Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “DEXAMETHASONE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,315 records · Page 73Linked to original sources
PubMed1999

Temporal changes in fetal cardiovascular, behavioural, metabolic and endocrine responses to maternally administered dexamethasone in the late gestation fetal sheep.

OBJECTIVE: To determine the primary (0-12 h) and secondary (12-24 h) effects of dexamethasone on fetal heart rate, short term heart rate variation, blood pressure, breathing movements and electrocortical activity, blood gas exchange, metabolism and adrenocortical function in the late gestation sheep fetus. DESIGN: Comparison of the effects of a single maternally administered intramuscular injection of dexamethasone (12 mg) with those of saline vehicle from 1 h before injection to 24 h post-injection. Fetal cardiovascular and behavioural parameters were recorded continuously. Fetal and maternal blood samples were taken at regular intervals for blood gas, glucose and lactate, cortisol and adrenocorticotrophin measurements. SAMPLE: Sixteen chronically instrumented singleton fetal sheep at 127-133 days of gestation (term is about 147 days). RESULTS: During the primary phase short term heart rate variation fell (P < 0.001), and this was associated with a transient fall in the incidence of fetal breathing movements, a fall in fetal heart rate and a rise in fetal blood pressure. By 12 h there was a significant increase in short term heart rate variation (P < 0.001) and a rise in fetal heart rate, but blood pressure and fetal breathing movements had returned to normal. Dexamethasone significantly reduced fetal PaO2 throughout most of the experimental period, particularly 1 h post-injection (P < 0.005). Fetal and maternal plasma cortisol and adrenocorticotrophin concentrations fell significantly from 1 h post-injection. CONCLUSIONS: The effects of dexamethasone on fetal heart rate variation are more complex than previously described with both a fall and an increase observed depending on the time at which heart rate variation was measured after injection. Dexamethasone also caused a significant fall in fetal PaO2, and although this was not to hypoxic levels in normoxic fetuses it does raise questions about the potential impact of dexamethasone on chronically hypoxic fetuses.

Adrenocorticotropic Hormone↗
PubMed1984

Influence of protein-calorie malnutrition on the pharmacokinetics, placental transfer and tissue localization of dexamethasone in rats.

The influence of protein-calorie malnutrition (PCM) on the pharmacokinetics, transplacental passage and tissue localization of dexamethasone was determined in Sprague-Dawley rats. PCM increased the plasma half-life and volume of distribution of dexamethasone in pregnant but not in nonpregnant rats. Ratios of foetal to maternal serum dexamethasone concentrations were 0.2-0.4 at different dose levels (0.8-20 mumol kg-1), time intervals (0.25-12 h) and gestational ages (day 14-21). PCM increased the foetal serum and tissue concentrations of dexamethasone but exerted no significant effect on its binding to maternal and foetal serum proteins or on its metabolism by the placenta. It is suggested that significantly lower foetal than maternal serum levels of dexamethasone are due to efficient elimination of this agent by the foeto-placental unit and an impairment of this mechanism may account for the observed increase in dexamethasone levels in the foetuses of PCM rats.

Animals↗
PubMed1986

Investigation of the maternal to foetal serum concentration gradient of dexamethasone in the rat.

The basis of the maternal to foetal serum concentration gradient of dexamethasone was investigated in the rat on day 20 of gestation. The pregnant rat was assumed to behave as a two-compartment open model with one maternal and one foetal pool exchanging with each other and each to outside. Bolus injections of unlabelled dexamethasone were made into the mother and of [3H]-dexamethasone into its foetuses and serial maternal and foetal blood samples were collected a number of times. The monitoring of both forms of the drug in each sample permitted the estimation by a non-linear least square approach of two placental and two non-placental clearances. After both maternal and foetal injections of dexamethasone, its concentrations were higher in the maternal than in the foetal serum. Placental clearance of dexamethasone from the foetus to the mother was 824 +/- 40 ml kg-1 h-1 and 8.5 +/- 1 times greater than the placental clearance from the mother to foetus (103 +/- 2 ml kg-1 h-1). Foetal non-placental clearance was zero. It is suggested that a maternal to foetal serum gradient of dexamethasone is caused by its active transfer from the foetal to maternal side.

