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PubMed1997

Transcriptional induction of cholesterol 7alpha-hydroxylase by dexamethasone in L35 hepatoma cells requires sulfhydryl reducing agents.

It is known that hepatic levels of reduced glutathione correlate with the activity of the liver-specific enzyme cholesterol-7alpha-hydroxylase. We examined the possibility that sulfhydryl reducing agents activate transcription of cholesterol 7alpha-hydroxylase. Adding dithiothreitol (DTT, 1 mM) and dexamethasone to L35 hepatoma cells increased the content of 7alpha-hydroxylase mRNA 3-fold above the levels observed with dexamethasone alone. Without dexamethasone, DTT had no affect. The addition of reduced glutathione to L35 cells demonstrated a similar potentiation of expression dependent on dexamethasone. Nuclear run-on assays showed that in the presence of both dexamethasone and DTT, the transcription of the 7alpha-hydroxylase gene was clearly increased. In contrast, by itself, dexamethasone did not cause a detectable increase in the transcription of the 7alpha-hydroxylase gene. Dexamethasone and DTT did not affect the transcription of beta-actin, suggesting a selective induction of the 7alpha-hydroxylase gene. DTT reversed repression of 7alpha-hydroxylase expression by insulin but not the repression by phorbol ester. Our data show for the first time that the sulfhydryl redox potential of the hepatocyte (i.e. level of reduced glutathione) has a marked influence on the transcription and expression of the liver-specific gene 7alpha-hydroxylase.

Animals↗
PubMed1998

Effects of dexamethasone in rat neonatal model of axotomy-induced motoneuronal cell death.

In this study the effect of dexamethasone on the motoneuronal cell death and the nuclear and somatic morphology changes occurring after peripheral nerve transection in the neonatal rats has been determined. The study was performed on 3 day old Wistar rats. Animals were divided into 3 groups--control, axotomised, and axotomised and dexamethasone-treated. The nerve transection was performed bilaterally. A dose of 0.5 mg/kg/24h dexamethasone, administered i.p., was used. On day 7 after the operation the animals were sacrificed and the motoneurons in segments L4 and L5 in the spinal cord were counted and their morphology was analysed. 25. 88% cell loss was found in the axotomised group (p<0.001 vs. control) versus 43.33% cell loss in the dexamethasone-treated and axotomised animals (p<0.01 vs. control). Dexamethasone significantly decreased the number of the surviving motoneurons (p<0.05 vs. axotomised). The axotomised group showed enlargement of the somatic area and the maximal and minimal diameters of the cell while the dexamethasone-treated and axotomised group showed soma shrinkage and decrease in the minimal cell diameter. Our results propose a possible hazard towards the application of dexamethasone in the treatment of new-borns with concomitant nerve injuries.

Animals↗
PubMed1999

Effect of topically applied 0.1% dexamethasone on endothelial healing and aqueous composition during the repair process of rabbit corneal alkali wounds.

PURPOSE: The effects of topical dexamethasone on the endothelial healing and the change of aqueous compositions were investigated during the repair process of alkali-wounded rabbit cornea. METHODS: A central corneal alkali wound was produced by a 60 sec application of a 5.5 mm round filter paper soaked in 1N NaOH onto one eye of each rabbit. The eyes subsequently were treated topically with either 0.1% dexamethasone or a balanced salt solution (BSS) 4 times per day for 8 weeks. Endothelial wound morphometry was performed after alizarin red and trypan blue staining. The concentrations of ascorbic acid, glucose, and the ions, Na+, K+, Ca2+ and Mg2+, were measured in the aqueous humor. RESULTS: Endothelial healing in control (alkali-wounded but not treated with dexamethasone) corneas showed a biphasic pattern of healing: an initial short-term healing for the first week and then a late long-term healing following the secondary endothelial breakdown. Topical administration of 0.1% dexamethasone deterred endothelial healing during the early period and prevented the secondary endothelial breakdown. However, the total repair process of endothelium was accelerated by the dexamethasone-treatment. Among the various components of the aqueous humor examined, ascorbic acid seemed the most sensitive to change caused by the alkali injury and dexamethasone treatment. CONCLUSIONS: The present data indicate that dexamethasone may have a therapeutic potential in the management of endothelial healing after corneal alkali injury.

