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PubMed1981

The effect of dexamethasone on the radiation survival response and misonidazole-induced hypoxic-cell cytotoxicity in Chinese hamster cells V-79-753B in vitro.

Overnight exposure of Chinese hamster cells, V-79-753B, to microgram quantities of the synthetic corticosteroid, dexamethasone, resulted in a decrease in sensitivity towards radiation, both in air and in hypoxia. The effect was dose-modifying and the oxygen enhancement ratio did not change appreciably. Similarly, when dexamethasone-treated hypoxic cells were irradiated in the presence of misonidazole, a hypoxic cell radiosensitizer, there was a decrease in radiation sensitivity compared with untreated hypoxic cells irradiated with misonidazole. The effect of dexamethasone cannot be attributed to classical radioprotection since administration of the drug immediately or 4.5 h before irradiation does not alter the survival response of hypoxic cells with or without misonidazole. Neither can this increased radioresistance be attributed to synchronization to a more resistant phase of the cell cycle since pretreated cells remain more radioresistant for at least 6 h after the removal of the drug. The data suggest that dexamethasone induces metabolic changes in cells which alter their radiosensitivity. Whatever metabolic changes may be occurring there was no effect on the uptake of 14C-misonidazole into dexamethasone-treated or control cells. However, there was a pronounced decrease in hypoxic-cell cytotoxicity induced by misonidazole in cells pretreated with dexamethasone. The implications of these results are discussed.

Animals↗
PubMed2005

Interaction between dexamethasone treatment and the corticotropin stimulation test in septic shock.

OBJECTIVE: To review dexamethasone interaction with corticotropin stimulation testing, particularly as it applies to treating septic shock. DATA SOURCES: Pertinent literature was identified through MEDLINE (1966-February 2004) using combinations of the key words dexamethasone, adrenocorticotropic hormone stimulation, and pretreat. Only articles written in the English language and evaluating human subjects were considered. Reference lists of identified articles were reviewed for additional citations. DATA SYNTHESIS: Accurate interpretation of the corticotropin stimulation test is important to identify patients with septic shock who may benefit from corticosteroid supplementation. In healthy volunteers, short-term dexamethasone administration prior to the corticotropin stimulation test may depress the baseline cortisol level, but does not inhibit the response to the corticotropin challenge. This may result in a slight increase in the difference between baseline and post-stimulation values. CONCLUSIONS: In 2 small trials in healthy adults, short-term, low-dose dexamethasone pretreatment decreased baseline cortisol levels, but values following corticotropin stimulation were unaffected. Accordingly, caution in interpreting corticotropin stimulation test results is warranted. However, the application of the findings from these studies to patients with septic shock is difficult, given the important differences in physiology between normal and septic patients. As of December 29, 2004, a dexamethasone dose >2 mg or prolonged dexamethasone therapy (>2 days, totaling 4 mg) preceding corticotropin stimulation has not been studied in any population.

Adrenocorticotropic Hormone↗
PubMed1994

Effect of intratracheal dexamethasone on oleic acid-induced lung injury in the rat.

The therapeutic efficacy of single-dose intratracheal dexamethasone (2.5 mg/kg) in oleic acid-induced acute lung injury in the rat was established by showing significant improvement in bronchoalveolar lavage parameters and lung compliance at 24 h after oleic acid as compared with animals not treated with oleic acid. An equivalent dose of intraperitoneal dexamethasone demonstrated no therapeutic benefit at 24 h after oleic acid. The therapeutic effect of this single-dose intratracheal dexamethasone regimen was accompanied by recovery to normal bronchoalveolar parameters and lung compliance at 7 days, in contrast to previous observations made with high-dose sustained intraperitoneal dexamethasone (4 mg/kg for 7 days). This improved benefit:toxicity ratio of intratracheal dexamethasone compared with systemic dexamethasone may be due to enhanced topical anti-inflammatory potency relative to systemic potency and toxicity.

Animals↗
PubMed1989

Dexamethasone as prophylaxis for acute mountain sickness. Effect of dose level.