Animals↗
PubMed1992

Dexamethasone-induced gastric mucosal damage in the rat: possible role of platelet-activating factor.

1. The aim of the present experiments was to study the possible role of platelet-activating factor (PAF) in mediating gastric mucosal damage induced by dexamethasone in the rat by measuring gastric tissue levels of PAF during dexamethasone-treatment and by investigating the effects of specific PAF receptor antagonists on dexamethasone-induced gastric lesions. PAF-like bioactivity extracted from the rat glandular stomach was determined by a platelet aggregation assay. 2. Dexamethasone treatment (0.4-4 mg kg-1, daily for 1-6 days) produced time- and dose-dependent damage to the glandular mucosa of the stomach as characterized by extensive, uniform hyperaemia with multiple, focal petechiae and erosions. 3. These changes were accompanied by a time-, and dose-dependent increase in PAF content of the glandular stomach. Control rat stomach contained small amounts of PAF (0.14 +/- 0.04 ng per g wet weight), which increased over 40 fold in response to dexamethasone treatment (4 mg kg-1, daily for 6 consecutive days). The presence of PAF-like material in the stomach extract was ascertained by thin-layer chromatography, high performance liquid chromatography and by alkaline hydrolysis. 4. Pretreatment of the animals with one or other of the structurally unrelated PAF receptor antagonists, BN 52021 (10 mg kg-1, i.p.) or BN 50727 (1 mg kg-1, i.p.) significantly reduced dexamethasone-induced gastric damage. In these animals neither petechiae nor erosions were observed. 5. These observations suggest that PAF is a likely endogenous mediator of glucocorticoid-induced gastric mucosal damage in the rat.

Animals↗
PubMed1994

Sensitization by dexamethasone of lymphocyte cyclic AMP formation: evidence for increased function of the adenylyl cyclase catalyst.

1. Glucocorticoids and elevations of intracellular adenosine 3':5'-cyclic monophosphate (cyclic AMP) may affect lymphocyte activation, proliferation and effector functions in similar ways. Therefore, we have investigated the effects of the glucocorticoid, dexamethasone, on human lymphocyte cyclic AMP formation. 2. Treatment of resting human lymphocytes with the glucocorticoid, dexamethasone, sensitized prostaglandin E2-stimulated cyclic AMP accumulation in a time- and concentration-dependent manner. 3. In membranes of lymphocytes treated for 24 h with 100 nM dexamethasone, maximal adenylyl cyclase activity stimulated by prostaglandin E2, isoprenaline, guanosine 5'-triphosphate (GTP), forskolin and MnCl2 was significantly enhanced; the EC50 for these agents was not significantly altered. 4. beta 2-Adrenoceptor density, immunodetectable alpha-subunits of the G-proteins Gs and Gi, and pertussis toxin-substrates were not significantly altered by dexamethasone treatment. 5. In dexamethasone-treated lymphocytes, prostaglandin E2-mediated inhibition of concanavalin A-induced Ca2+ elevations was doubled compared to control cells. 6. Based on these data and the observation that enhancement of forskolin- and MnCl2-stimulated adenylyl cyclase activity could quantitatively account for the enhancement of prostaglandin E2-, isoprenaline- or GTP-stimulated adenylyl cyclase activity, we conclude that dexamethasone treatment sensitizes cyclic AMP formation in resting human lymphocytes by altering the adenylyl cyclase catalyst rather than G-proteins or hormone receptors. This results in an enhanced capability of cyclic AMP generating agonists to inhibit early steps of lymphocyte activation.

Adenylyl Cyclases↗
PubMed1996

Effects of dexamethasone and cyclosporin A on the accumulation of eosinophils in acute cutaneous inflammation in the guinea-pig.

