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PubMed2002

Pharmacokinetics of betamethasone in twin and singleton pregnancy.

OBJECTIVE: The aims of the study were to compare the pharmacokinetics of betamethasone in singleton pregnancy with the pharmacokinetics in twin pregnancy and to assess the adrenal suppression produced by betamethasone. STUDY DESIGN: We measured serial betamethasone and cortisol levels in 30 singleton and 21 twin pregnancies after the first dose of betamethasone and calculated the pharmacokinetic parameters for betamethasone including volume of distribution, half-life, and clearance. We also measured cord and maternal blood levels of betamethasone at the birth of infants of 13 singleton and 9 twin pregnancies. RESULTS: The half-life of betamethasone in mothers with twin pregnancies was significantly shorter than that in mothers with singleton pregnancies (7.2 +/-2.4 versus 9.0 +/- 2.7 hours; P <.017). Clearance of betamethasone in the twin pregnancies appeared greater than in singleton pregnancies (8.4 +/- 6.4 versus 5.7+/- 3.1 L/h; P =.06) but did not reach statistical significance. Volume of distribution was similar in the two groups. Because the time between the last dose of betamethasone and birth varied widely (range, 2-158 hours), mothers with a longer interval after treatment tended to have a higher cord-to-maternal betamethasone ratio than did mothers with a shorter interval in both twin and singleton pregnancies. This finding indicated delayed fetal clearance, but the correlation was weak (R (2) = 0.29 for twins and 0.08 for singletons). CONCLUSION: The shorter half-life of betamethasone in twin pregnancy than in singleton pregnancy may cause the level of betamethasone to be subtherapeutic for lung maturation in twin pregnancy.

Adult↗
PubMed1996

Single dose fetal betamethasone administration stabilizes postnatal glomerular filtration rate and alters endocrine function in premature lambs.

UNLABELLED: These studies determined the effects of fetal treatment with betamethasone alone, or in combination with thyroid hormone (thyroxine; T4), on postnatal renal and endocrine adaptations in preterm newborn lambs. Ovine fetuses (126 d of gestation; term = 150 d) received single, ultrasound-guided intramuscular injections of saline, 0.5 mg/kg betamethasone (Celestone Soluspan, or 0.5 mg/kg betamethasone plus 60 micrograms/kg T4. After 48 h, lambs were delivered, treated with surfactant (Survanta, 100 mg/kg), and ventilated for 3 h. Due to maintained urine flow in the betamethasone-treated animals and a significant decrease in the saline group, betamethasone versus saline urine flow values (0.11 +/- 0.03 versus 0.03 +/- 0.004 mL.min-1.kg-1) were significantly elevated by the end of studies. GFR (1.5 +/- 0.3 versus 0.8 +/- 0.2 mL.min-1.kg-1) and mean blood pressure (61 +/- 4 versus 42 +/- 3 mm Hg) values also were higher in the betamethasone-treated animals. Although renal blood flow, renal plasma flow, and fractional sodium excretion rates did not differ, betamethasone versus saline values for the filtration fraction (11.9 +/- 1.5 versus 7.4 +/- 1.5%) and total sodium reabsorption (196 +/- 38 versus 81 +/- 16 microEq.min-1.kg-1) were increased. Betamethasone versus saline treatment also was associated with significant reductions in plasma angiotensin II (125 +/- 23 versus 550 +/- 140 pg/mL) and AVP (116 +/- 19 versus 230 +/- 77 pg/mL) levels. Overall, the effects of combined betamethasone + T4 treatment were similar to the effects of betamethasone alone. CONCLUSIONS: 1) fetal betamethasone injection 48 h before delivery stabilizes GFR and significantly alters endocrine function in preterm newborn lambs, and 2) the addition of T4 does not augment betamethasone-induced renal and endocrine responses.

Angiotensin II↗
PubMed2006

Kinetics of betamethasone and fetal cardiovascular adverse effects in pregnant sheep after different doses.