Administration, Topical↗
PubMed2006

Effect of topical dexamethasone versus rimexolone on middle ear inflammation in experimental otitis media with effusion.

CONCLUSION: The lipopolysaccharide (LPS)-induced chinchilla otitis media (OM) model was proven useful in screening anti-inflammatory agents for topical use. Both 1% rimexolone and 1% dexamethasone are effective in reducing the volume of middle ear effusion and mucosal thickness compared with control groups. Topical corticosteroid therapy was efficacious in reducing middle ear mucosal inflammation. OBJECTIVE: OM is one of the most common diseases in the pediatric population. Our previous studies have shown that treatment with systemic antibiotics and corticosteroids was more efficacious than antibiotics alone. The purpose of this study was to determine the effectiveness of topically applied corticosteroids on the outcome of OM. The long-term goal of this study was to develop a better method of OM treatment by demonstrating effectiveness of topically applied anti-inflammatory agents, such as corticosteroids, avoiding systemic side effects. MATERIALS AND METHODS: Three experimental groups were studied in chinchillas. OM with effusion was induced in all groups by injecting LPS. Group 1 consisted of controls in three subgroups as follows. Control-LPS alone, vehicle of dexamethasone (control-dexa), vehicle of rimexolone (control-rimex). Group 2 was treated with dexamethasone and included subgroups of separate concentrations of dexamethasone: 0.1% and 1% suspensions. Group 3 was treated with rimexolone and included subgroups of separate concentrations of rimexolone: 0.1% and 1% suspensions. A total of 58 animals were used: 18 for controls and 40 for experimental groups. All test substances (saline, control-dexa, control-rimex, dexamethasone and rimexolone, 200 microl) were injected at -2, 48 and 60 h; LPS was injected at 0 h. Animals were monitored by daily otomicroscopy. After 4 days, samples of middle ear effusion (MEE) were collected for analysis and temporal bones were harvested for histopathological studies. RESULTS: At the end of 4 days, only in five ears (3/20 with 1% dexamethasone, 1/20 with 1% rimexolone, and 1/20 with 0.1% rimexolone) had the fluid diminished to the point of being unobservable. The volume of MEE, thickness of mucoperiosteum, and the degree of inflammation of middle ear mucosa with 1% dexamethasone and 1% rimexolone was significantly less compared with other groups.

Administration, Topical↗
PubMed1998

Effects of early postnatal dexamethasone therapy on calcium homeostasis and bone growth in preterm infants with respiratory distress syndrome.

The effects of dexamethasone therapy on calcium homeostasis and bone growth were evaluated in 49 infants (24 placebo and 25 dexamethasone) who participated in a double-blind trial of early dexamethasone therapy for the prevention of chronic lung disease. Dexamethasone (0.25 mg kg(-1) b.i.d. on d 1-7; 0.12 mg kg(-1) b.i.d. on d 8-14; 0.05 mg kg(-1) b.i.d. on d 15-21; 0.02 mg kg(-1) b.i.d. on d 22-28) or saline placebo was given i.v. Serum calcium (Ca), phosphorus (P) and parathyroid hormone (PTH), and the corresponding urinary excretion of calcium (FECa) and phosphorus (FEP) were measured on d 2, 3, 7, 10, 14, 21 and 28 after starting the study. Radiographic evaluations of bone growth were also evaluated. Infants in the dexamethasone group had significantly higher PTH on d 2 (p < 0.01), 7 and 14 (p < 0.05) than infants in the placebo group. The dexamethasone-treated infants also had significantly higher FEP on d 2, 7 and 14 (p < 0.05) and lower FECa on d 7 and 14 (p < 0.05) than control infants. There was no significant difference between the groups in bone growth during the study. It was concluded that early dexamethasone therapy causes a transient elevation in PTH without apparent change in bone growth. The long-term effect remains to be evaluated further.

Age Factors↗
PubMed2003

Effects of short-term dexamethasone treatment on collagen synthesis and degradation markers in preterm infants with developing lung disease.