1. Eosinophils are thought to play an important role in the pathophysiology of allergic diseases and pharmacological suppression of their recruitment is considered to be of therapeutic benefit. In the present study we have assessed and compared the effects of treatment with dexamethasone and cyclosporin A on the accumulation of 111In-labelled eosinophils and local oedema formation in sites of acute inflammation in guinea-pig skin. 2. When injected locally 150 min prior to i.d. administration of antigen in a passive cutaneous anaphylactic (PCA) reaction, dexamethasone (10(-9) to 3 x 10(-7) mol per site) dose-dependently inhibited oedema formation by up to 50%. Similarly, oedema formation induced by PAF and lipopolysaccharide (LPS), but not by zymosan-activated plasma (ZAP), was significantly inhibited by dexamethasone. In contrast, 111In-eosinophil accumulation measured in response to i.d. injection of PAF, LPS and ZAP or in the PCA reaction was not altered. 3. Systemic treatment with dexamethasone (4 mg kg-1, i.v., 150 min pretreatment period) inhibited both oedema formation and 111In-eosinophil accumulation induced by PAF, ZAP, LPS and in the PCA reaction. 4. The effects of i.d. injection of cyclohexamide (2 x 10(-7) mol per site) on 111In-eosinophil accumulation and oedema formation induced by PAF, ZAP or in a PCA reaction were evaluated in order to assess the dependency of these responses on protein synthesis. Cycloheximide had no effect on the responses measured. In contrast, 111In-eosinophil accumulation, but oedema formation, induced by LPS was inhibited by 30%. 5. Acute (10 mg kg-1, i.v., 15 min pretreatment) or prolonged (10 mg kg-1, s.c. daily for 3 days) systemic treatment with cyclosporin A had no effect on 111In-eosinophil accumulation or oedema formation induced by PAF, ZAP, LPS or in the PCA reaction. 6. In conclusion, we demonstrate preferential inhibitory effects of dexamethasone on 111In-eosinophil accumulation according to its site of administration. In addition we show that dexamethasone inhibits protein synthesis-independent acute inflammation in guinea-pig skin. Finally, our results do not support the concept that eosinophils are an important cellular site of action for the inhibitory effects of cyclosporin A in a guinea-pig model of allergic inflammation.

Animals↗
PubMed2003

A taste comparison of three different liquid steroid preparations: prednisone, prednisolone, and dexamethasone.

OBJECTIVES: To determine whether significant differences exist in the taste, texture, smell, and aftertaste of three commonly used liquid steroid preparations: prednisone, prednisolone, and dexamethasone. METHODS: This was a double-blind study of medical students and residents. Participants were asked to drink 5 mL of each steroid preparation, and grade each on a one-to-five-point scale for the categories of smell, texture, taste, and aftertaste. A score of 5 was considered most positive, 3 neutral, and 1 most negative. The medications were placed in small cups with the letter A, B, or C on them. The steroids were then administered in an advancing alphabetical format. A saltine cracker and water were administered between tastings in an attempt to remove any residual flavor. Data were analyzed using mean score and standard deviations, and mean rank and standard deviation by the Friedman test. Statistical significance was set at p < 0.05. RESULTS: Eighty-six adult volunteers participated in the study: 53 (62%) were male and 33 were female. The overall mean scores and standard deviations (+/-SDs) for prednisolone, dexamethasone, and prednisone were 3.43 (+/-1.05), 3.19 (+/-1.01), and 2.29 (+/-0.98), respectively. Using the Friedman test, the mean ranks for smell, texture, taste, and aftertaste for dexamethasone were 2.37, 2.06, 2.19, and 2.22. The corresponding mean ranks for prednisone were 1.80, 1.52, 1.31, and 1.27; and for prednisolone, the mean ranks were 1.83, 2.41, 2.51, and 2.52, respectively. Dexamethasone scored better in all four categories than prednisone (p < 0.05). Prednisolone scored better than prednisone in the categories of texture, taste, and aftertaste (p < 0.05); there was no statistical difference in smell. Dexamethasone had a higher mean rank than prednisolone for smell (p < 0.05); for the remaining three categories, there was no statistical difference. CONCLUSIONS: In adult volunteers, both prednisolone and dexamethasone liquid were more palatable than prednisone liquid.

