous major depressive episodes. Weight loss, gender, and symptom severity added little to the endogenous/nonendogenous dichotomy. The Research Diagnostic Criteria (RDC) primary/secondary and Winokur and colleagues' family history subtypes for unipolar depression were not strongly validated by the DST. The 4 p.m. and 11 p.m. samples together detected 91.0% of those inpatients with abnormal three-sample DST results. The 8 a.m. sample alone detected 30% of those, the 4 p.m. sample alone detected 67%, and the 11 p.m. sample alone detected 62%. CONCLUSION: The RDC endogenous/nonendogenous dichotomy was validated by the DST.

Adult↗
PubMed1999

Effects of dexamethasone administration on serum trypsin-like immunoreactivity in healthy dogs.

OBJECTIVE: To determine whether administration of dexamethasone altered serum trypsin-like immunoreactivity (TLI) in healthy dogs. ANIMALS: 12 healthy dogs. PROCEDURE: Dexamethasone (0.25 mg/kg, p.o., q 24 h) was administered for 7 days. Serum TLI, alpha-amylase and alanine aminotransferase (ALT) activities, and urea and creatinine concentrations were determined on days 0, 7, 14, and 21 of the study. RESULTS: Serum TLI and ALT activities were significantly increased, and serum alpha-amylase activity was significantly decreased after administration of dexamethasone for 7 days. However, values obtained on days 14 and 21 were not significantly different from baseline values. Dexamethasone administration was not associated with any significant changes in serum creatinine or urea concentrations. Serum TLI and alpha-amylase activities were significantly correlated prior to dexamethasone administration. Dogs did not develop clinical signs of pancreatitis. CONCLUSIONS AND CLINICAL RELEVANCE: Dexamethasone administration was associated with an increase in serum TLI. However, values returned to baseline 7 days after dexamethasone administration was discontinued. Serum TLI may be falsely high in dogs that have been treated with dexamethasone in the week preceding analysis.

Alanine Transaminase↗
PubMed1999

Albumin microsphere as a drug delivery system for dexamethasone: pharmacokinetics in sheep, residue amount in cows and distribution in rats.

The aim of this study was to evaluate the potential use of albumin microspheres as a drug delivery system to provide sustained release of dexamethasone in vivo. Pharmacokinetic studies were carried out in sheep and tissue distribution in rats given dexamethasone in two injectable forms--water suspension of dexamethasone associated with albumin microspheres and water-ethanol solution of dexamethasone. When dexamethasone was associated with albumin microspheres the amount of free dexamethasone, available for absorption did not reach the high values typical of the pattern of release of dexamethasone from water-ethanol solution. The time of withdrawal in lactating cows after i.m. administration of DXM-AM was found to be 5 days. The release of dexamethasone from the albumin microspheres was accomplished gradually thus allowing sustained levels of the corticosteroid to be maintained for several days in blood plasma, milk, liver, kidney and muscles.

Albumins↗
PubMed1998

[Effects of dexamethasone on apoptosis of airway inflammatory cells in asthmatic guinea-pigs].

OBJECTIVE: Clearance of airway inflammatory cells is the key point of therapeutic effect in asthma. Apoptosis, a form of cell death, is thought to be critically important to promote the clearance of inflammatory cells and the resolution of inflammation. To investigate the effects of dexamethasone on apoptosis of airway inflammatory cells in asthma showed be very important. METHOD: Dexamethasone was used for the treatment of asthma model of guinea pigs set up by inhaling ovalbumin. Apoptotic cells were labelled with TdT-mediated dUTP nick end labeling(TUNEL) technique on formalin-fixed paraffin-embedded trachea and lung tissue sections. By way of immunohistochemistry, eosinophils were stained with EG2 antibody and T lymphocytes with CD3+, CD4+ and CD8+ antibodies on sections. RESULT: (1) The quantity of airway eosinophils and lymphocytes decreased in dexamethasone group, which could not be observed in the control one (P < 0.01). (2) Apoptotic index of lymphocytes was significantly elevated following dexamethasone treatment(P < 0.05). But no difference was found in the proportion of apoptotic eosinophils between these two groups. (3) The percentage of EG2 positive eosinophils and CD4+ positive lymphocytes decreased significantly following dexamethasone treatment. On the contrary, the number of CD8+ lymphocytes increased in dexamethasone group when compared with the control one (P < 0.05). CONCLUSION: (1) The quantity of airway eosinophils decreases following dexamethasone treatment in guinea-pigs asthma, and its mechanism may not be ascribed mainly to the apoptosis of eosinophils. (2) The number of lymphocytes, mainly CD4+, decreased following dexamethasone treatment in guinea-pig airways, and apoptosis may represent the mechanism that promotes the clearance of lymphocytes in asthma.