Rapid exposure of unacclimatized persons to high altitude causes the syndrome acute mountain sickness (AMS). Prophylactic treatment with frequent high doses of dexamethasone has been shown to prevent AMS. To determine whether lower, less frequent doses were effective in preventing AMS, 28 men between the ages of 18 and 32 were exposed to a simulated altitude of 4,570 m for 45 h in a hypobaric chamber on two occasions while taking one of three doses of dexamethasone (4 mg, 1 mg, or .25 mg every 12 h) or a placebo in a double-blind, crossover design. The 4-mg dose of dexamethasone reduced the incidence of AMS symptoms compared with placebo and the other dose levels. Dexamethasone did not alter fluid balance or plasma volume changes, but treatment with 1 mg and 4 mg suppressed cortisol secretion. There was no evidence of adrenal cortical suppression after treatment with dexamethasone or placebo 48 h after discontinuing altitude exposure and drug treatment. The results indicate that 4 mg of dexamethasone twice daily is an effective prophylactic treatment for AMS, while lower doses are relatively ineffective.

Adolescent↗
PubMed2006

Adiponectin and resistin in the neonatal rat: effects of dexamethasone and hypoxia.

Hypoxia is a common neonatal stress that induces insulin resistance and a decrease in body weight gain. Dexamethasone is often used to treat neonatal cardiopulmonary disease, and also leads to insulin resistance and a decrease in body weight gain. The current study addressed the hypothesis that serum concentrations of the adipokines adiponectin and/or resistin are altered during hypoxia and/or dexamethasone therapy in neonatal rats. Rat pups with their lactating dams were exposed to hypoxia (11% O2) from birth and treated with a tapering regimen of dexamethasone from postnatal day (PD) 3-6. Serum adiponectin and resistin were measured on PD7. Hypoxia and dexamethasone independently decreased body weight gain and increased adiponectin levels. The combination of hypoxia and dexamethasone did not further increase adiponectin. Dexamethasone caused a small increase in resistin in normoxic pups, which may facilitate the hyperinsulemic- normoglycemic state we previously described. We also conclude that adiponectin is increased during hypoxia in response to a decrease in the sensitivity to insulin.

Adiponectin↗
PubMed1981

[The effects of dexamethasone and captopril on plasma aldosterone response to exogenous angiotensin II in normal men (author's transl)].

The response of plasma aldosterone to exogenous angiotensin II was evaluated in five normal volunteers on three occasions, once without endogenous ACTH or angiotensin II suppression (control), once with ACTH suppression (dexamethasone) and once with ACTH and angiotensin II suppression (dexamethasone and captopril). Plasma aldosterone concentration (PAC) fell from a control of 6.8 +/- 1.6 (mean +/- SEM) to 4.4 +/- 0.4 ng/dl with dexamethasone (p less than 0.05) and to 1.8 +/- 0.2 ng/dl with dexamethasone and captopril (p less than 0.001). PAC increased dose-dependently upon infusion rates of angiotensin II (0.2, 0.4, 0.8, 1.0, 1.2, 2.5 and 5.0 ng/kg/min) on each occasion, but aldosterone responsiveness to infused angiotensin II (change and percentage from base line levels) was not altered by the suppression of endogenous ACTH secretion with dexamethasone with each incremental infusion of the octapeptide. However, change in PAC caused by angiotensin II in the suppression of ACTH and angiotensin II was greater than that in the control at an infusion rate of 0.2 ng/kg/min (p less than 0.05), 1.2 ng/kg/min (p less than 0.05) and 2.5 ng/kg/min (p less than 0.01), and it was also greater than that in the suppression of ACTH at an infusion rate of 0.2 ng/kg/min (p less than 0.05) and 2.5 ng/kg/min (p less than 0.01). These results demonstrate that in normal men, base line aldosterone levels are controlled not only by the renin-angiotensin system, but also, in part, by ACTH. The aldosterone response to angiotensin II, however, does not depend upon endogenous ACTH secretion, an action of angiotensin II on the pituitary to release ACTH. Simultaneous administration of dexamethasone and captopril may be a useful tool to assess the sensitivity of aldosterone production in the adrenal glomerulosa with exogenous angiotensin II since endogenous ACTH and angiotensin II can be suppressed by these medications.

Adult↗
PubMed1998

Long term follow-up of a 46,XY phenotypic girl with 17alpha-hydroxylase deficiency treated with alternate-day dexamethasone.