OBJECTIVE: To study the pharmacokinetics of different betamethasone doses and preparations used to enhance fetal lung maturation in the maternal and fetal circulation of sheep and the adverse effects on fetal blood pressure. METHODS: Doses of 170 (n = 6) and 110 microg/kg (n = 6) betamethasone phosphate equivalent to 12 or 8 mg, respectively, administered to a 70 kg pregnant woman or 170 microg/kg (n = 6) of a depot formulation (50% betamethasone phosphate and 50% betamethasone acetate) were injected intramuscularly to chronically instrumented pregnant sheep. RESULTS: Both betamethasone preparations produced highest maternal concentrations after 15 min followed by an exponential decline with a t(1/2) of about 3 hours. The drug fell below the limit of detection at 8 to 12 hours. Betamethasone was first detectable in the fetal circulation at 1 hour, peaked at 3 hours, and decreased below the limit of detection at 8 hours independently of the dose or preparation. Maternal and fetal betamethasone concentrations achieved with the phosphate and acetate formulation were one half of those obtained with betamethasone phosphate, suggesting that very little betamethasone is released from the acetate within the first 8 hours when the effect on lung maturation is needed. Betamethasone led to a maximal increase of mean fetal blood pressure from 42+/-1 to 51+/-1 mm Hg (P < .05) and did not differ between the doses and preparations, although plasma concentrations showed a clear dose-concentration relationship. CONCLUSION: The doses of betamethasone used in obstetrics are supramaximal in terms of cardiovascular effects in sheep. Risk-benefit studies are needed to find the effective steroid dose with the least adverse effects.

Animals↗
PubMed1997

A comparative study of cardiovascular, endocrine and behavioural effects of betamethasone and dexamethasone administration to fetal sheep.

1. Chronically instrumented, late-gestation fetal sheep were prepared to: (1) characterize cardiovascular, endocrine and behavioural effects of fetal treatment with clinical doses of betamethasone and dexamethasone; (2) define specific differences, if any, in the actions of betamethasone and dexamethasone of measured fetal responses; and (3) assess the contribution of changes in peripheral vascular resistance to the glucocorticoid-induced hypertension. 2. Following baseline, either saline (n = 9), betamethasone (n = 9), or dexamethasone (n = 6) was infused for 48 h in fetal sheep commencing at 125 days of gestation. A pronounced increase in fetal blood pressure occurred following both betamethasone and dexamethasone treatment. The nature and magnitude of this increase was similar following treatment with either glucocorticoid. 3. To address possible mechanisms contributing to the glucocorticoid-induced fetal hypertension, fetal plasma catecholamine levels and changes in fetal femoral haemodynamics were assessed following fetal glucocorticoid treatment. A fall in fetal plasma noradrenaline and adrenaline concentrations occurred during betamethasone and dexamethasone treatment. In contrast, a progressive femoral vasoconstriction occurred during betamethasone treatment. 4. A modest fall in the incidence of fetal breathing movements occurred during fetal treatment with either betamethasone or dexamethasone. The magnitude of this reduction was similar with treatment of either glucocorticoid. The fall in fetal breathing during betamethasone and dexamethasone treatment was not associated with a fall in the incidence of fetal low voltage electrocortical activity. 5. Our results indicate that prenatal betamethasone and dexamethasone treatment of late-gestation fetal sheep, in doses similar to those employed clinically, is associated with fetal cardiovascular, endocrine and behavioural effects. Both betamethasone and dexamethasone induce similar increases in fetal blood pressure and similar falls in the incidence of fetal breathing movements. The pronounced betamethasone-induced fetal hypertension is associated with an increase in fetal femoral vascular resistance.

Animals↗
PubMed2005

Lumbar radiculopathy: treatment with selective lumbar nerve blocks--comparison of effectiveness of triamcinolone and betamethasone injectable suspensions.