AIM: To assess the effects of dexamethasone treatment on collagen turnover in preterm infants. METHODS: The serum concentrations of the amino-terminal propeptide of type I and III procollagens (PINP and PIIINP), which reflect rates of type I and III collagen synthesis, respectively, and the carboxy-terminal telopeptide of type I procollagen (ICTP), which reflects the rate of type I collagen degradation, were monitored in 13 preterm infants receiving dexamethasone and 13 matched control infants without glucocorticoid treatment for a total period of 12 mo. Dexamethasone was started at a median age of 12 d and continued at tapering doses for a median total duration of 10 d. Blood samples were taken immediately after birth, at 7, 14 and 28 d of age and at 2, 3, 6, 9 and 12 mo. The same markers were also measured just before the initiation of dexamethasone and on days 1, 3, and 7 of treatment. RESULTS: A striking decrease in all of the markers was already observed in every case on day 1 of dexamethasone, the suppression being greatest on day 3 and still considerable on day 7. The percentages from the pretreatment levels recorded on days 1, 3 and 7 were: for PINP 51, 26 and 45%; for PIIINP 63, 44% and 52%; and for ICTP 64, 41 and 51%. A rebound rise in PINP levels was seen in dexamethasone-treated infants, the levels exceeding those of the controls at 3 and 6 mo of age. A similar phenomenon was noted concerning PIIINP at 3 mo. The levels settled down at 9 and 12 mo. CONCLUSION: Dexamethasone causes an immediate, inevitable, deep suppression of type I and III collagen synthesis and also type I collagen degradation. This should be taken into consideration, e.g. when assessing for the indications for steroid treatment in sick preterm infants and its dosing and duration.

Anti-Inflammatory Agents↗
PubMed1996

Regulation of type I 5'-deiodinase by thyroid hormone and dexamethasone in rat liver and kidney cells.

Type I 5'-deiodinase (5'D-I) is crucial for the generation of circulating 3,5,3'-triiodothyronine (T3) and so is a major determinant of thyroid hormone action. Liver and kidney 5'D-I activity is reduced in nonthyroidal illness (NTI), but the exact cause of reduced 5'D-I activity remains unknown. Elevated circulating glucocorticoid hormone concentrations are one factor postulated to play a role. We have studied regulation of 5'D-I expression in cultured rat liver (phi 1) and kidney (NRK-52E) cells in response to treatment with T3 and the glucocorticoid dexamethasone. 5'D-I mRNA was measured by Northern hybridization and 5'D-I activity was measured in a sub-strate conversion assay. Expression of the sodium pump alpha 1-subunit (Na+/K(+)-ATPase alpha 1-subunit) mRNA was measured as an index of T3 and dexamethasone effects. In ø1 liver cells, T3 increased 5'D-I mRNA by 76 +/- 17% and 5'D-I activity by 101 +/- 30% (all results mean +/- SEM; n = 9). Dexamethasone increased 5'D-I mRNA by 55 +/- 16% and 5'D-I activity by 128 +/- 6%. In NRK-52E rat kidney cells, 5'D-I mRNA increased by 87 +/- 15% with T3 treatment and by 76 +/- 14% with dexamethasone. 5'D-I activity in NRK-52E cells was measurable only after stimulation by combined T3 and dexamethasone treatment. Na+/K(+)-ATPase alpha 1-subunit mRNA expression was stimulated following T3 and dexamethasone treatment in both cell lines. These results provide evidence for direct pretranslational regulation of 5'D-I by T3 and dexamethasone in both rat liver and kidney cells. Our findings do not support the hypothesis that glucocorticoids are directly responsible for inhibition of 5'D-I enzyme activity in NTI.

Animals↗
PubMed1995

Dexamethasone treatment impairs calcium regulation and reduces bone mineralization in infant pigs.

