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One hundred and twenty-one patients were treated in a double-blind fashion with .025% betamethasone benzoate gel and 0.1% betamethasone valerate cream. Results were not statistically significant, although 14 of 16 patients with psoriasis showed excellent results with betamethasone benzoate gel, as opposed to six of 14 patients given betamethasone valerate cream.
Irritative effects of three steroidal anti-inflammatory drugs on the gastrointestinal tract of rats and dogs were determined. With either single or repeated subcutaneous administration these drugs dose dependently irritated the gastric mucosa of both species. The intestinal mucosa was less affected. Concomitant oral administration of aspirin or subcutaneous administration of indomethacin revealed an aggravation of aspirin-induced gastric ulcers by betamethasone valerate and inhibition of indomethacin-induced intestinal ulcers by beta-methasone dipropionate. These two steroidal drugs had no noxious effect on healing of chronic gastric ulcers induced in rats and dogs. Betamethasone valerate, however, delayed the healing of gastric ulcer in rats. Indomethacin, a non-steroidal anti-inflammatory drug, also induced serious damage to the gastric and intestinal mucosa both of rats and dogs. Indomethacin ingestion delayed the healing of chronic gastric ulcer in rats but not in dogs. Since both steroidal and non-steroidal drugs induce damage to the gastrointestinal tract, a careful monitoring of the patients' complaints should be carried out when these compounds are used as a systemic treatment. Steroidal drugs used in this study, however, appear to be highly safe from the point of dose inasmuch as they are used as a topical treatment.
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The concentration of betamethasone has been measured in maternal peripheral plasma, umbilical cord artery and vein, and amniotic fluid following maternal administration of betamethasone phosphate and betamethasone acetate on 3 consecutive days. Betamethasone was measured by radioimmunoassay following column chromatography. The findings show that betamethasone is transferred across the human placenta, circulates in the fetus and appears in amniotic fluid. During the 3 days after the start of treatment, levels of the betamethasone were similar in maternal and umbilical cord blood and in amniotic fluid. Thereafter, although levels in the mother were measurable for up to 7 days after the initial injection, the drug was detected in the cord plasma of only one baby. In vitro incubation studies of human placental tissue with 3H betamethasone identified 11-keto betamethasone as the major metabolite of betamethasone.
In the oxazolone-induced delayed hypersensitivity inflammation in the rat ear, betamethasone 17-valerate, in contrast to other topical corticosteroids, is incapable of suppressing oedema. When given in combination with triamcinolone acetonide, betamethasone 17-valerate competitively antagonizes the anti-inflammatory action of the active steroid. When tested in the mouse, betamethasone 17-valerate behaved as an anti-inflammatory agent 15 and 80 times as potent as betamethasone and hydrocortisone respectively. In an in vivo lymphocyte culture system in which preincubation with corticosteroids prevents subsequent phytohaemagglutinin induced DNA synthesis, betamethasone 17-valerate was less active than even hydrocortisone when rat lymph node cells were used, but with human cell preparations it was more potent than either hydrocortisone or betamethasone. Betamethasone 17-valerate behaves uniquely in the rat as an anticorticosteroid; in mouse and in man the compound behaves as a normal corticosteroid.
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.
Out of a group of 189 pregnant women, who were in the 28th to 37th week of gestation, 57 women received i.m. injections of betamethasone. 132 premature infants whose mothers were not treated served as controls. Betamethasone caused a significant decrease in established respiratory distress syndrome (RDS). In the betamethasone group there was an incidence of 7% of respiratory distress syndrome as compared to 23,5% in the control group. Neonatal mortality was 1,8% in the treated group versus 10,6% in the control group. The occurrence of suspected respiratory distress syndrome also was significantly lowered after betamethasone. In the control group premature rupture of membranes or administration of tocolytic drugs did not have any effect on the frequency of respiratory distress syndrome. However, the premature babies who were delivered by caesarian section had a significantly higher incidence of respiratory distress syndrome than those who were delivered vaginally. After betamethasone treatment the occurrence of respiratory distress syndrome after caesarian section was as low as in the group with vaginal delivery. The present study of a larger group of premature babies has confirmed previous positive results of betamethasone treatment.
