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PubMed1998

Placebo-controlled comparison between a single dose and a multidose of betamethasone in accelerating lung maturation of mice offspring.

OBJECTIVE: Our purpose was to determine, in a placebo-controlled manner with a mouse model, whether a multidose of betamethasone is more beneficial than a single dose in accelerating fetal lung maturation. STUDY DESIGN: Ninety gravid CD-1 mice were randomly assigned to 1 of 3 groups (n = 30) to receive either a placebo (0.25 mL subcutaneously) or betamethasone (0.1 mg subcutaneously) as a single dose on gestational day 14 or as a multidose twice daily on gestational day 14 and 15. Ten pregnancies in each group were terminated at gestational day 16.5 to observe the neonatal breathing pattern (scale 0 to 5; 5 is unlabored breathing) and the lung histologic findings (scale 0 to 5; 5 is alveolar budding). The lungs of the offspring belonging to the remaining 20 pregnancies in each group were removed and weighed at postnatal day 1, 3, 5, or 120. RESULTS: Fetuses exposed to a multidose of betamethasone displayed a higher breathing score at gestational day 16.5 than either to a single dose or to the placebo (mean score 4.6 vs 3.8 or 1.3; P <. 001). Alveolar development was greater after exposure to a multidose of betamethasone than after a single dose or after a placebo (mean score 4.4 vs 3.5 or 1.6; P <.001). The lung weights at gestational day 16.5 were less after a multidose of betamethasone than after a single dose of either betamethasone or a placebo (18.3 +/- 1.0 g vs 21.4 +/- 1.3 g or 23.3 +/- 1.3 g; P <.02). The lung/body weight ratio was similarly affected. This reduced weight of the lungs persisted postnatally into adulthood. CONCLUSIONS: With a CD-1 mouse model, a multidose of antenatal betamethasone accelerated fetal lung maturation more than after a single dose but was accompanied with a decrease in lung weight that persisted into adulthood.

Animals↗

PubMed1997

Changes in leukocyte, granulocyte and lymphocyte counts following antenatal betamethasone administration to pregnant women.

OBJECTIVE: Preterm labor and premature rupture of membranes are associated with a mild leukocytosis. However, we have observed a higher maternal leukocyte count after antenatal betamethasone therapy. We planned this study to evaluate the effects of antenatal betamethasone treatment on maternal leukocyte, granulocyte and lymphocyte count. METHODS: Forty-six pregnant women with the diagnosis of preterm labor between 28 and 33 weeks of gestation age received 12 mg betamethasone at a 12-h interval. The control group consisted of 50 pregnant women between 28 and 33 weeks of gestational age with no medical or obstetrics problems. After a baseline venous sampling, serial leukocyte, granulocyte and lymphocyte counts were obtained every 6 h until it returned to baseline value. RESULTS: There were no statistically significant differences in the control group with respect to the total leukocyte, lymphocyte, and neutrophil count. Total leukocyte and granulocyte counts were increased by 29.8% and 17.8% within 24 and 12 h after betamethasone injection, respectively (P < 0.01). A significant reduction in lymphocyte count was observed within 12 h (45.4%) after betamethasone injection (P < 0.01). All changes in leukocyte, granulocyte and lymphocyte counts returned to baseline values within 3 days. CONCLUSION: Antenatal betamethasone therapy leads to an increase in maternal leukocyte count and a decrease in lymphocyte count. This effect is transient and any leukocytosis persisting for more than 3 days is not due to betamethasone administration.

Betamethasone↗

PubMed2003

Differential effects of maternal and fetal betamethasone injections in late-gestation fetal sheep.

OBJECTIVE: To determine the effects of single or repeated intramuscular injections of betamethasone, given maternally or directly to the fetus, on chronically catheterized, late-gestation fetal sheep. METHODS: Fetal or maternal sheep received either repeated intramuscular injections of betamethasone (0.5 mg/kg body weight at 104, 111, and 118 days' gestation), single betamethasone injection (at 104 days' gestation, followed by saline at 111 and 118 days' gestation), or repeated saline injections; n = 6 or 7 per group. At approximately 130 days' gestation fetuses were catheterized for serial measurements of heart rate, arterial pressure, blood gases, metabolites, and electrolytes. RESULTS: Repeated maternal betamethasone injections reduced birth weight (P =.03) without fetal hypoxemia or hypoglycemia. Circulating fetal calcium and lactate concentrations were reduced (P =.002 and P =.014, respectively) by repeated maternal betamethasone only. Fetal hematocrit tended to be lower after fetal (P =.3) and maternal (P =.07) betamethasone. CONCLUSION: Growth restriction caused by repeated maternal betamethasone treatments is not due to overt chronic placental insufficiency but may be caused by alterations in hormonal mediators of fetal growth or impairment of placental transport of specific nutrients.