PURPOSE: To retrospectively determine if there is a difference in the effectiveness of triamcinolone acetonide injectable suspension versus betamethasone sodium phosphate and betamethasone acetate injectable suspension in the treatment of radiculopathy and low back pain with selective lumbar nerve blocks. MATERIALS AND METHODS: This retrospective study was approved by the institutional review board and was HIPAA compliant; informed consent was not required. Charts and self-reported pain score evaluations were retrospectively reviewed in 114 patients (56 men, 58 women; age range, 36-84 years; mean age, 60 years) treated for radiculopathy from 1997 to 2003 with 130 selective lumbar nerve blocks with triamcinolone or betamethasone. Perineural location was confirmed with fluoroscopic guidance. Forty-nine patients received a mixture of 1 mL of the triamcinolone, 40 mg/mL, and 1 mL of 0.5% bupivacaine hydrochloride. Eighty-one patients received a mixture of 1 mL of the betamethasone, 6 mg/mL, and 1 mL of 0.5% bupivacaine hydrochloride. Patients completed standardized pain evaluation sheets and compared their pain with baseline levels during 14 days after injection. Fisher exact test was used for data analysis. RESULTS: From day 0 to 1 after the procedure, there was no statistically significant difference in improvement in low back pain and lower extremity pain between groups. On day 3, 42% of triamcinolone recipients and 58% of betamethasone recipients demonstrated improvement in low back pain (P = .04, Fisher exact test), whereas 55% of triamcinolone recipients and 57% of betamethasone recipients had lower extremity pain improvement (P = .33). On day 7, 45% of triamcinolone recipients and 58% of betamethasone recipients had improvement in low back pain (P = .38), whereas 52% of triamcinolone recipients and 57% of betamethasone recipients had improvement in lower extremity pain (P = .69). On day 14, 42% of triamcinolone recipients and 53% of betamethasone recipients had improvement in low back pain (P = .26), whereas 49% of triamcinolone recipients and 55% of betamethasone recipients had improvement in lower extremity pain (P = .69). CONCLUSION: Selective nerve root blocks with betamethasone and triamcinolone reduced low back pain and lower extremity pain, although there was no significant difference in effectiveness between the two.

Adult↗
PubMed1995

Simultaneous diffusion and metabolism of betamethasone 17-valerate in the living skin equivalent.

Simultaneous diffusion and metabolism of betamethasone 17-valerate was studied using betamethasone 17-valerate, betamethasone 21-valerate, and betamethasone as permeants. These corticosteroids were suspended in silicone adhesive and applied to an artificial living skin equivalent (LSE) for 72 h. When betamethasone was applied, no metabolites were detected in the receptor medium. Conversely, with betamethasone 21-valerate application, only betamethasone but no betamethasone 21-valerate was detected in the receptor medium indicating the metabolism of the latter by skin esterases. When tested with the theory for simultaneous diffusion and metabolism, the result is consistent with the enzyme rate constant in the LSE homogenate measured in a previous study. When betamethasone 17-valerate was applied to the LSE, more than half of the total amount of corticosteroids detected in the receptor medium was unchanged, consistent with the previously reported chemical (as opposed to enzymatic) degradation half-life of about 8 h. This result also indicated that very little metabolism of betamethasone 17-valerate occurred in the skin.

Betamethasone↗
PubMed1983

Pharmacokinetics of betamethasone in healthy adults after intravenous administration.

The pharmacokinetics of betamethasone and its phosphate ester are described in 8 healthy adults after i.v. bolus injection of 10.6 mg betamethasone phosphate. Both compounds were measured by high-performance liquid chromatography with ultraviolet detection using sample handling methods which prevented hydrolysis of the ester in vitro. Betamethasone phosphate disappeared rapidly from plasma (mean half-life = 4.7 min) as betamethasone levels rose. Betamethasone plasma levels reached a peak 10-36 min after administration of the phosphate before declining in a biexponential manner. The terminal slow disposition phase had a mean half-life of 6.5 h. Only about 5% of the dose was recovered from urine as betamethasone, indicating extensive extrarenal clearance of betamethasone. Protein binding and blood/plasma concentration ratio were also determined. In comparison with its stereoisomer, dexamethasone, betamethasone is also cleared mainly by metabolism but has a lower plasma clearance, is less plasma bound, has a higher blood/plasma concentration ratio, and a higher volume of distribution. Endogenous cortisol levels were measured in the subjects who received betamethasone phosphate and in a matched control group of 4 subjects who did not. Betamethasone abolished the normal episodic secretion of cortisol and rapidly reduced its plasma concentration to a basal level. Cortisol plasma levels were not restored at 24 h but had returned to normal by 48 h after dosing.

Adult↗
PubMed2000

Adrenal suppression induced by betamethasone in women at risk for premature delivery.