We report an 18-year-old 46,XY phenotypic girl who has been on alternate-day dexamethasone therapy for 10 years. The patient was seen at our hospital for right-sided inguinal hernia at the age of 4 years. Biopsy of the herniated gonad showed testicular tissue, and the karyotype of the peripheral lymphocytes was 46,XY. The diagnosis of 17alpha-hydroxylase deficiency was established by the evaluation of adrenal steroidogenesis at the age of 6.1 years when hypertension was clearly recognized, and was confirmed later by the gene analysis of CYP17 which disclosed a compound heterozygote. The growth rate was suppressed during the initial treatment with daily administration of 0.25-0.5 mg dexamethasone. Switching to alternate-day regimen of dexamethasone 0.5 mg/dose improved height velocity. Subsequent addition of low-dose estrogen therapy induced pubertal growth spurt. The blood pressure and adrenal hormone levels remained almost within the normal range throughout the course. Adrenal function was evaluated at the age of 15 years. Plasma ACTH and corticosterone levels were high only just before the next administration, when the plasma dexamethasone concentration should be at the nadir. Since corticosterone possesses glucocorticoid activity and can work as a glucocorticoid reserve, it is assumed that this mode of dexamethasone administration can be a safe treatment for this disorder. We conclude that the patient with childhood 17alpha-hydroxylase deficiency can be safely and effectively treated with alternate-day dexamethasone without interfering with linear growth.

Adolescent↗
PubMed1983

The glucagon-insulin antagonism and glucagon-dexamethasone synergism in the induction of phosphoenolpyruvate carboxykinase in cultured rat hepatocytes.

In hepatocytes precultured for 24 h with dexamethasone glucagon increased phosphoenolpyruvate carboxykinase activity 3-4-fold with a half maximal activity increase at 30 pM. The half maximal effective glucagon concentration was enhanced 10-fold to 300 pM when insulin was added simultaneously. The glucagon-insulin antagonism was maximally expressed when glucagon was present at low physiological concentrations. At equimolar doses it was only in the concentration range around 0.1 nM that glucagon and insulin became powerful antagonists; at higher levels glucagon was the dominant hormone. In hepatocytes not pretreated with dexamethasone glucagon still enhanced phosphoenolpyruvate carboxykinase activity, but the half maximal effective dose raised more than 30-fold to 1 nM. The degree of stimulation, however, remained essentially unchanged. Thus dexamethasone shifted the glucagon sensitivity of the cells into the physiological concentration range; it exerted a half maximal effect at 10 nM. Dexamethasone was not required for the enzyme induction proper if the cells had been pretreated with the glucocorticoid. The amount of the glucagon-stimulated enzyme induction was dependent on the time period of cell pretreatment with dexamethasone. Glucagon enhanced enzyme activity to the same constant suboptimal level irrespective of whether cells had been pretreated with glucocorticoid for 1 or for 14 h. If cells were pretreated for more than 15 h, glucagon linearly increased enzyme activity further until the maximal value was reached after 24 h pretreatment. The glucagon-insulin antagonism and the glucagon-glucocorticoid synergism were observed at physiological hormone concentrations indicating that the interaction should be effective also in vivo. Dexamethasone does not seem to be generally permissive for the inducing action of glucagon, but rather sensitizes the cell towards lower physiological hormone concentrations.

Animals↗
PubMed1985

Cyclic Cushing's syndrome combined with cortisol suppressible, dexamethasone non-suppressible ACTH secretion: a new variant of Cushing's syndrome.

A 55 year old woman with an unusual form of Cushing's disease was studied. During several periods (periods lasting up to 84 days) evidence of cortisol hypersecretion with cycles occurring every 6 days was found. Suppression of plasma cortisol through orally administered dexamethasone (up to 32 mg per day) could not be achieved either during periods of cyclic cortisol hypersecretion or during apparent remission with normal cortisol secretion. Marked suppression of plasma ACTH was measured in response to an iv infusion of 50 mg cortisol over a period of 55 min whereas a similar test with 2 mg dexamethasone (iv bolus) did not suppress ACTH secretion. Transsphenoidal exploration of the sella revealed a tumour surrounding the anterior pituitary. Examination of the pituitary showed a few tiny tumour structures embedded in normal tissue which could not be removed, when the tumour was resected selectively under preservation of normal appearing tissue. Post-operatively, clinical and chemical remission (normal response to 1 mg dexamethasone) was observed for about 4 months. Thereafter, cortisol hypersecretion occurred again necessitating bilateral adrenalectomy. Our results are compatible with the assumption that normal hypothalamic-pituitary-adrenal suppressibility with cortisol, but not with dexamethasone, was caused by the loss of feedback receptors for dexamethasone in the presence of cortisol receptors in the cells which secrete ACTH or CRF. The combination of cyclic hypercortisolism with dexamethasone non-suppressible Cushing's syndrome has not been reported before and thus represents a new variant of Cushing's syndrome.