Animals↗

PubMed2001

A prospective, randomized trial comparing the efficacy of dexamethasone and betamethasone for the treatment of antepartum HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome.

OBJECTIVE: This study was undertaken to determine whether dexamethasone or betamethasone is superior for the antepartum treatment of HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome. STUDY DESIGN: This prospective, randomized, clinical investigation compared intravenously administered dexamethasone and intramuscularly administered betamethasone in the treatment of gravid women with HELLP syndrome. Efficacy end points included laboratory values (platelet count, lactate dehydrogenase activity, aspartate aminotransferase activity) and clinical parameters (mean arterial pressure, urinary output). RESULTS: Forty patients were enrolled in the study, 19 in the dexamethasone arm and 21 in the betamethasone arm. The adjusted time-averaged changes from baseline were significant for aspartate aminotransferase activity (dexamethasone, -20.4 +/- 9.6 U/L; betamethasone, 9.9 +/- 8.9 U/L; P =.029), mean arterial pressure (dexamethasone, -15.6 +/- 1.4 mm Hg; betamethasone, -8.1 +/- 1.4 mm Hg; P <.001), and urinary output (dexamethasone, 12.9 +/- 8.6 mL/h; betamethasone, -11.9 +/- 8.2 mL/h; P =.043). CONCLUSION: Intravenously administered dexamethasone appears to be more effective than intramuscularly administered betamethasone for the antepartum treatment of mothers with HELLP syndrome.

Adult↗

PubMed2002

A new calcipotriol/betamethasone formulation with rapid onset of action was superior to monotherapy with betamethasone dipropionate or calcipotriol in psoriasis vulgaris.

In this study, we compared a new combination ointment containing both calcipotriol and betamethasone dipropionate with betamethasone dipropionate ointment (Diprosone) and calcipotriol ointment (Daivonex) in patients with psoriasis vulgaris; 1106 patients were randomized to twice daily double-blind treatment with combination, betamethasone dipropionate or calcipotriol for 4 weeks. Patients then received twice daily calcipotriol, unblinded, for a further 4 weeks. Mean percentage change in PASI at end of the double-blind phase was -74.4 (combination group), -61.3 (betamethasone group) and -55.3 (calcipotriol group). Mean difference (95% Cl) combination-betamethasone was -13.1 (-16.9 to -9.3, p < 0.001) and for combination-calcipotriol -19.0 (-22.8 to -15.2, p <0.001). The differences in PASI were also statistically significant after 1 week. In the double-blind phase, 8.1% of patients (combination) reported lesional/ perilesional adverse reactions compared to 4.7% (betamethasone) and 12.0% (calcipotriol). In the combination group, mean PASI at the end of the double-blind phase was 2.5, and at end of the unblinded phase 3.6, compared with 3.9 and 4.1 (betamethasone) and 4.4 and 3.7 (calcipotriol). Calcipotriol/betamethasone combination is more effective and has a more rapid onset of action than either active constituent used alone, and is well tolerated. It is safe to transfer patients from combination to calcipotriol, with maintenance of clinical effect.

Administration, Topical↗

PubMed1994

Comparative effects of calcipotriol solution (50 micrograms/ml) and betamethasone 17-valerate solution (1 mg/ml) in the treatment of scalp psoriasis.