Calcium and vitamin D metabolism, bone mineralization, and growth were studied in piglets randomly assigned to 15 d of dexamethasone (0.5 mg.kg-1.d-1, orally) or placebo. Growth velocity was significantly reduced by dexamethasone treatment (P < 0.001). Pigs in the dexamethasone group demonstrated lower 45Ca absorption by in situ intestinal perfusion (P < 0.01). Plasma 25-hydroxycholecalciferol (calcidiol) and 1,25-dihydroxycholecalciferol (calcitriol) were lower (P < 0.05) and the urinary ratio of calcium to creatinine was higher (P < 0.05) after 15 d of dexamethasone compared with placebo. Differences between pre- and postosteocalcin (P < 0.01) and pyridinoline (P < 0.01) were higher and wholebody, lumbar, and femur bone mineral density were lower (P < 0.05) in dexamethasone-treated piglets. Dexamethasone-induced reductions in bone mineral mass likely result from reduced vitamin D status, reduced intestinal calcium absorption, elevated urinary calcium loss and direct effects of the steroid on bone. When dexamethasone is used in premature infants to improve lung function, negative effects on growth and bone metabolism could occur.

Animals↗
PubMed1998

Antenatal dexamethasone therapy does not affect circulating concentrations of insulin-like growth factor binding protein-1.

In animals, dexamethasone administration during pregnancy leads to fetal growth restriction due to enhanced expression of insulin-like growth factor binding protein-1 (IGFBP-1). In humans, there is also a significant inverse correlation between maternal and fetal concentrations of IGFBP-1 and birth weight. During pregnancy, maternal IGFBP-1 is derived from the decidualized endometrium. We have studied the effect of dexamethasone on circulating concentrations of IGFBP-1 in 12 pregnant women who received dexamethasone therapy for fetal lung maturation in anticipation of premature delivery before 34 completed weeks of gestation. Blood samples were collected before dexamethasone administration, at 24 h and 48 h after the course of dexamethasone, and within 24 h of delivery, for the measurement of IGFBP-1. There was no significant change in plasma IGFBP-1 concentrations at 24 and 48 h following dexamethasone therapy, and at delivery (P = 0.666, 0.307 and 0.398, respectively). Therefore, antenatal dexamethasone therapy does not influence decidual synthesis of IGFBP-1.

Adult↗
PubMed1999

Effect of antenatal dexamethasone therapy on maternal plasma human chorionic gonadotrophin, oestradiol and progesterone.

The aim of this study was to determine whether the current regimen of dexamethasone administration to induce fetal lung maturation affected the circulating concentrations of placental hormone. A standard regimen of dexamethasone that comprised two doses of 12-mg intramuscular injections, 12 h apart was administered to 12 pregnant women to promote fetal lung maturation in anticipation of premature delivery before 34 completed weeks of gestation. Blood samples were collected before starting the dexamethasone therapy, 24 h, and 48 h after completing therapy for the measurement of the plasma concentrations of human chorionic gonadotrophin (HCG), oestradiol and progesterone. There was a progressive fall in the plasma concentrations of HCG following dexamethasone therapy (P = 0.049 and P = 0.034, 24-h and 48-h post therapy respectively). There was an initial fall in the plasma concentrations of oestradiol after dexamethasone therapy (z = 3.059; P = 0.002, 24-h post therapy), which recovered by 48 h (P = 0.239). There was no difference between the plasma concentrations of progesterone at the three time points. The effect of dexamethasone on HCG concentrations suggests that it has a direct inhibitory effect on placental hormone synthesis or secretion. Further studies are needed to define the mechanism of action of dexamethasone on placental HCG production.

Adult↗
PubMed1991

Intestinal metallothionein gene expression and zinc absorption in rats are zinc-responsive but refractory to dexamethasone and interleukin 1 alpha.

The effects of dexamethasone and interleukin 1 alpha on intestinal metallothionein gene expression and zinc absorption were studied. Rats given parenteral zinc served as positive controls. A single intraperitoneal or intravenous dose of dexamethasone, interleukin 1 alpha or zinc markedly increased liver metallothionein synthesis 3-9 h after injection. Intestinal metallothionein mRNA and metallothionein protein were not affected by dexamethasone or interleukin 1 alpha, but were markedly increased by parenteral zinc. Absorption of 65Zn from isolated duodenal segments was inversely related to intestinal metallothionein concentration in rats given zinc, but was not affected by dexamethasone or interleukin 1 alpha. Plasma zinc concentrations decreased in rats given dexamethasone or interleukin 1 alpha and increased in those given zinc, but they were not related to 65Zn absorption. Similarly, multiple intraperitoneal administration of either dexamethasone or interleukin 1 alpha, or oral administration of dexamethasone, for 7 d markedly increased liver metallothionein synthesis but did not affect intestinal metallothionein concentration or 65Zn absorption. These results suggest that intestinal metallothionein gene expression and 65Zn absorption are refractory to glucocorticoid hormone and interleukin 1 alpha.