OBJECTIVE: To determine whether betamethasone administered to women at risk of preterm delivery causes adrenal suppression. METHODS: Ten women at risk of preterm delivery had three weekly low-dose (1 microg) ACTH stimulation tests with the first one between 24 and 25 weeks' gestation. Immediately after the first and second ACTH stimulation tests, we gave each woman a 12-mg betamethasone dose intramuscularly and repeated it 24 hours later. The third ACTH stimulation test was 1 week after the second course of betamethasone. Serum cortisol levels were measured before (baseline) and 30 minutes after ACTH administration. RESULTS: All subjects had normal baseline and stimulated cortisol levels for the first ACTH stimulation test. Mean baseline serum cortisol levels decreased with each ACTH stimulation test, from 25.4 +/- 4.8 microg/dL (before betamethasone) to 4.3 +/- 4.0 microg/dL (1 week after the second course of betamethasone) (P <.001). The mean stimulated cortisol levels also decreased from 33.0 +/- 4.3 microg/dL (before betamethasone) to 11.8 +/- 6.4 microg/dL (1 week after the second course of betamethasone) (P <.001). Compared with initial ACTH stimulation tests, laboratory evidence of adrenal suppression occurred in four patients 1 week after the first course of betamethasone and in seven patients after the second course. No signs or symptoms of Addisonian crisis occurred antepartum or intrapartum. CONCLUSION: Antenatal administration of betamethasone produced measurable adrenal suppression in women at risk of preterm delivery. The number of women with adrenal suppression increased each week that antenatal betamethasone was repeated. (Obstet Gynecol 2000;96:287-90.)

Adrenal Cortex↗
PubMed2006

Outbreak of Serratia marcescens infections following injection of betamethasone compounded at a community pharmacy.

BACKGROUND: In June 2001, following the report of 4 patients with Serratia marcescens meningitis who received epidural injections of betamethasone compounded at a community pharmacy, we initiated an outbreak investigation. METHODS: All patients who received injections of betamethasone from the production lot common to the 4 patients were evaluated. A case patient was defined as a patient who received compounded betamethasone and had S. marcescens isolated from a sterile site or clinical and laboratory evidence of infection. We cultured all recovered betamethasone, environmental specimens from the pharmacy, and medications recovered from an ambulatory surgery center. The California Board of Pharmacy reviewed the procedures used to prepare the betamethasone. RESULTS: We identified 11 patients with culture-confirmed S. marcescens (8 patients) or clinical infection (3 patients) following injection of compounded betamethasone from 25 May through 31 May 2001. Case patients had meningitis (5 patients, with 3 deaths), epidural abscesses (5 patients), or an infected hip (1 patient). S. marcescens was isolated from 35 (69%) of 51 betamethasone vials recovered, from pharmacy specimens of 1% carboxymethylcellulose stock solution, from pharmacy surfaces, and from multiple parenteral materials used at the ambulatory surgery center. Pulsed-field gel electrophoresis patterns of S. marcescens isolates of representative specimens from patients, the betamethasone, the pharmacy, and the ambulatory surgery center were identical. Deficient practices in compounding of betamethasone included inadequate autoclaving temperatures and failure to perform terminal sterilization. CONCLUSIONS: This outbreak of serious S. marcescens infection followed improper compounding of betamethasone in a community pharmacy. Enforceable national standards for pharmaceutical compounding are needed to reduce the risk of such outbreaks.

Bacterial Typing Techniques↗
PubMed2005

Betamethasone pharmacokinetics after two prodrug formulations in sheep: implications for antenatal corticosteroid use.

Maternal administration of betamethasone to enhance fetal lung maturation for women who threaten preterm labor is common clinical practice. However, recommendations regarding the choice of betamethasone formulations for perinatal use are vague. The disposition of betamethasone from two commonly used antenatal formulations is poorly understood. We therefore designed a study to capture the true pharmacokinetic profiles of betamethasone from these fast acting and dual-release formulations. Betamethasone in sheep plasma was measured by a newly designed, highly sensitive liquid chromatography/tandem mass spectrometry assay after intramuscular injection (n = 4) of 0.25 mg/kg betamethasone phosphate and 0.5 mg/kg betamethasone phosphate/acetate formulations. Compartmental modeling was performed using the ADAPT II program. Betamethasone pharmacokinetics could be captured for 24 h for the phosphate and for 5 days for the phosphate/acetate formulations. The phosphate formulation profile had the appearance of a traditional Bateman function with a terminal half-life of 4 h, whereas the phosphate/acetate formulation produced a biexponential decline with a terminal half-life of 14 h. The latter is much longer than is commonly reported and has been missed in the literature due to assay limitations. Extrapolations to humans indicate that although both formulations might have similar therapeutic indices, the dual formulation might be associated with a lower safety profile. In light of this newly identified long terminal half-life for the betamethasone dual formulation, dosing practices for betamethasone in pregnancy need to be reassessed.