Percutaneous absorption was studied in patients following topical application of betametahsone 17-benzoate cream and gel with occlusion by means of a sensitive and specific radioimmunoassay method. Concentrations of betamethasone 17-benzoate in plasma were between 0.3 and 5 ng/ml, indicating approximately 0.05 to 0.3% of the steroid applied to the skin was detected in plasma. Plasma betamethasone 17-benzoate levels increased in proportion to the amount of the steroid applied to the skin. High correlation between plasma betamethasone 17-benzoate levels and percent inhibition of plasma cortisol was also observed. Approximately 3 ng/ml levels of betamethasone 17-benzoate in plasma induced 90% inhibition of plasma cortisol. The data suggest that betamethasone 17-benzoate in gel base was more readily absorbed than in cream base.
The effect of oral administration of betamethasone (25 microgram kg-1 day-1) on the duodenal absorption of calcium has been studied in chicks using the ligated loop technique in vivo. The chicks were fed normal calcium, normal phosphorus (NCaNP), low calcium, normal phosphorus (LCaNP) or normal calcium, low phosphorus (NCaLP) diets. Daily oral administration of betamethasone for 2-3 weeks markedly reduced the absorption of calcium in chicks fed the NCaNP diet, but did not significantly affect the adaptation in absorption when the NCaLP or LCaNP diets were fed for the same period of time. In one group of chicks, betamethasone was administered daily for 10 days before the birds were transferred to the NCaLP or LCaNP diets. Adaptation was again unaffected by betamethasone treatment. Administration of betamethasone caused a marked retardation in growth-rate, hypercalcaemia and an increased percentage of ash in the tibiae.
One hundred forty-six pregnant women were enrolled in a prospective double-blind study to assess the effectiveness and side-effects of antenatal administration of betamethasone in the prevention of respiratory distress syndrome (RDS) in potentially premature infants. On admission to the study, the women were given, at random, either 12 mg of betamethasone or placebo. The same dose was repeated 24 hours later and then weekly up to 34 weeks of gestation. Gestational age of the infants ranged from 25 to 34 weeks, and birth weights ranged between 730 and 2,650 gm. Statistically significant differences in favor of the infants in the betamethasone group were found in the incidence of RDS, 20.7% in the betamethasone group compared with 59.5% in the control group (P less than .005); in the severity of RDS (P less than .05); and in the death rate (P less than .05). A higher incidence of hypoglycemia was found among infants in the betamethasone group (P less than .05). Prolonged rupture of the membranes played no protective role against RDS, and the incidence of infection was similar in both groups.
The effect of betamethasone on plasma cortisol concentrations was studied in 6 healty adult men. Each of them was administered 8 mg of betamethasone in a single intravenous injection. Blood samples were obtained serially for 2 days before the injection of betamethasone and for a week after the injection. Plasma cortisol was measured by competitive protein binding analysis. Before the injection of betamethasone plasma cortisol levels showed the normal diurnal rhythm in all the cases. After the injection plasma cortisol levels decreased rapidly and a mean half life time was about 1.7 hours. The low levels of plasma cortisol under 2 microgram/ml were observed for 48 hours after the injection, and then the diurnal rythm of plasma cortisol reappeared, but the levels of plasma cortisol at this time were still lower than the control levels. Then plasma cortisol levles increased gradually and they returned to the control levels 5 days after the injection. Thus, it was clarified that the suppressive effect of 8 mg or betamethasone on plasma cortisol concentrations lasted at least for 48 hours. From this point of view the time interval or repetitive glucocorticoid administration for the treatment of brain edema will further be studied.