Adrenocorticotropic Hormone↗
PubMed1994

Oral dexamethasone administration: new pharmacological test for the assessment of growth hormone secretion.

Acute intravenous (i.v.) dexamethasone administration has been described recently as a new test for the diagnosis of growth hormone (GH) deficiency. In the present study, a new protocol of dexamethasone administration was evaluated. Twelve normal adults and 18 normal prepubertal children were studied. The dexamethasone i.v. test was performed in six adults at a dose of 4 mg and 12 children at a dose of 2 mg/m2. Blood samples were collected 15 min before, at time zero and every 15 or 30 min during 5 h, resulting in a total of 16 samples. In the remaining six adults and six children, 8 and 4 mg, respectively, of dexamethasone were administered orally at the subject's home, and blood sampling started 90 min later when they arrived at the hospital. Plasma GH was measured by radioimmunoassay. The dexamethasone-induced GH response (mean +/- SEM, micrograms/l) to the i.v. or oral protocol did not differ in either the adults (i.v. 8.2 +/- 2.1; oral 8.0 +/- 1.6) or the children (i.v. 14.9 +/- 1.3; oral 13.6 +/- 1.8). It is concluded that the simpler protocol of acute oral dexamethasone administration hereby presented can be a safe and suitable test of GH secretion.

Administration, Oral↗
PubMed1995

Lack of growth hormone response to acute administration of dexamethasone in anorexia nervosa.

High plasma growth hormone (GH) levels, associated with abnormal hormone responses to provocative stimuli, point to an altered GH secretion in anorexia nervosa. The GH-releasing effect of acutely administered glucocorticoids, firmly established in normal subjects, has not been reported in these patients. In this study, acute iv administration of 4 mg of dexamethasone, compared with saline, increased plasma GH in nine normal-weight women (AUC 848.2 +/- 127.95 vs 242.8 +/- 55.35 micrograms.l-1.min-1, p < 0.05, respectively) but was ineffective in 11 anorectic patients (AUC 3271.8 +/- 1407.11 vs 2780.0 +/- 1162.04 micrograms.l-1.min-1, NS). After dexamethasone, a significant lowering of plasma cortisol was observed in normal women (AUC 25367.0 +/- 3128.43 vs 47347.1 +/- 4456.61 nmol.l-1.min-1, after dexamethasone and saline, respectively, p < 0.05), but not in anorectic patients (AUC 77809.3 +/- 8499.92 vs 78454.9 +/- 7603.62 nmol.l-1.min-1, NS). In both groups, plasma adrenocorticotrophin (ACTH) displayed a significant decrease after dexamethasone (AUC 523.6 +/- 92.08 vs 874.2 +/- 115.03 pmol.l-1.min-1, p < 0.05, after dexamethasone and saline, respectively, in anorectic patients and 377.5 +/- 38.41 vs 1004.9 +/- 200.51 pmol.l-1.min-1, p < 0.05, in controls). However, when considering the hormonal decremental areas, a significant dexamethasone-induced ACTH inhibition, compared to saline, was evidenced in normal (delta AUC -414.4 +/- 65.75 vs 222.9 +/- 42.40 pmol.l-1.min-1, p < 0.05) but not in anorectic women (delta AUC -254.2 +/- 96.92 vs 2.9 +/- 132.32 pmol.l-1.min-1, NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1999

Randomized placebo-controlled trial of a 42-Day tapering course of dexamethasone to reduce the duration of ventilator dependency in very low birth weight infants.