Adrenal Cortex Hormones↗
PubMed2006

Betamethasone does not prevent nausea and vomiting induced by the dopamine-agonist apomorphine.

PURPOSE: The mechanism of the antiemetic actions of corticosteroids is not known. The purpose of this study was to evaluate if betamethasone can prevent nausea, vomiting or increase of vasopressin induced by apomorphine. Metoclopramide, a dopamine antagonist, was used as a control substance. METHODS: Ten healthy volunteers were studied on three occasions. In a randomized order they were allocated to receive pretreatment with betamethasone 8 mg iv, metoclopramide 10 mg iv, and normal saline 2 mL as placebo on the three different occasions, 15 min before the administration of apomorphine 30 microg x kg(-1) s.c.. After administration of apomorphine, episodes of vomiting were recorded, and the intensity of nausea was estimated by the subject on a visual analogue scale (VAS 0-10 cm). Blood samples for analysis of plasma concentrations of vasopressin were analyzed. RESULTS: One volunteer decided to withdraw, as he experienced akathisia after receiving metoclopramide. During the first two hours after apomorphine, eight of nine volunteers vomited both after betamethasone and placebo. One volunteer did not vomit after betamethasone and placebo but he experienced nausea. None of the volunteers vomited after metoclopramide (P < 0.01 vs betamethasone and placebo). The maximum VAS for nausea was significantly higher after betamethasone and placebo compared to metoclopramide (P < 0.01). The vasopressin levels increased after betamethasone and placebo, but there was no increase in any volunteer after pretreatment with metoclopramide. CONCLUSION: This study demonstrates that betamethasone does not prevent nausea, vomiting and increase of vasopressin induced by apomorphine, whereas metoclopramide prevents apomorphine-induced emesis. Our work suggests that betamethasone does not have dopamine-antagonistic effects.

Adult↗
PubMed2004

Effect of betamethasone administration to the pregnant baboon at 0.75 gestation on placental eNOS distribution and activity.

Betamethasone is frequently administered to pregnant women at risk of premature labor to accelerate fetal lung maturation. Maternally administered betamethasone produces pronounced changes in the fetal peripheral vasculature, raises fetal blood pressure and produces fetal growth restriction. Endothelial nitric oxide synthase (eNOS) plays an important role in regulating vascular tone. We hypothesized that effects of betamethasone on the fetal vasculature include decreased eNOS activity. We determined a significant depression of total placental eNOS protein measured by ELISA (betamethasone treated vs control, 0.48 +/- 0.28 vs 1.57 +/- 0.45, p < 0.05) and immunohistochemistry in both syncytiotrophoblast and vascular endothelium. Following betamethasone exposure, eNOS mRNA and enzyme activity showed decreasing trends which were not statistically significant. eNOS protein was higher in the placentas of both control and betamethasone treated baboons in the presence of a female fetus compared with a male fetus. The same effect of the sex of the fetus was observed in the betamethasone group for eNOS mRNA. In conclusion, maternally administered betamethasone produces a consistent decrease in several indices of placental eNOS function that may play a role in the altered cardiovascular dynamics and fetal growth retardation produced by betamethasone administration in late pregnancy.

Animals↗
PubMedDate not supplied

Effect of in utero exposure to betamethasone on motivation/anxiety testing in mice offspring.

In utero exposure to a single dose of the long-acting corticosteroid betamethasone at GD 14 has been shown to induce specific differences in motivation/anxiety testing among offspring. Because multidosings are desired to enhance fetal lung maturation, our objective was to compare effects of multidosings of betamethasone with a placebo on postnatal tests of motivation and anxiety. Sixty gravid CD-1 mice were randomly assigned to receive one of six treatment regimens (n = 10) that consisted of a single or a double SC dosing of either betamethasone (Celestone soluspan 0.2 mg on GD 14; 0.1 mg on GD 13 to 16; 0.1 mg b.i.d. on GD 14 and 15; 0.1 mg b.i.d. on GD 13 to 16) or saline (0.25 ml on GD 13 to 16; 0.25 ml b.i.d. on GD 13 to 16). The percent of pups exhibiting separation vocalization was temporarily less at PND 5 after betamethasone exposure to four doses (p < 0.05) and to eight doses (p < 0.01). The percents of pups being successful in homing (PND 9) and in responding to startle stimulation (PND 12-15) were not different between the betamethasone-exposed and placebo-exposed groups. Exploratory performance in the radial arm maze revealed no delay in the activities of juvenile and adult offspring exposed to betamethasone. The percent of male offspring that fought as juveniles and as adults was not different between the betamethasone-exposed and the placebo-exposed groups. The previously reported altered responses using the elevated plus maze, among juvenile and adult offspring, after a single dose of betamethasone was not replicated in this multidose study. These data indicate that prenatal exposure to betamethasone did not affect the mouse offspring's long-term responses to motivation/anxiety testing.