Animals↗
PubMed1984

Endometrial prostaglandins and phospholipase activity related to implantation in rabbits: effects of dexamethasone.

The anti-inflammatory steroid, dexamethasone, was demonstrated to have an antifertility effect in rabbits when administered systemically on Days 5-7 of pregnancy. The effects of this agent on prostaglandin (PG) concentrations and phospholipase activity in endometrium were determined. Using a highly specific and sensitive gas chromatography-mass spectometry (GC-MS) method, it was established that PGF2 alpha, PGE2 and 6-keto-PGF1 alpha concentrations are all significantly elevated in implant site endometrium relative to nonimplant regions on Day 7 postcoitus (p.c.). Although these levels were strikingly lowered in indomethacin-treated females, the administration of dexamethasone altered the balance between the various PGs but did not reduce tissue levels greatly. Determinations of PG levels in uterine venous plasma likewise demonstrated that neither synthesis nor release of PGs had been drastically curtailed by dexamethasone treatment. Endometrial phospholipase activity was determined on Days 6, 7 and 8 of pregnancy. Enzyme activity was elevated on Day 7 relative to the other days and implant site activity was significantly greater than nonimplant region activity on both Days 6 and 7. Treatment with either dexamethasone or indomethacin reduced the Day 7 activity to baseline levels and obliterated the differential between implant and nonimplant regions. The dexamethasone effect appears to be mediated by induction of a transferable inhibitory factor. Thus, while indomethacin and dexamethasone have similar effects on pregnancy when present during the implantation period, their respective mechanisms of action may be different. Even though dexamethasone inhibits endometrial phospholipase activity, this is not attended by inhibition of PG generation.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Induction of parturition, progesterone secretion, and delivery of placenta in beef heifers given relaxin with cloprostenol or dexamethasone.

Sixty primiparous beef heifers from a crossbreeding study were used to examine the effects of inducing parturition with relaxin (3,000 U/mg) combined with cloprostenol (500 micrograms, i.m., n = 30) or dexamethasone (20 mg, i.m., n = 30) at Day 273, 10 +/- 1 days before expected parturition (Day 283). Heifers were assigned at random within cloprostenol and dexamethasone groups to receive relaxin (1 mg, n = 5/treatment), i.m. or in the cervical os (OS), at 0 h (the same time as cloprostenol and dexamethasone) or 24 h later. Eleven and six first-calving heifers and sixteen and nine second-calving cows also received cloprostenol + relaxin and cloprostenol + phosphate-buffered saline, respectively. Radioimmunoassay of daily plasma samples indicated an abrupt decrease in progesterone with time (p less than 0.001), from 7.5 +/- 0.50 to 1.0 +/- 0.30 ng/ml (mean +/- SE) within 48 h for all groups. The mean rate of progesterone decrease (ng/ml in 24 h) was accelerated (p less than 0.01) in relaxin-treated heifers (5.3 +/- 0.36), in contrast to dexamethasone- and cloprostenol-treated control heifers (2.8 +/- 0.40). Relaxin combined with cloprostenol or dexamethasone shortened the calving period in these heifers by reducing the interval between treatment and calving (33 vs. 56 h; p less than 0.01). The incidence and duration of retained placenta were reduced by 22 vs. 75% and 14 vs. 34 h for relaxin combined with cloprostenol or dexamethasone as compared with cloprostenol- or dexamethasone-treated controls, respectively (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Dexamethasone inhibits luteinizing hormone-induced synthesis of steroidogenic acute regulatory protein in cultured rat preovulatory follicles.