Animals↗
PubMed2001

Dexamethasone enhances follicle stimulating hormone-induced P450scc mRNA expression and progesterone production in pig granulosa cells.

The effect of dexamethasone on follicle-stimulating hormone (FSH)-stimulated expression of cholesterol side-chain cleavage (P450scc) enzyme and production of progesterone by ovarian granulosa cells was studied in vitro. Granulosa cells from 3- to 5-mm pig antral follicles were cultured for 48 h in the presence or absence of FSH and/or dexamethasone. Treatment with FSH resulted in a dose-dependent increase in the level of P450scc mRNA that reached a submaximum at 100 ng FSH/ml. This increase was associated with an increase in progesterone production. Treatment of the cells with increasing concentrations (10(-9)-10(-6) M) of dexamethasone for 48 h increased constitutive and potentiated FSH-stimulated P450scc mRNA levels and progesterone production in a dose-dependent manner. Increasing duration (12-48 h) of treatment with dexamethasone (100 nM) led to a time-dependent increase in basal and FSH-stimulated progesteorne production, achieving statistical significance by 48 and 24 h, respectively. Dexamethasone also increased P450scc mRNA level and progesterone production induced by the adenylate cyclase activator forskolin (10 microM) or a cAMP analog 8-Br-cAMP (1 mM). The effects of dexamethasone on FSH-induced progesterone production were blocked by cotreatment of the cells with glucocorticoid receptor antagonist RU-486. These results demonstrate that dexamethasone potentiates FSH actions on steroidoogenesis in the pig ovary. Possible mechanisms for this potentiation include the ability of dexamethasone to stimulate P450scc gene expression.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2001

Prevention of PONV with dexamethasone in female patients undergoing desflurane anesthesia for thyroidectomy.

BACKGROUND: Desflurane is associated with a higher incidence of 24-h postoperative nausea and vomiting (PONV) as compared with sevoflurane or isoflurane. Dexamethasone 5 mg i.v. is suggested to be the minimum effective dose for prophylaxis of PONV in women undergoing thyroidectomy with isoflurane anesthesia. The objective of this study was to investigate whether a 5 mg dose of dexamethasone could be enough for, or a larger dose at 8 mg, could be more capable of preventing PONV in women undergoing desflurane anesthesia for thyroidectomy. METHODS: One hundred and thirty five patients were assigned to receive one of three treatment regimens prior to induction i.e., dexamethasone 8 mg i.v. (Group D8), dexamethesone 5 mg i.v. (Group D5) or saline (Group S). RESULTS: It was demonstrated that the prophylactic administration of either dexamethasone 8 mg or 5 mg significantly reduced the overall incidence of PONV in patients undergoing thyroidectomy with desflurane anesthesia (P < 0.001, Group D8 vs. Group S; Group D5 vs. Group S). However, patients who received dexamethasone 8 mg showed a higher incidence of complete responses (no vomiting or need of rescue antiemetic medication for a 24-h postoperative period) in comparison with those receiving dexamethasone 5 mg (86% vs. 67%; P < 0.01). CONCLUSIONS: The results of this study showed that in PONV prophylaxis, in female patients undergoing desflurane anesthesia for thyroidectomy, the effect of dexamethasone 8 mg was superior to that of dexamethasone 5 mg.

Adult↗
PubMed2002

Dexamethasone therapy for bacterial meningitis in adults: a double blind placebo control study.

Routine use of steroids in the treatment of bacterial meningitis remains controversial. A prospective placebo controlled double blind study of dexamethasone was carried out in 40 patients (age>10 years) of acute bacterial meningitis. The patients were randomly assigned to receive either placebo (n=20) or dexamethasone (n=20) in addition to injection ceftriaxone 100 mg/kg/day (maximum 4 gm/day) for 14 days. Dexamethasone sodium phosphate was given in dose of 0.6 mg/kg/day in 4 divided doses, for first 4 days of therapy. First dose of dexamethasone was given 15 minutes prior to first dose of ceftriaxone. Baseline demographics, clinical and laboratory features of the two groups were similar. Clinical improvement of signs of meningeal irritation was rapid in dexamethasone group than in the placebo group, but no significant difference was observed regarding resolution of fever, headache and vomiting. Secondary fever (mean+/-SD 15.00), gastrointestinal tract bleeding (mean+/-SD 15.00) and psychiatric manifestations (mean+/-SD 10.00) were more common in dexamethasone group. Neurological complications and hearing loss were more common and severe in placebo group as compared to the dexamethasone group (p<0.05). It is concluded that dexamethasone may be beneficial in some aspects of bacterial meningitis, in adults. A study with a larger number of cases in each group is recommended.