Animals↗
PubMed2004

Is 1-hour glucose screening test reliable after a short-term administration of antenatal betamethasone?

This study was designed to determine whether betamethasone has any effect on 1-hour (50-g) glucose screening test in nongestational diabetic pregnancy, and if any exists, to determine if this effect is transient or permanent. If the effect is temporary, the study was designed to determine the duration of this glucose intolerance effect and to determine the timing of 1-hour glucose screening test after betamethasone usage. One hundred fourteen pregnant women with a diagnosis of preterm labor at 24 to 34 weeks gestation were enrolled into the prospective study. One-hour glucose screening test was performed before initiation of hydration treatment. Forty pregnant women with normal 1-hour glucose results, who also had responded to hydration therapy, made up our study group. Twenty-four hours, 72 hours, and 1 week after administration of betamethasone, 50-g glucose challenge tests were again performed. A 3-hour glucose tolerance test was performed in pregnant women, whose 1-hour screening test had been positive 1 week after corticosteroid administration. In the evaluation of data, one-way, variance analysis and Tukey's multiple comparison test were used. The mean value of 1-hour glucose results of 50-g challenge test at the 24 hours was significantly higher than the mean value of 1-hour glucose results of the test done initially before betamethasone administration and than those of the tests done at 72 hours and 1 week (p < 0.001 for these three groups). There was no statistically significant difference between the mean values of 1-hour glucose results of the test done before betamethasone administration and both the results of the tests done at 72 hours (p = 0.96) and 1 week (p = 0.99), separately. There was no significant difference between the mean 1-hour glucose results of the tests at 72 hours and 1 week (p = 0.99). The test results were positive in 42.5%, 10%, and 5% of the patients, respectively at 24 hours, 72 hours, and 1 week. The betamethasone administration significantly deteriorates 1-hour glucose screening test results in the nongestational diabetic patients but this effect of betamethasone is transient. Because of its high false-positivity at 24 hours (42.5%) and at 72 hours (10%) in women with initial negative 1-hour glucose screening test, we suggest that 1-hour glucose screening test in pregnant women be postponed at least 1 week after betamethasone administration or perform the test before administration of betamethasone.

Adolescent↗
PubMed1984

Disposition of betamethasone in parturient women after intramuscular administration.

When betamethasone phosphate equivalent to 8 mg betamethasone was administered intramuscularly in solution (Celestone Injection) to pregnant women, a large proportion of this ester was absorbed unchanged. Bioavailability of betamethasone from the phosphate ester was as high as after intravenous injection. When pregnant patients received the equivalent of either 6 or 12 mg betamethasone in a formulation containing 3.1 mg/ml betamethasone acetate suspended in a solution of 4 mg/ml betamethasone phosphate (Celestone Chronodose), much of the phosphate ester was absorbed intact but betamethasone acetate was not detected in plasma. Availability of betamethasone from Celestone Chronodose was much lower than from Celestone Injection. After administration of either formulation, maternal plasma cortisol concentrations fell towards a basal level but were rising again within 2 to 3 days of the last dose. We conclude that Celestone Chronodose does not provide prolonged release of betamethasone and offers no advantage over Celestone Injection.

Betamethasone↗
PubMed2006

Long term effects of antenatal betamethasone on lung function: 30 year follow up of a randomised controlled trial.