Adult↗
PubMed2003

Intramuscular versus oral dexamethasone for the treatment of moderate-to-severe croup: a randomized, double-blind trial.

UNLABELLED: Glucocorticoids are an effective treatment for croup, although the most beneficial route of administration remains unclear. Recent studies have concluded that both intramuscular dexamethasone and oral dexamethasone are effective treatments, but there are few data directly comparing the two for moderate-to-severe croup. OBJECTIVES: The authors' primary objective was to determine whether there is a difference in proportion of children with resolution of symptoms attributable to croup at 24 hours, when treated with oral or intramuscular dexamethasone. Secondarily, the authors sought to estimate whether there is a difference in proportion of children with resolution of symptoms attributable to croup at 10 days and to estimate the interval to complete resolution of symptoms between these two routes. METHODS: The authors performed a prospective, randomized, double-blind trial involving children aged 3-84 months with moderate-to-severe croup, presenting to a suburban teaching emergency department (ED). Patients were eligible for enrollment if they had inspiratory stridor or a barky cough and a croup score of 2 or greater after 10-15 minutes of cool mist therapy. The patients were randomized to one of two intervention groups. In both groups, the parents were not present in the treatment room during study drug administration. One group received 0.6 mg/kg of intramuscular dexamethasone and an oral placebo, while the other group received 0.6 mg/kg of oral dexamethasone and direct pressure on their thigh with the hub of a syringe. A nurse placed a Band-Aid on the site of the real or mock injection. Parents were contacted by telephone approximately 1 and 10 days after the index visit to ask about their child's symptoms using a standardized questionnaire. Data were analyzed using an intention-to-treat approach. RESULTS: Of 126 patients eligible, 96 were recruited, with complete follow-up on 95. The groups were similar in all baseline characteristics, treatments received in the ED, and disposition. At 24 hours and 10 days after the visit, there were no statistical differences between the groups for the proportion with stridor, expiratory sounds, barky cough, sleep pattern, the degree of improvement, or the proportion with complete resolution of symptoms at one day. CONCLUSIONS: No statistical differences for any parameters were observed between intramuscular and oral dexamethasone treatments for children with moderate-to-severe croup at 24 hours or at any time the week after treatment. The durations of symptoms were similar between the treatment groups.

Administration, Oral↗
PubMed1996

Effects of dexamethasone on sleep.

The purpose of this study was to evaluate the effects of acute systemic corticosteroid administration on sleep structure in healthy individuals. We conducted a randomized, prospective, double-blind, placebo-controlled cross-over study of the effects of dexamethasone, 3 mg every eight hours for 48 hr on the sleep architecture of six normal volunteers (mean age 28 years, five males and one female). The subjects were participants blood pressure. Each subject was studied with a full polysomnogram on two successive nights when receiving either placebo or dexamethasone. Only the second night was used for analysis. Placebo and dexamethasone periods were separated by at least two weeks. There were significant increases in the REM latency, percent time spent awake and percent time spent in slow wave sleep in subjects taking dexamethasone when compared to their sleep while taking placebo. There were also significant decreases in the percent time spent in REM and the number of REM periods while on dexamethasone. We conclude that pharmacologic doseas of dexamethasone alter sleep architecture in healthy humans.

Adult↗
PubMed2005

Dexamethasone up-regulates skeletal muscle maximal Na+,K+ pump activity by muscle group specific mechanisms in humans.