The effect of dexamethasone on LH-induced synthesis of steroidogenic acute regulatory (StAR) protein was studied in a serum-free culture of preovulatory follicles. StAR protein is a steroidogenic tissue-specific, hormone-induced, rapidly synthesized protein previously shown to be involved in the acute regulation of steroidogenesis, probably by promoting the transfer of cholesterol to the inner mitochondrial membrane and the cytochrome P450 side-chain cleavage (P450(scc)) enzyme. Treatment of preovulatory follicles dissected from ovaries of cyclic adult rats on the morning of proestrus with LH for 24 h resulted in a dose-dependent increase in the level of StAR protein that reached a maximum at 10 ng LH/ml. This increase was associated with an increase in progesterone production. Treatment of the follicles with increasing concentrations (1-1000 ng/ml) of dexamethasone suppressed LH (10 ng/ml)-induced StAR protein levels and progesterone production in a dose-dependent manner. The amount of P450(scc) was not affected by this dexamethasone treatment, indicating that the loss of steroidogenic capacity was not a result of inhibition of P450(scc). Dexamethasone also decreased StAR protein levels and progesterone production induced by the adenylate cyclase activator forskolin (10(-5) M) or a cAMP analogue 8-Br-cAMP (0.5 mM). The effects of dexamethasone on 8-Br-cAMP-induced StAR protein levels and progesterone production were blocked by cotreatment of the follicles with glucocorticoid receptor antagonist RU-486. These results demonstrate that dexamethasone inhibits the LH-induced StAR protein levels and that the effects of dexamethasone are mediated by the glucocorticoid receptor.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1997

Prophylaxis for vomiting by children after tonsillectomy: dexamethasone versus perphenazine.

UNLABELLED: The effects of dexamethasone and perphenazine on vomiting after tonsillectomy in children were compared in 226 healthy children aged 2-12 yr. The study was randomized, stratified, blocked, and double-blind. Anesthesia was induced intravenously (I.V.) with propofol or by inhalation with halothane and N2O. Dexamethasone 150 microg/kg or perphenazine 70 microg/kg was administered I.V. after the induction of anesthesia in a double-blind fashion. Perioperative management of emesis, pain, fluids, and patient discharge was all standardized. The groups had similar demographic characteristics. Perphenazine significantly reduced the incidence of in-hospital vomiting compared with dexamethasone (13% vs 36%, P < 0.001). The incidence of out-of-hospital vomiting was almost identical. Overall, the incidence was significantly different for perphenazine vs dexamethasone (33% vs 46%, P = 0.04) using logistic regression analysis. Of note, sex and induction technique were significant predictors of postoperative vomiting (P < 0.05) using logistic regression analysis, with male patients and those patients undergoing I.V. induction vomiting less. In conclusion, perphenazine more effectively decreases vomiting by children after tonsillectomy in an ambulatory hospital setting compared with dexamethasone. IMPLICATIONS: Postoperative vomiting can have many debilitating effects, and children undergoing tonsillectomy are at particular risk. We compared the effects of dexamethasone and perphenazine on vomiting after tonsillectomy in 266 children. We found perphenazine more effective than dexamethasone before discharge from hospital but that the two drugs have similar effects after discharge.

Anesthesia↗
PubMed1997

The effects of dexamethasone on antiemetics in female patients undergoing gynecologic surgery.

UNLABELLED: This randomized, double-blind study compared the effects of dexamethasone plus either droperidol, metoclopramide, or granisetron with each antiemetic alone for preventing postoperative nausea and vomiting (PONV) in 270 female patients undergoing general anesthesia for major gynecological surgery. Patients were randomly assigned to receive either droperidol 1.25 mg (Group D1, n = 45), droperidol 1.25 mg plus dexamethasone 8 mg (Group D2, n = 45), metoclopramide 10 mg (Group M1, n = 45), metoclopramide 10 mg plus dexamethasone 8 mg (Group M2, n = 45), granisetron 40 micrograms/kg (Group G1, n = 45), or granisetron 40 micrograms/kg plus dexamethasone 8 mg (Group G2, n = 45) immediately before the induction of anesthesia. A standard general anesthetic technique and postoperative analgesia were used throughout the study. Complete response, defined as no PONV and no administration of rescue antiemetic medication during the first 24 h after anesthesia, was 49% in Group D1, 60% in Group D2 (P = 0.199 versus Group D1), 51% in Group M1, 62% in Group M2 (P = 0.198 versus Group M1), 80% in Group G1, and 96% in Group G2 (P = 0.025 versus Group G1). Our results suggest that dexamethasone enhances the antiemetic efficacy of granisetron but does not potentiate the other antiemetics-droperidol and metoclopramide-in female patients undergoing major gynecological surgery. IMPLICATIONS: We compared the efficacy of dexamethasone plus three different antiemetics-droperidol, metoclopramide, and granisetron-for the prevention of nausea and vomiting after gynecologic surgery. The granisetron-dexamethasone combination was the most effective for preventing post-operative emetic symptoms.