The efficacy, tolerability and safety of calcipotriol solution and betamethasone 17-valerate solution were compared in a multicentre, prospective, randomized, double-blind, parallel group study. Four hundred and seventy-four patients with scalp psoriasis were recruited from six European countries and Canada. Following a 2-week washout period, either calcipotriol solution (50 micrograms/ml) or betamethasone 17-valerate solution (1 mg/ml) was applied twice daily for 4 weeks. After this time, patients who required no further active treatment were observed for relapse. Retreatment with calcipotriol was offered to those patients who relapsed, and who were originally in the calcipotriol-treated group. The two treatment groups were well matched at baseline. At the end of treatment, the proportion of patients who had 'cleared' or 'markedly improved' was statistically significantly greater in the betamethasone group (75%) than in the calcipotriol group (58%) (P < 0.001) (95% confidence interval of difference 25.3-->8.6). The decrease in total sign score (sum of scores for erythema, thickness and scaliness) at the end of treatment was also statistically significantly greater in the betamethasone group (61%) than the calcipotriol group (45%) (P < 0.001) (95% confidence interval of difference 9.7-->23.1). Adverse events were reported by 87 patients in the calcipotriol group, and 31 patients in the betamethasone group; the most common was lesional or perilesional irritation, which occurred significantly more frequently with calcipotriol (26%) than with betamethasone (8%) (P < 0.001). Fifteen patients (6%) in the calcipotriol group and four (1%) in the betamethasone group withdrew from the study because of adverse events or unacceptable treatment response (P = 0.017).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1999

Betamethasone-mediated vascular dysfunction and changes in hematological profile in the ovine fetus.

Glucocorticoid administration to fetal sheep induces a sustained systemic blood pressure rise and an associated increase in femoral vascular resistance. We utilized a small vessel myograph to compare isometric vascular responses of small femoral arterial branches from fetal sheep infused intravenously with either betamethasone or vehicle in vivo from 128 days gestation. Changes in hematological parameters were also determined. Betamethasone was infused for 48 h to produce fetal plasma betamethasone concentrations similar to those observed in human fetuses after maternal treatment with betamethasone to accelerate fetal lung maturation. When compared with vessels removed from vehicle-infused fetuses, vessels obtained from betamethasone-treated fetuses exhibited 1) enhanced sensitivity to depolarizing potassium solutions; 2) no differences in response to the thromboxane mimetic U-46619 or norepinephrine; and 3) differential responses to vasodilators, enhanced sensitivity to ACh, but decreased response to bradykinin and forskolin. In addition, erythrocyte and leukocyte counts were increased in betamethasone-infused fetuses. These observations indicate that multiple mechanisms operate to increase fetal vascular resistance during antenatal betamethasone exposure.

Animals↗

PubMed2003

Late-gestation betamethasone enhances coronary artery responsiveness to angiotensin II in fetal sheep.

Antenatal glucocorticoids are used to promote the maturation of fetuses at risk for preterm delivery. While perinatal glucocorticoid exposure has clear immediate benefits to cardiorespiratory function, there is emerging evidence of adverse long-term effects. To determine if antenatal betamethasone alters vascular reactivity, we examined isometric contraction of endothelium-intact coronary and mesenteric arteries isolated from twin fetal sheep at 121-124 days gestation (term being 145 days). One twin received betamethasone (10 microg/h iv) while the second twin received vehicle (0.9% NaCl) for 48 h immediately before the final physiological measurements and tissue harvesting. Fetuses that received betamethasone had higher mean arterial blood pressures than the saline-treated twin controls (53 +/- 1 vs. 48 +/- 1 mmHg, P < 0.05). Coronary vessels from betamethasone-treated fetuses exhibited enhanced peak responses to ANG II (72 +/- 17 vs. 23 +/- 6% of the maximal response to 120 mM KCl, P < 0.05). There was no significant difference in response of the coronary arteries to other vasoactive compounds [KCl, U-46619, sodium nitroprusside, 8-bromo-cGMP (8-BrcGMP), isoproterenol, and forskolin]. Contractile responses to ANG II were similar in betamethasone and control mesenteric arteries (48 +/- 17 vs. 36 +/- 12% of the maximal response to 10-6 M U-46619). Western blot analysis revealed AT1 receptor protein expression was increased by betamethasone in coronary but not in mesenteric arteries. These findings demonstrate that antenatal betamethasone exposure enhances coronary but not mesenteric artery vasoconstriction to ANG II by selectively upregulating coronary artery AT1 receptor protein expression.