Dexamethasone, a widely clinically used glucocorticoid, increases human skeletal muscle Na+,K+ pump content, but the effects on maximal Na+,K+ pump activity and subunit specific mRNA are unknown. Ten healthy male subjects ingested dexamethasone for 5 days and the effects on Na+,K+ pump content, maximal activity and subunit specific mRNA level (alpha1, alpha2, beta1, beta2, beta3) in deltoid and vastus lateralis muscle were investigated. Before treatment, maximal Na+,K+ pump activity, as well as alpha1, alpha2, beta1 and beta2 mRNA levels were higher (P < 0.05) in vastus lateralis than in deltoid. Dexamethasone treatment increased Na+,K+ pump maximal activity in vastus lateralis and deltoid by 14 +/- 7% (P < 0.05) and 18 +/- 6% (P < 0.05) as well as Na+,K+ pump content by 18 +/- 9% (P < 0.001) and 24 +/- 8% (P < 0.01), respectively. Treatment with dexamethasone resulted in a higher alpha1, alpha2, beta1 and beta2 mRNA expression in the deltoid (P < 0.05), but no effects on Na+,K+ pump mRNA were detected in vastus lateralis. In conclusion, dexamethasone treatment increased maximal Na+,K+ pump activity in both vastus lateralis and deltoid muscles. The relative importance of transcription and translation in the glucocorticoid-induced regulation of Na+,K+ pump expression seems to be muscle specific and possibly dependent on the actual training condition of the muscle, such that a high Na+,K+ pump maximal activity and mRNA level prior to treatment prevents the transcriptional response to dexamethasone, but not the increase in Na+,K+ pump content and maximal activity.

Administration, Oral↗
PubMed2003

Inhibition of inflammation and remodeling by roflumilast and dexamethasone in murine chronic asthma.

Phosphodiesterase (PDE) inhibitors have potential as alternatives or adjuncts to glucocorticoid therapy in asthma. We compared roflumilast (a selective PDE4 inhibitor) with pentoxifylline (a nonselective inhibitor) and dexamethasone in ameliorating the lesions of chronic asthma in a mouse model. BALB/c mice sensitized to ovalbumin were chronically challenged with aerosolized antigen for 6 weeks. During weeks 5 and 6, groups of animals were treated with roflumilast or dexamethasone by daily gavage or with pentoxifylline by daily intraperitoneal injection. Airway hyper-reactivity (AHR) was evaluated by whole-body plethysmography and airway lesions by histomorphometry and immunohistochemistry. Compared with vehicle alone, treatment with roflumilast or dexamethasone significantly reduced accumulation of eosinophils and chronic inflammatory cells, subepithelial collagenization, and thickening of the airway epithelium. Dexamethasone also reduced goblet cell hyperplasia/metaplasia, subepithelial accumulation of transforming growth factor-beta1, and epithelial cytoplasmic immunoreactivity for nuclear factor-kappaB. Treatment with pentoxifylline inhibited only eosinophil recruitment and epithelial thickening. Roflumilast and dexamethasone slightly decreased AHR, whereas this was significantly reduced by pentoxifylline. Thus, in this model of chronic asthma, both roflumilast and dexamethasone were potent inhibitors of airway inflammation and remodeling. Roflumilast did not diminish accumulation of transforming growth factor-beta1, suggesting that it might affect remodeling by mechanisms distinct from glucocorticoids.

Aminopyridines↗
PubMed1978

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

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

Amniotic Fluid↗
PubMed2003

Staphylococcal enterotoxin B-induced acute inflammation is inhibited by dexamethasone: important role of CXC chemokines KC and macrophage inflammatory protein 2.

This study was conducted to examine the anti-inflammatory mechanisms of dexamethasone during leukocyte recruitment and expression of the CXC chemokines macrophage inflammatory protein 2 (MIP-2) (CXCL2) and cytokine-induced neutrophil chemoattractant (KC) (CXCL1) in staphylococcal enterotoxin B (SEB)-induced acute inflammation. To do this, SEB was injected into murine air pouches with or without dexamethasone pretreatment for 2 h. SEB induced infiltration of leukocytes in a dose- and time-dependent manner, with the maximal response observed after 4 h of treatment with 10 microg of SEB. The recruited leukocytes comprised more than 77% neutrophils. Moreover, SEB challenge (10 microg) provoked time-dependent secretion of CXC chemokines, which peaked after 1 h. Local administration of antibodies against MIP-2 and KC significantly reduced SEB-triggered neutrophil accumulation by 38 and 59%, respectively. Dexamethasone (10 mg kg(-1)) significantly decreased neutrophil recruitment by 82% and reduced secretion of MIP-2 and KC by 89 and 85%, respectively, in response to SEB challenge. Our data demonstrate that dexamethasone potently inhibits neutrophil recruitment in SEB-induced inflammation. Moreover, we provide evidence that MIP-2 and KC are key mediators in the neutrophil response to SEB. Furthermore, our findings demonstrate that dexamethasone attenuates SEB-induced expression of MIP-2 and KC. Thus, this study elucidates important signaling pathways of SEB-induced neutrophil recruitment and anti-inflammatory mechanisms of action of dexamethasone.