Adolescent↗
PubMed2003

[Therapeutic effect of dexamethasone and mannitol on global brain ischemia-reperfusion injury in rats].

OBJECTIVE: To determine the effect of dexamethasone and mannitol on reperfusion injury after global brain ischemia in rats. METHODS: Forty-two Wistar rats were randomly divided into six groups: normal group (n = 5), normal rats without any surgical operation; sham operative group (n = 6), the rat bilateral vertebral arteries were electrocauterized; ischemia group (n = 7), bilateral vertebral arteries were electrocauterized, and both carotid arteries were occluded temporarily by atraumatic artery clasp for 10 minutes; dexamethasone group (n = 8), intraperitoneal dose of dexamethasone of 10 mg.kg-1 (body weight) was received immediately after vessel occlusion (VO), twice a day; mannitol group (n = 8), intravenous dose of 20% mannitol of 10 ml.kg-1 was received 4 hours after VO, three times a day; dexamethasone combined with mannitol group (n = 8), both intraperitoneal dexamethasone of 10 mg.kg-1, twice a day, and intravenous 20% mannitol of 10 ml.kg-1, three times a day were administered. All rats were sacrificed and brains were removed after 72 hours. A 3 mm thick coronal brain was sliced from temporal lobe for histopathological examination. Ischemic neurons and neuron density in hippocampal CA1 region were measured with paraffin sections stained by HE methods. Apoptosis of cells was observed by TUNEL method. The rest of the brain was used to measure water contents by means of wet-dry method. RESULTS: All drug-treated groups could effectively reduce brain edema. Dexamethasone exacerbated ischemic neuronal injury but dexamethasone combined with mannitol was the most effective treatment for brain ischemia injury compared with other groups. CONCLUSION: Dexamethasone aggravates brain ischemic-reperfusion injury, mannitol is effective for reducing brain ischemia-reperfusion injury, and application of the combined agents is the most effective treatment.

Animals↗
PubMed2003

Complete protection by high-dose dexamethasone against the hepatotoxicity of the novel antitumor drug yondelis (ET-743) in the rat.

Yondelis (ET-743) is a promising antitumor drug with hepatotoxic properties in animals and humans. Here the hypothesis was tested that dexamethasone can ameliorate manifestations of yondelis-induced hepatotoxicity in the female Wistar rat, which is the animal species with the highest sensitivity toward the adverse hepatic effect of yondelis. Hepatotoxicity was adjudged by measurement of plasma levels of alkaline phosphatase, aspartate aminotransferase, and bilirubin, and by liver histopathology. Yondelis (40 micro g/kg i.v.) alone caused a dramatic elevation of plasma alkaline phosphatase, aspartate aminotransferase, and bilirubin levels, and degeneration and patchy focal necrosis of bile duct epithelial cells. Pretreatment of rats with dexamethasone (5-20 mg/kg, p.o.) 24 h before yondelis ameliorated or abrogated the biochemical and histopathological manifestations of yondelis-induced liver changes. In contrast, when dexamethasone was administered simultaneously with yondelis, its toxicity was not reduced. Pretreatment with dexamethasone (10 mg/kg) also reversed the gene expression changes induced by yondelis in rat liver. However, dexamethasone pretreatment did not interfere with the antitumor efficacy of yondelis in rats bearing the 13762 mammary carcinoma or in four murine models. Dexamethasone (10 mg/kg) administered 24 h before yondelis decreased hepatic levels of yondelis dramatically compared with those obtained after administration of yondelis alone, whereas yondelis plasma levels after the drug combination were not markedly different from those in rats on yondelis alone. The results suggest that pretreatment with high-dose dexamethasone effectively protects rats against yondelis-mediated hepatic damage by decreasing hepatic exposure to yondelis, perhaps linked to induction of metabolism by cytochrome P450 enzymes. Pretreatment with high-dose dexamethasone should be investigated in patients who receive yondelis to ameliorate its unwanted effect on the liver.

Animals↗