Adult↗
PubMed2001

Dexamethasone facilitates discharge after outpatient anorectal surgery.

UNLABELLED: Corticosteroids can decrease pain and postoperative nausea and vomiting after ambulatory surgery. Therefore, we designed a study to evaluate if the routine use of dexamethasone would facilitate the early recovery process after anorectal surgery. A secondary aim of the study was to determine if dexamethasone would increase the incidence of postoperative wound complications. Eighty adult outpatients undergoing anorectal surgery with a standardized monitored anesthesia care technique were randomly assigned to receive either dexamethasone 4 mg IV or an equal volume of saline before the start of surgery. All patients were premedicated with midazolam 2 mg IV and received ketorolac 30 mg IV as a preemptive analgesic. A propofol infusion, 50 microg. kg(-1). min(-1) IV, was initiated and subsequently titrated to maintain an observer's assessment of alertness/sedation score of 2 or 3 (with 5 = awake/alert to 1 = asleep). Fentanyl 25 microg IV was administered 3-5 min before infiltrating the surgical field with a 30-mL local anesthetic mixture containing 15 mL of lidocaine 1% and 15 mL of bupivacaine 0.25% (with epinephrine 1:200,000 and sodium bicarbonate 3 mL). All patients were fast-tracked directly from the operating room to the step-down recovery area. Even though the incidences of postoperative pain and postoperative nausea and vomiting were small in both treatment groups, the time to "home readiness" was significantly shorter in the dexamethasone group. Importantly, there was no increase in the incidence of wound infections (8% vs 12%) or hematoma formation (3% vs 5%) in the dexamethasone (versus saline) group. We conclude that the administration of dexamethasone, 4 mg IV, shortened the time to home readiness without increasing the incidence of postoperative wound infections in a high-risk outpatient population undergoing anorectal surgery. IMPLICATIONS: A single dose of dexamethasone (4 mg IV) decreased the time to "home readiness" without increasing the incidence of postoperative wound complications in an outpatient population undergoing anorectal surgery.

Adult↗
PubMed2001

The effect of dexamethasone on postoperative vomiting after tonsillectomy.

UNLABELLED: In this double-blinded, randomized, placebo-controlled study, we assessed the effect of dexamethasone 0.5 mg/kg IV administered preoperatively in 110 children 2-12 yr old, undergoing electrodissection adenotonsillectomy, using a standardized anesthetic technique. The incidence of early and late vomiting, the time to first oral intake, the quality of oral intake, the satisfaction scores, and the duration of IV hydration were compared in both groups. The overall incidence of vomiting, as well as the incidence of late vomiting, was significantly less in the Dexamethasone group as compared with the Saline group (23% and 19% vs 51% and 34%, respectively). The time to first oral intake and the duration of IV hydration were shorter in the Dexamethasone group compared with the Saline group (P < 0.05). The quality of oral intake and the satisfaction scores were better in the Dexamethasone group than in the Saline group (P < 0.05). This report confirms the beneficial effect of IV dexamethasone on both vomiting and oral intake in children undergoing electrodissection adenotonsillectomy. IMPLICATIONS: In this double-blinded, placebo-controlled study, we examined the efficacy of a single dose of dexamethasone 0.5 mg/kg IV on posttonsillectomy vomiting and oral intake in children 2-12 yr old. Dexamethasone significantly decreased the incidence of postoperative vomiting during the first 24 h, shortened the time to the first oral intake and the duration of IV hydration, and improved the quality of oral intake and the satisfaction scores of the patients.

Age Factors↗