Acute Disease↗
PubMed1992

Catabolic effect of dexamethasone in the preterm baby.

Most babies treated with dexamethasone for bronchopulmonary dysplasia exhibit an appreciable rise in the blood urea concentration, from a mean of 2.3 mmol/l before steroid to a mean of 7.1 mmol/l after. In order to discover whether this was primarily the result of increased protein catabolism, nitrogen balance studies before and after the start of dexamethasone were performed and a mean deficit in nitrogen retention of 158 mg/kg/24 hours was found. Similarly the urinary 3-methylhistidine (3MH):creatinine ratio before and after the commencement of dexamethasone treatment in a group of preterm babies was measured. It was found that there was a substantial increase in 3MH excretion after dexamethasone: from a mean 3MH:creatinine ratio of 46 in the week before steroids to a mean ratio of 77 in the week after. As 3MH emanates almost exclusively from the breakdown of actin in skeletal muscle cell, this finding implies the loss of muscle tissue. It was also found that the babies were in less positive nitrogen balance after dexamethasone, to a degree which is significant relative to their protein reserves. The long term consequences of a period of increased catabolism are not yet known but the authors suggest caution in the use of dexamethasone, at least in babies with milder degrees of bronchopulmonary dysplasia in whom the ratio of benefit to risk may be less favourable.

Bronchopulmonary Dysplasia↗
PubMed1996

Dexamethasone and bacterial meningitis in Pakistan.

The objective of this study was to assess, in a developing country setting, the effect of dexamethasone therapy on bacterial meningitis outcomes. A prospective double blind placebo controlled trial was conducted in 89 children aged from 2 months to 12 years suffering from bacterial meningitis. Neurological, developmental, and hearing assessments were conducted at one, four, and 12 months after discharge. Forty eight patients received dexamethasone and 41 placebo. Initial antimicrobial drugs used were ampicillin and chloramphenicol. For all patients at the time of admission the mean duration of illness was 5.7 days; 47% had had seizures and 56% had impaired consciousness. Seventeen of 89 (19%) patients died. The mortality for the dexamethasone group was 25% as compared with 12% in the group receiving placebo. Presentation to the hospital after four days of symptoms and with impaired conscious state were independent predictors of death. Of the dexamethasone group survivors, 26.5% had neurological sequelae and 42.3% had hearing impairment, whereas in the placebo group it was 24% and 30% respectively. Altered state of consciousness was a predictor of neurological sequelae. The presence of neurological sequelae and high cerebrospinal fluid protein independently predicted hearing loss. No beneficial effect of dexamethasone was observed on morbidity or mortality of this group of patients with bacterial meningitis. Dexamethasone is therefore not useful in developing countries as adjunctive treatment in patients seriously ill with bacterial meningitis, who present late for treatment and have been partially treated.

Ampicillin↗
PubMed2000

Effects of cyclosporin at various concentrations on dexamethasone intracellular uptake in multidrug resistant cells.