Angiotensin II↗

PubMed1980

Steroid and growth hormone levels in premature infants after prenatal betamethasone therapy to prevent respiratory distress syndrome.

Prenatal maternal therapy with glucocorticoid reduces the incidence of respiratory distress syndrome (RDS) in premature infants. To investigate the effects of this treatment on the fetal endocrine system, we determined serum concentrations of betamethasone, cortisol, dehydroepiandrosterone sulfate, growth hormone, and prolactin in cord blood of 215 treated infants and 117 untreated infants of 26--36 wk of gestation. Cortisol levels are suppressed within 6 hr of betamethasone treatment, decrease to 45% of the concentration in untreated infants (8.4 micrograms/dl), and return to normal by 7 days. Dehydroepiandrosterone sulfate is reduced maximally by 65% and returns to normal concentrations (123.5 micrograms/dl in 7 1/2 days. The suppression of both steroids was similar after treatment with 12 mg betamethasone (acetate and phosphate) daily 2 times or with 6 mg betamethasone (alcohol) twice daily 4 times. Peak betamethasone levels were higher after the 12 mg dose, but the two-treatment regimens produced a similar total exposure of the fetus to elevated serum glucocorticoid activity for 2 1/2 days and decreased plasma activity for the subsequent 4 1/2 days. Treated infants with low cortisol concentrations at birth increased their cortisol levels severalfold after birth in response to either intrapartum asphyxia or RDS. Betamethasone therapy did not affect cord serum prolactin levels, but the concentration of growth hormone was reduced at all ages. The suppression was greatest (53% decrease) among infants of 28 less than 32 wk, and, among older infants, there was a subsequent increase above control levels between 2 and 4 days after treatment. This study indicates that prenatal betamethasone treatment causes a transient suppression of fetal growth hormone and presumably those pituitary hormones which regulate steroid production by both the definitive and fetal zones of the fetal adrenal. However, the suppression of fetal cortisol does not interfere with the pituitary-adrenocortical response to stress after birth.

Betamethasone↗

PubMed1989

Increased constriction of the ductus arteriosus with combined administration of indomethacin and betamethasone in fetal rats.

To find a better treatment for patient ductus arteriosus of preterm infants, we studied the combined effect of indomethacin and betamethasone on the fetal ductus in rats. We used a rapid whole-body freezing technique, and the ratio of the inner diameter of the ductus to the main pulmonary artery, which was 1.0 in controls, was used as an index of constriction. Indices of ductal constriction 4 h after administration of indomethacin (1 mg/kg) alone, betamethasone (1 mg/kg) alone or in combination in near-term rats were 0.56 +/- 0.05 (mean +/- SEM), 0.76 +/- 0.06, and 0.17 +/- 0.03, respectively. In preterm rats too, a marked increase in fetal ductus constriction was observed with the combined administration of these two drugs. Study of the dose effect of betamethasone revealed that maximal effects were obtained with 1 mg/kg of betamethasone combined with indomethacin in both preterm and near-term fetal rats. Increased constriction of the fetal ductus with combination treatment persisted from 1 to 8 h after administration. Administration of betamethasone 24 h before the rat was killed did not augment constriction of the fetal ductus by indomethacin administered 4 h before they were killed. Fetal ductus constriction by sulindac, another nonsteroidal antiinflammatory drug with little inhibitory effect on renal function, also was augmented by combined use with betamethasone (1 mg/kg). In conclusion, ductal constriction was markedly increased by combined administration of indomethacin and betamethasone in near-term and preterm fetal rats.

Animals↗

PubMed2004

Circulating glucocorticoid bioactivity in the preterm newborn after antenatal betamethasone treatment.