OBJECTIVE: To assess the effect on duration of ventilator dependency of a 42-day tapering course of dexamethasone in very low birth weight neonates. METHODS: Infants (N = 118) were assigned randomly, within birth weight/gender strata, to treatment with either a 42-day tapering course of dexamethasone or an equal volume of saline as placebo. Entry criteria were 1) birth weight <1501 g; 2) age between 15 and 25 days; 3) <10% decrease in ventilator settings for 24 hours and FIO2 >/=0.3; 4) absence of patent ductus arteriosus, sepsis, major congenital malformation, congenital heart disease; and 5) no evidence of maternal HIV or hepatitis B infection. The dosage schedule was 0.25 mg/kg bid for 3 days, then 0.15 mg/kg bid for 3 days, then a 10% reduction in the dose every 3 days until a dose of 0.1 mg/kg had been given for 3 days, from which time a dose of 0.1 mg/kg qod was continued until 42 days after entry. The primary endpoint was the number of days on assisted ventilation after study entry. Secondary outcomes of interest included days on supplemental oxygen, days of hospitalization, and potential adverse effects, such as infection, gastrointestinal bleeding, left ventricular hypertrophy, and severe retinopathy of prematurity. RESULTS: Infants in the dexamethasone- and placebo-treated groups were similar in terms of baseline attributes, including birth weight, gestational age, gender, race, and ventilator settings at entry. Infants treated with dexamethasone were on assisted ventilation and supplemental oxygen for fewer days after study entry (median days on ventilator, 5th and 95th percentiles, 13 [1-64] vs 25 [6-104]; days on oxygen, 59 [6-247] vs 100 [11-346]). No differences were found in risk of death, infection, or severe retinopathy. In subgroup analyses, the association of dexamethasone with more rapid weaning from the ventilator was weaker among infants enrolled before the 16th day of life, infants with chest radiographs showing cystic changes and/or hyperinflation, and infants requiring an FIO2 >/=0.7 or a peak inspiratory pressure >/=19 at study entry. CONCLUSIONS: A 42-day tapering course of dexamethasone decreases the duration of ventilator and oxygen dependency in very low birth weight infants and is not associated with an increased risk of short-term adverse effects.

Confounding Factors, Epidemiologic↗
PubMed1999

Dexamethasone therapy increases infection in very low birth weight infants.

BACKGROUND: Infection is a major complication of preterm infants, resulting in increased morbidity and mortality. We recently reported the results of a multicenter trial of dexamethasone initiated at 14 or 28 days in very low birth weight (VLBW) infants who were at risk for chronic lung disease; the results showed an increase in nosocomial bacteremia in the group receiving dexamethasone. This study is an in-depth analysis of bacteremia/sepsis and meningitis among infants enrolled in the trial. METHODS: Data on cultures performed and antibiotic therapy were collected prospectively. Infections were classified as definite or possible/clinical. RESULTS: A total of 371 infants were enrolled in the trial. There were no baseline differences in risk factors for infection. For the first 14 days of study, infants received either dexamethasone (group I, 182) or placebo (group II, 189). During this period, infants in group I were significantly more likely than those in group II to have a positive blood culture result (48% vs 30%) and definite bacteremia/sepsis/meningitis (22% vs 14%). Over the 6-week study period, 47% of those cultured had at least one positive blood culture result (53% in group I vs 41% in group II) and 25% of the infants had at least one episode of definite bacteremia/sepsis/meningitis (29% in group I vs 21% in group II). Among infants with definite infections, 46.8% were attributable to Gram-positive organisms, 26.6% to Gram-negative organisms and 26.6% to fungi. The factors present at randomization were evaluated for their association with infection. Group I assignment and H(2) blocker therapy (before study entry) were associated with increased risk of definite infection, whereas cesarean section delivery and increasing birth weight were associated with decreased risk. CONCLUSIONS: Infants who received a 14-day course of dexamethasone initiated at 2 weeks of age were more likely to develop a bloodstream or cerebrospinal fluid infection while on dexamethasone therapy than were those who received placebo. Physicians must consider this increased risk of infection when deciding whether to treat VLBW infants with dexamethasone.

Cross Infection↗
PubMed2000

Outpatient treatment of moderate croup with dexamethasone: intramuscular versus oral dosing.