BACKGROUND: The multidrug resistance phenomenon results from the expression of P-glycoprotein (P-gp), a drug-efflux pump. Corticosteroids are substrates for P-gp, whose function can be inhibited by cyclosporin. This study evaluates the ability of cyclosporin to modulate dexamethasone uptake in multidrug resistant cells. METHODS: The K 562 cell line, which does not express P-gp and a P-gp expressing clone, K562/ADM, were used. Cells were incubated with H3-dexamethasone in the absence or presence of cyclosporin at various concentrations. Then, cells were washed, lysed, and radioactivity was measured. RESULTS: The uptake of dexamethasone alone was higher in sensitive than in resistant cells. Addition of cyclosporin induced a dose dependent increase of dexamethasone uptake in resistant cells, whereas the drug did not influence dexamethasone uptake in parental cells. CONCLUSION: Cyclosporin, at therapeutic concentrations induces a moderate, but significant increase in dexamethasone accumulation in multidrug resistant cells. Thus, cyclosporin might increase the intestinal absorption of corticosteroids or their accumulation in mononuclear cells, or both, thereby increasing their therapeutic efficacy.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1996

Effect of dexamethasone on IL-2 and IL-3 production by mononuclear cells in neonates and adults.

The effect of dexamethasone on interleukin 2 (IL-2) and interleukin 3 (IL-3) production by mononuclear cells in preterm and term infants and adults was evaluated. The capacity of mononuclear cells to produce these cytokines, in preterm infants with bronchopulmonary dysplasia (BPD) and treated with dexamethasone, was compared with that before treatment. Twenty six preterm and 36 term neonates and 24 healthy adults were included in the study. Mononuclear cells isolated from neonatal cord blood (CBMC) and adult peripheral blood (PBMC) were stimulated with phytohaemagglutinin (PHA) in the absence or presence of dexamethasone at concentrations between 10(-8)M and 10(-5)M. IL-2 and IL-3 activities in the supernatant fluids were tested using bioassays. The in vivo effect of the drug on the production of these cytokines by PBMC in 10 preterms was determined before and 24 hours after dexamethasone administration (0.5 mg/kg/day). The production of both cytokines was inhibited in a dose dependent manner. A difference in the sensitivity of mononuclear cells to the inhibitory effect of the drug was found between neonatal cord blood cells and adult PBMC, the former being more sensitive. PBMC from preterm infants treated with dexamethasone for BPD produced significantly less IL-2 and IL-3 as early as 24 hours after the initiation of the treatment (43% and 31%; P < 0.05, respectively). It is concluded that mononuclear cells from preterm and term neonates are more sensitive to the inhibitory effect of dexamethasone on IL-2 and IL-3 production.

Adult↗
PubMed1998

Cardiac effects of short course dexamethasone in preterm infants.

AIM: To examine the incidence and natural history of left ventricular hypertrophy (LVH) associated with the shorter 2-3 week course of dexamethasone, now more usual, for chronic lung disease. METHOD: Thirty one infants, gestational age 23-34 (median 26) weeks, birthweight 500-2054 (median 815)g, received dexamethasone, starting at 0.4-0.6 mg/kg/day, at a median of 11 days of age (range 2-34), weaning over a period of 2-3 weeks. Eighteen preterm neonates were studied as controls over a similar time period. Serial echocardiographic measurements of end diastolic interventricular septum (IVSd) and left ventricular posterior wall (LVPWd) thicknesses were taken before, and up to 48 days after, starting dexamethasone. Maximum Doppler blood flow velocities from the left ventricular outflow tract (LVOT) were measured. RESULTS: Left ventricular hypertrophy (LVH) occurred in 29 babies (94%). Median hypertrophy of the IVSd in those receiving dexamethasone was 67% and LVPWd 56% of baseline measurements, significantly greater than control infants (p < 0.001). LVH appeared by a median of three days, peaking by a median of 10 days. All resolved by a median of 27 days. LVOT obstruction was not seen. There was no significant correlation with birthweight, gestation, blood pressure, or glucose tolerance. CONCLUSIONS: LVH developed in almost all preterm neonates receiving a 2-3 week course of dexamethasone, but was of little clinical importance and always resolved. Echocardiography is probably not required routinely in infants receiving such short course dexamethasone for chronic lung disease.

Anti-Inflammatory Agents↗