Antenatal glucocorticoid treatment of mothers at risk of premature delivery is highly cost-effective in reducing neonatal mortality and morbidity. However, there is only limited information on the actual glucocorticoid bioactivity (GBA) reaching the fetus. By employing a recently developed recombinant cell bioassay, we studied circulating GBA in preterm newborns exposed to the standard antenatal betamethasone regimen (12 mg betamethasone twice, 24-h interval, for the mother; repeated in 7-10 d if required). Plasma GBA and cortisol concentrations were measured in cord blood of 71 infants (mean gestational age, 28.9 wk; range, 24.6-32 wk; mean birth weight, 1208 g; range, 480-2010 g). The median time between the last administered betamethasone dose and birth was 2.0 d. Cord GBA ranged from less than 15.6 to 170 nmol/liter cortisol equivalents. The level was highly dependent on the time between the last betamethasone dose and birth, i.e. infants born shortly (<12 h) after the last steroid dose displayed on average 4-fold higher GBA than that in the reference group (infants with >7 d since the last betamethasone dose before birth or without treatment; 74 vs. 21 nmol/liter cortisol equivalents; P < 0.0001). By contrast, if more than 72 h had elapsed between the last steroid dose and birth, circulating GBA was strongly dependent on cord cortisol (r = 0.85; P < 0.0001; n = 30). In multiple regression analysis adjusted for cord cortisol concentration and the time since the last steroid dose, increased umbilical artery resistance, a sign of severe fetal distress, was associated with lower cord GBA (P = 0.01). In conclusion, antenatal exposure of preterm fetuses to betamethasone causes a sizeable, but brief, peak of supraphysiological GBA, and approximately 3 d after the last betamethasone dose, circulating GBA derives from cord cortisol concentration.

Betamethasone↗

PubMed2000

Effects of repeated maternal betamethasone administration on growth and hypothalamic-pituitary-adrenal function of the ovine fetus at term.

Synthetic glucocorticoids have become an important clinical tool with which to advance fetal lung maturation in women at risk of early preterm birth, and this has succeeded in reducing neonatal mortality and morbidity from respiratory distress syndrome. Although previous studies have shown that glucocorticoids have deleterious consequences on fetal development, there is little information regarding the effects of clinically relevant repeated maternal doses of glucocorticoids on fetal growth and hypothalamic-pituitary-adrenal (HPA) function. We hypothesised that repeated prenatal exposure to increased concentrations of glucocorticoids would alter fetal growth and HPA axis development. Pregnant ewes were injected with betamethasone (0.5 mg/kg) or vehicle at 104, 111 and 118 days of gestation (term 150 days). Animals were sacrificed at 125 and 146 days of gestation, at which time fetal weights were recorded. Maternal and fetal blood samples were gathered and fetal tissue collected. Maternal oestradiol concentrations were significantly greater than those in controls at 125 days of gestation, but were not different at 146 days. Maternal plasma progesterone concentrations were similar between groups at both 125 and 146 days of gestation. Weight at birth was significantly reduced by 23% at 125 days and 19% at 146 days of gestation (P<0.05) after exposure to glucocorticoid. Cord plasma ACTH concentrations were not significantly different between groups at day 125, but were significantly increased in day 146 fetuses of ewes that had received betamethasone (P<0.05). Cord plasma cortisol concentrations followed the same trend, although differences were not statistically significant. Cord plasma corticosteroid binding capacity (CBC) was significantly increased at 125 days of gestation in fetuses of betamethasone-treated animals (P<0.05), but not at 146 days of gestation. To examine the mechanisms regulating the increase in cord plasma ACTH of 146-day fetuses, we used in situ hybridisation to determine the distribution and levels of mRNA encoding key pituitary and hypothalamic neuropeptides of the HPA axis. In pituitaries of 146-day fetuses, there were no significant differences in the regional pattern of distribution or amounts of pro-opiomelanocortin (POMC) mRNA between betamethasone-treated animals and controls, in either the pars intermedia or the inferior and superior regions of the pars distalis. Neither prohormone convertase (PC)-1 nor PC-2 mRNA levels in pituitaries of 146-day fetuses were significantly different between treatment groups. After maternal betamethasone, immunoreactive ACTH peptide content in the fetal pars distalis was not different but glucocorticoid receptor (GR) mRNA levels in the pars distalis were increased significantly (P<0.05). No significant difference in distribution pattern or concentrations of corticotrophin-releasing hormone (CRH) mRNA, GR mRNA, oxytocin mRNA and pre-proenkephalin mRNA were found in hypothalami from fetuses at 146 days of gestation after betamethasone treatment. We conclude that antenatal betamethasone given to pregnant sheep in a manner similar to that used in human obstetric practice results in reduced weight at birth at 125 and 146 days, and altered basal cord levels of plasma ACTH and corticosteroid binding capacity, but these changes are not reflective of changes in steady state concentrations of POMC and CRH mRNA in the fetal pituitary or hypothalamus.