OBJECTIVE: Steroid use for the treatment of croup has been supported by several studies, although few have addressed the use of oral dexamethasone for outpatient management. The efficacy of oral (PO) versus intramuscular (IM) dosing of dexamethasone in the outpatient treatment of moderate croup are compared in this study. METHODS: Patients between the ages of 3 months and 12 years with moderate croup (history or presence of stridor, cyanosis, or retractions) were eligible for enrollment in this single-blind, prospective study. Patients were randomized to receive a single dose (0.6 mg/kg, maximum 8 mg) of IM or PO dexamethasone. Parents were contacted by phone to assess resolution of symptoms and need for further evaluation. RESULTS: Two hundred seventy-seven patients were enrolled (median age: 2.1 years). One hundred thirty-nine patients received IM dexamethasone, and 138 received PO. At phone follow-up, 141 (51%) had total resolution of symptoms (75 in IM, 66 in PO). Eighty patients (29%) returned for further evaluation (45 in IM, 35 in PO). Twenty-three (8%) received either more steroids, racemic epinephrine, or admission (11 in IM, 12 in PO). CONCLUSION: No statistically significant difference was found in the need for subsequent interventions after a single dose of either IM or PO dexamethasone. A single PO dose of dexamethasone can be effectively and safely used for the outpatient treatment of moderate croup.

Administration, Oral↗
PubMed2002

Controlled trial of early dexamethasone treatment for the prevention of chronic lung disease in preterm infants: a 3-year follow-up.

OBJECTIVE: There is increasing concern in regard to the possible long-term adverse effects of postnatal dexamethasone treatment in preterm infants. The purpose of this study was to assess growth and neurodevelopmental outcome in preterm infants at high risk of chronic lung disease (CLD), treated with early (<96 hours) postnatal dexamethasone. DESIGN: Three-year follow-up data of physical growth and neurodevelopmental outcome of preterm infants enrolled in a controlled trial to study the effectiveness of early postnatal dexamethasone administration for the prevention of CLD were reviewed. The original trial included 25 treated neonates who received dexamethasone intravenously from the fourth day of life for 7 days (0.5 mg/kg/d for the first 3 days, 0.25 mg/kg/d the next 3 days, and 0.125 mg/kg/d on the seventh day), and 25 untreated neonates as controls. Forty-five surviving infants (22 untreated and 23 treated) completed the 3-year follow-up. RESULTS: At the end of follow-up, infants pertaining to both study groups had similar values for body weight, height, and head circumference, and a similar incidence of infants with anthropometrics data below the third percentile. Moreover, no differences were detected between the groups in regard to incidence of major cranial ultrasound abnormalities, cerebral palsy, major neurosensory impairment or IQ scores, and distribution. CONCLUSIONS: Early (<96 hours) postnatal dexamethasone administration at the doses employed in this study did not impair physical or neurodevelopmental outcome in preterm infants at high risk of CLD. However, the small sample size of our study was not tailored to look for long-term outcomes and our results are not in agreement with those of larger trials and systematic reviews. The real risks of postnatal dexamethasone administration could be definitely assessed only when more well-designed trials using long-term neurodevelopmental assessment as the primary outcome will be reported.

Anti-Inflammatory Agents↗
PubMedDate not supplied

Prenatal tracheal ligation or intra-amniotic administration of surfactant or dexamethasone prevents some structural changes in the pulmonary arteries of surgically created diaphragmatic hernia in rabbits.

PURPOSE: Characterization of the structural changes occurring in the pulmonary arteries resulting from surgically produced congenital diaphragmatic hernia in rabbits, with particular emphasis on the preventive effects of prenatal tracheal ligation or administration of intra-amniotic dexamethasone or surfactant. METHODS: Twenty rabbit fetuses underwent surgical creation of a left-sided congenital diaphragmatic hernia on the 24th or 25th gestational day. They were divided according to the following procedures: congenital diaphragmatic hernia (n = 5), congenital diaphragmatic hernia plus tracheal ligation (n = 5), congenital diaphragmatic hernia plus intra-amniotic administration of dexamethasone 0.4 mg (n = 5) or surfactant (Curosurf 40 mg, n = 5). On gestational day 30, all the fetuses were delivered by caesarean section and killed. A control group consisted of five nonoperated fetuses. Histomorphometric analysis of medial thickness, cell nuclei density, and elastic fiber density of pulmonary arterial walls was performed. RESULTS: Arteries with an external diameter > 100 microm have a decreased medial thickness, lower cell nuclei density, and greater elastic fiber density when compared with arteries with external diameter < or = 100 microm. Congenital diaphragmatic hernia promoted a significant decrease in medial thickness and an increase in cell nuclei density in artery walls with external diameter > 100 microm. Prenatal treatments with tracheal ligation or intra-amniotic administration of dexamethasone or surfactant prevented these changes. In arteries with external diameter < or = 100 microm, congenital diaphragmatic hernia promoted a significant increase in medial thickness and in cell nuclei density and a decrease in elastic fiber density. The prenatal treatments with tracheal ligation or intra-amniotic administration of dexamethasone or surfactant prevented these changes, although no effect was observed in elastic fiber density in the congenital diaphragmatic hernia plus dexamethasone group. CONCLUSIONS: Congenital diaphragmatic hernia promoted different structural changes for large or small arteries. The prenatal intra-amniotic administration of dexamethasone or surfactant had positive effects on the lung structural changes promoted by congenital diaphragmatic hernia, and these effects were comparable to the changes induced by tracheal ligation.