BACKGROUND: Antenatal betamethasone is routinely used for the prevention of neonatal respiratory distress syndrome in preterm infants. However, little is known of the long term effects of exposure to antenatal betamethasone on lung function in adulthood. METHODS: Five hundred and thirty four 30 year olds whose mothers had participated in the first and largest randomised controlled trial of antenatal betamethasone were followed. Lung function was assessed by portable spirometric testing. The prevalence of asthma symptoms was assessed using the European Community Respiratory Health Survey questionnaire. RESULTS: Fifty (20%) betamethasone exposed and 53 (19%) placebo exposed participants met the criteria for current asthma (relative risk 0.98 (95% CI 0.74 to 1.30), p = 0.89). 181 betamethasone exposed and 202 placebo exposed participants had acceptable spirometric data. There were no differences in lung function between betamethasone and placebo exposed groups (mean (SD) forced vital capacity in the betamethasone and placebo groups 105.9 (12.0) v 106.6 (12.6)% predicted, difference = -0.7 (95% CI -3.2 to 1.8), p = 0.59; mean (SD) forced expiratory volume in 1 second in the betamethasone and placebo groups 98.9 (13.4) v 98.5 (13.6)% predicted, difference = 0.3 (95% CI -2.4 to 3.1, p = 0.80)). CONCLUSIONS: Antenatal exposure to a single course of betamethasone does not alter lung function or the prevalence of wheeze and asthma at age 30.

Asthma↗
PubMed1980

Relative potency in acute and chronic suppressive effects of prednisolone and betamethasone on the hypothalamic-pituitary-adrenal axis in man.

The relative potency in the hypothalamic-pituitary-adrenal (HPA) suppression of both prednisolone and betamethasone was examined in an acute study with normal volunteers and in a chronic study with glucocorticoid-treated patients. Circadian rhythm of plasma cortisol was studied after a single dose administration of 5 to 30 mg prednisolone or 0.5 to 3.0 mg betamethasone at 8:00 hr. Morning-rise of plasma cortisol occurred on the morning after the administration of 30 mg or less prednisolone but no morning rise was noted after the administration of 1.0 mg or more betamethasone. Plasma ACTH was slightly elevated on the morning after 30 mg prednisolone administration but showed low levels throughout the night after 3.0 mg betamethasone administration. Plasma cortisol responsiveness to ACTH was examined in patients before and during therapy with either prednisolone or betamethasone. The basal cortisol level was not suppressed and the responsiveness to ACTH remained nearly normal during long-term 5 mg prednisolone therapy, but these were completely suppressed during long-term 5 mg betamethasone therapy. The responsiveness to ACTH was nearly normal in patients receiving alternate-day therapy with prednisolone in such large doses as 50 or 60 mg every other day, but was completely suppressed in patients receiving 1.0 mg betamethasone every other day. The relative potency of betamethasone in acute and chronic suppressive effects on the HPA system seems to be much stronger than that of prednisolone in equivalent doses with comparable anti-inflammatory effects. It is also suggested that the alternate-day therapy with such long-acting steroids as betamethasone are useless in preventing HPA suppression.

Adrenocorticotropic Hormone↗
PubMed2006

Adverse neonatal outcomes associated with antenatal dexamethasone versus antenatal betamethasone.

OBJECTIVE: Antenatal dexamethasone and betamethasone may not be equally efficacious in the prevention of adverse neonatal outcomes. We compared the risks of periventricular leukomalacia (PVL), intraventricular hemorrhage (IVH), retinopathy of prematurity (ROP), and neonatal death among very low birth weight infants who were exposed to dexamethasone, betamethasone, or neither steroid. METHODS: Infants (401-1500 g) in the National Institute of Child Health and Human Development Neonatal Research Network were studied. Multivariate logistic regression analyses compared the 3 groups with regard to PVL, IVH, ROP, and neonatal death, adjusting for network center and selected covariates. RESULTS: A total of 3600 infants met entry criteria. Compared with no antenatal steroids, there were trends for a reduced risk for PVL associated with dexamethasone and betamethasone but no difference in risk between dexamethasone and betamethasone. Dexamethasone reduced the risk for IVH and severe IVH, compared with no antenatal steroid exposure. Betamethasone reduced the risk for IVH, severe IVH, and neonatal death, compared with no antenatal steroids. Compared with betamethasone, dexamethasone had a statistically significant increased risk for neonatal death. There were trends for greater risks associated with dexamethasone compared with betamethasone for IVH and severe ROP. CONCLUSIONS: Betamethasone was associated with a reduced risk for neonatal death, with trends of decreased risk for other adverse neonatal outcomes, compared with dexamethasone. It may be in the best interest of neonates to receive betamethasone rather than dexamethasone when available.

Betamethasone↗