Adrenocorticotropic Hormone↗

PubMed1982

Defleecing effect of betamethasone and other long-acting corticosteroids, their influence on wool growth and some physiological processes in sheep.

The defleecing effects of the long-acting derivatives of prednisolone, triamcinolone and dexamethasone were compared with those of betamethasone alcohol when these steroids were administered at the rate of 3.3 mg/kg liveweight in three equal intramuscular injections of 1.1 mg to Merino wethers. Prednisolone showed no defleecing activity whereas the other steroids produced positive but variable responses. Prolonged depression of wool growth was evident following treatment with dexamethasone esters. Betamethasone alcohol injected intramuscularly at 1.1 mg/kg daily for 3 days produced a similar defleecing response to intravenous infusion of 3.3 mg/kg betamethasone phosphate over 8 days. A range of dose rates (0.3-3.3 mg/kg) of betamethasone as multiple and single intramuscular injections indicated that the minimum effective defleecing dose was approximately 2.1 mg/kg. The response to simultaneous administration of betamethasone and insulin or chlorpropamide (to increase glucose utilization) and glucose or xylazine (to increase hyperglycaemia) suggested that the gluconeogenic role of this steroid had little effect on fibre shedding. Thyroxine (300 micrograms per sheep) administered on the first day with an injection of betamethasone (0.9 mg/kg), and alone daily for 20 days thereafter, did not influence the changes in wool production resulting from betamethasone treatment. These results are discussed in relation to the molecular structure and physiological characteristics of a potentially specific defleecing steroid.

Adrenal Cortex Hormones↗

PubMedDate not supplied

The effect of betamethasone on intraocular pressure in nephrotic children.

Intraocular pressure (IOP) was measured by Goldmann's or Schiotz's method in 46 nephrotic children, who were treated with betamethasone, and in 40 age-matched normal controls at the Taipei Municipal Chung-Hsin Hospital, from July 1, 1987 to June 30, 1990. We found the difference in mean IOP between patients treated at the end of a full-dose course of betamethasone and normal controls or patients before treatment, was statistically significant. This difference was also found between the measurement of IOP at the end of a full-dose course of betamethasone, and after stopping betamethasone therapy two to four weeks later. Although six of all patients had high IOP and suffered from headache or ocular pain, clinically, at the end of full-dose betamethasone therapy, the symptoms disappeared quickly after tapering or stopping of the drug. Therefore, we believe it is very safe to treat the nephrotic syndrome with betamethasone. On the other hand, these observations indicate that corticosteroid is a causative factor in increasing IOP. Susceptibility to full-dose betamethasone is firmly recognized, and patients need to be monitored on an individual basis. Nephrotic syndrome is a chronic disease which often requires long-term corticosteroid treatment. Children with the syndrome are at risk of developing steroid-induced increasing IOP. Careful ophthalmological examination of nephrotic children, as well as other pediatric patients who received corticosteroid therapy, is highly recommended.

Adolescent↗

PubMedDate not supplied

Differential effects of betamethasone and dexamethasone fetal administration of parturition in sheep.

OBJECTIVE: We tested the hypothesis that betamethasone is more potent than dexamethasone in inducing the essential mechanisms of parturition in sheep. METHODS: Twenty-one sheep were instrumented under general anesthesia with maternal and fetal arterial and venous catheters and myometrial electromyogram electrodes at 117 days' gestation (dGA). At 125 dGA at 12:00 PM, after 2 days of baseline recording, either saline (n = 7, control group), betamethasone (n = 7), or dexamethasone (n = 7) was administered into the fetal jugular vein at a rate of 10 micrograms/hour. A total dose of 0.48 mg was given over the next 48 hours. The animals underwent autopsy 3 days after the end of the infusion period (130 dGA), or earlier if labor resulted from the glucocorticoid administration. Daily maternal and fetal arterial blood samples (4 mL) for hormone measurement were taken at 10:00 AM throughout the study period. Additional arterial blood samples were taken if the animal developed labor. Maternal plasma progesterone and fetal ACTH and cortisol concentrations were measured by radioimmunoassay, and corticosteroid-binding globulin (CBG) binding capacity was determined by saturation analysis. Myometrial activity was monitored continuously throughout the experimental protocol. RESULTS: All seven betamethasone-treated animals developed labor after the glucocorticoid infusion regimen. In contrast, only two of seven dexamethasone-treated animals developed labor. Fetal treatment with betamethasone produced a greater and earlier fall in maternal plasma progesterone than fetal treatment with dexamethasone. Both betamethasone and dexamethasone treatments elevated fetal plasma CBG to similar binding capacities. Elevated fetal plasma ACTH and cortisol concentrations at the end of the infusion period in both betamethasone-and dexamethasone-treated animals were not related to the development of labor-type contractions. CONCLUSION: These data support the hypothesis that betamethasone is more potent than dexamethasone in inducing the essential mechanisms of parturition in sheep.