Amnion↗
PubMed1999

Pharmacological and histopathological study of cyclophosphamide-induced hemorrhagic cystitis - comparison of the effects of dexamethasone and Mesna.

Chemotherapy with oxazaphosphorines, such as cyclophosphamide (CYP), is often limited by unacceptable urotoxicity. Without uroprotection, hemorrhagic cystitis (HC) becomes dose-limiting. To compare the uroprotective efficacy of classical 2-mercaptoethanesulfonic acid (Mesna) treatment with dexamethasone in CYP-induced HC, male Wistar rats (150-200 g; N = 6 in each group) were treated with saline or Mesna (40 mg/kg, ip) immediately and 4 and 8 h after ip administration of CYP (200 mg/kg). One, 2 or 3 doses of Mesna were replaced with dexamethasone (1 mg/kg, ip). The animals were sacrificed 24 h later. Cystitis was evaluated by determining the changes in bladder wet weight (BWW) and by macroscopic and microscopic analysis. CYP treatment induced a marked increased in BWW (162%, P<0.05), which was significantly inhibited by treatment with 3 doses of Mesna (P<0.05; 80%). The replacement of 1 or 2 doses of Mesna with dexamethasone reduced the increase in BWW by 83.3 and 95%, respectively. Macroscopic analysis of the bladder of rats with CYP-induced HC showed severe edema and hemorrhage, confirmed by microscopic analysis, that also showed mucosal erosion, inflammatory cell infiltration and ulcerations. The replacement of 1 or 2 doses of Mesna with dexamethasone inhibited the CYP-induced increase in BWW and almost abolished the macroscopic and microscopic alterations, with no significant difference between the effects of Mesna and dexamethasone, indicating that both drugs were efficient in blocking HC. However, although the replacement of all Mesna doses with dexamethasone reduced the edema, it did not prevent HC, suggesting that Mesna is necessary for the initial uroprotection.

Animals↗
PubMed2006

Effects of single dose of dexamethasone on patients with systemic inflammatory response.

CONTEXT AND OBJECTIVE: Systemic inflammatory response syndrome (SIRS) is a very common condition among critically ill patients. SIRS, sepsis, septic shock and multiple organ dysfunction syndrome (MODS) can lead to death. Our aim was to investigate the efficacy of a single dose of dexamethasone for blocking the progression of systemic inflammatory response syndrome. DESIGN AND SETTING: Prospective, randomized, double-blind, single-center study in a postoperative intensive care unit (Surgical Support Unit) at Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo. METHODS: The study involved 29 patients with SIRS. All eligible patients were prospectively randomized to receive either a single dose of 0.2 mg/kg of dexamethasone or placebo, after SIRS was diagnosed. The patients were monitored over a seven-day period using Sequential Organ Failure Assessment score (SOFA). RESULTS: The respiratory system showed an improvement on the first day after dexamethasone was administered, demonstrated by the improved PaO2/FiO2 ratio (p < 0.05). The cardiovascular system of patients requiring vasopressor therapy also improved over the first two days, with a better evolution in the dexamethasone group (p < 0.05). Non-surviving patients presented higher lactate assays than did survivors (p < 0.05) during this period. CONCLUSIONS: Dexamethasone enhanced the effects of vasopressor drugs and evaluation of the respiratory system showed improvements (better PaO2/FiO2 ratio), one day after its administration. Despite these improvements, the single dose of dexamethasone did not block the evolution of SIRS.

Adolescent↗