Adrenocorticotropic Hormone↗

PubMed1997

Betamethasone-induced ocular hypertension in rabbits.

The effect of subconjunctivally injected betamethasone on intraocular pressure (IOP) was studied in 85 albino New Zealand rabbits. IOP was measured with a Mentor Model 30 classic pneumatonograph that was manometrically calibrated to the rabbit eye. Ocular hypertension was induced by weekly subconjunctival injections of a betamethasone suspension into the left eye. In one experiment, 70 rabbits were given betamethasone for 4 weeks, while a second group of 10 rabbits received betamethasone for 11 weeks. The short-term effects of subconjunctival injections of betamethasone on IOP were also recorded in a third group of 5 rabbits. Weekly injections over 4 weeks resulted in an increase in IOP in the treated eye, which was prolonged to 11 weeks by repeated weekly injections. A sustained increase in IOP was observed in the treated eye for a period of 7 weeks. During the early hours after betamethasone injection, a transient decrease in IOP was registered in both eyes. The results show that weekly subconjunctival injections of betamethasone cause a predictable increase in IOP in the treated eye which may be suitable for testing the short- and long-term effects of antiglaucoma drugs. Evidence suggesting that endogenous glucocorticoids may play a role in the development of ocular hypertension in humans strengthens the potential value of this glaucoma model.

Animals↗

PubMed1997

The effects of betamethasone derivatives on endotoxin-induced uveitis in guinea pigs.

OBJECTIVE AND DESIGN: We reported previously that the betamethasone derivative betamethasone dipropionate behaves as an anti-glucocorticoid in rat endotoxin-induced uveitis (EIU). In the present study, we produced EIU in guinea pigs and investigated the effects of betamethasone dipropionate on the EIU. MATERIAL: Male Hartley guinea pigs were used. TREATMENT: Glucocorticoids were instilled into the eye. METHOD: To elicit EIU, lipopolysaccharide (LPS) was injected into the anterior chamber of the eye. Cell numbers in the aqueous humor after LPS injection were determined by flow cytometry. Prostaglandin E2 (PGE2) production after LPS injection into the anterior chamber was also examined. RESULTS: Intracameral injection of LPS (1 microgram/eye) induced cell infiltration into the anterior chamber and PGE2 production. Betamethasone dipropionate inhibited cell infiltration and PGE2 production more strongly than betamethasone. These results suggest that betamethasone dipropionate is a potent glucocorticoid in guinea pigs. CONCLUSIONS: Structure-activity relationships of glucocorticoids in the guinea pig EIL model may differ from those in the rat EIU model.

Animals↗

PubMed1978

Topical betamethasone 17-valerate is an anticorticosteroid in the rat. 1. Dermal atrophy.

In the albino rat, topical betamethasone 17-valerate acts as an anticorticosteroid. This steroid is inactive in a dermal atrophy assay over a dose range where betamethasone and hydrocortisone display atrophogenic activity. At appropriate concentrations betamethasone 17-valerate competitively inhibits the atrophogenic effects of both betamethasone and triamcinolone acetonide. Since betamethasone and betamethasone 17-valerate penetrate rat skin in vivo at essentially the same rate, it is concluded that the latter compound is relatively resistant to hydrolysis during penetration, and that it binds to rat corticosteroid receptor proteins in such a manner as to prevent expression of corticosteroid activity. Therefore, the rat cannot be used as a model species to predict activity in man for this compound.

Administration, Topical↗