The experimental and clinical studies on the protective effect of Betamethasone upon the myocardium particularly on the prevention of the subendocardial ischemia after the cardiopulmonary bypass was investigated on the ultrastructural alterations of the epicardium and the endocardium obtained by the transmural left ventricular myocardial biopsy. Pretreatment of Betamethasone, 5 mg/Kg, with single intravenous injection a half to one hour before cardiopulmonary bypass was effective to preserve the myocardial ultrastructure after the anoxic arrest and in the recovery period after restoring the coronary circulation. The intramyocardial gradient of the ultrastructure was diminished by Betamethasone hardly demonstrating the no-reflow phenomenon. Hemodynamic and metabolic changes did not show the significant effectiveness of Betamethasone. It was suspected that Betamethasone stabilized the cell membrane and lysosome and suppressed the interstitial edema in the myocardium during and after anoxic arrest.
The stability of betamethasone-17-valerate in semi-solid bases has been investigated. Emphasis has been placed on the stability problems which could arise upon dilution of proprietary preparations by the use of model systems. Betamethasone-17-valerate has been shown to decompose to betamethasone-21-valerate and betamethasone alcohol. Quantitation of the decomposition was by direct densitometry on thin layer chromatographic plates. The decomposition was found to be an apparent first order process and to depend on the diluent used and its concentration. Attempts were also made to relate the rate of decomposition to the pH of the base used, and to stabilize the products.
The effect of topical application of halcinonide cream and betamethasone valerate cream on plasma cortisol was studied in an acute usage study as well as a subacute study, which more closely approximated common clinical usage. In the acute study, halcinonide cream caused a marked decrease in plasma cortisol, both with and without occlusion, in patients with extensive psoriasis, but only with occlusion in normal subjects. Betamethasone valerate cream decreased plasma cortisol levels in patients with extensive psoriasis when applied with occlusion and, to a lesser extent, without occlusion. In a double-blind subacute usage study without occlusion, two of 23 patients treated with halcinonide cream showed decreased plasma cortisol levels during the treatment period, while none of the 21 patients treated with betamethasone valerate cream showed such decreases. Three patients in the halcinonide group developed striae. Clinical response to halcinonide was superior to that with betamethasone valerate cream, but a similar number of patients were resistant to treatment with each medication.
Administration of betamethasone (0.2 mg/kg, intramuscularly) to pregnant rabbits had the following effects on the fetal lung at 26--27 days gestation. It increased the amount of phosphatidylcholine in lung lavage by 70% and almost doubled the phosphatidylcholine/sphingomyelin ratio, it increased the rate of incorporation of choline into phosphatidylcholine in fetal lung slices by up to 90%, it increased the activities of pulmonary cholinephosphate cytidylyltransferase and phosphatidate phosphatase by 50% and it reduced the amount of lung glycogen to 60% of the amount in the controls. Betamethasone had no effect on the activities of pulmonary cholinephosphotransferase or lysolecithin: lysolecithin acyltransferase but it slightly decreased the activity of choline kinase. Betamethasone administration to the doe did not increase the amount of surfactant phospholipid in fetal lung lavage to as great an extent as did direct administration of cortisol to the fetuses. Neither did betamethasone stimulate the activity of pulmonary cholinephosphotransferase. These data suggest that agents other than glucocorticoids mediate the stress-induced acceleration of fetal lung maturation and surfactant production.
The commercially available betamethasone suspensions for injection used in this study have clearly shown quantitative differences in the combination of their easily hydrosoluble betamethasone esters and those difficult to dissolve in water, as well as in the shapes and sizes of their crystals. With regard to their influence on the endogenous cortisol production the two preparations have shown a highly deviating pharmaco-dynamic duration of action-corresponding to their different galenic composition (betamethasone phosphate/acetate approx. 7-8 days; betamethasone phosphate/dipropionate approx. 16-18 days). During the phase of suppression the reduced endogenous cortisol is largely compensated by the pharmaco-dynamic activity of the exogenous steroid.
Betamethasone 0.1% as valerate in an ointment base and fluocinonide 0.05% in a fatty alcohol propylene glycol (FAPG) base have been compared in a double-blind trial of 76 patients with either eczema or psoriasis. The results show betamethasone valerate ointment to be significantly (P less than.05) superior to fluocinonide FAPG in the treatment of both these skin conditions. In the light of publications from other studies on betamethasone valerate cream this trial indicates that the ointment base considerably increases the efficacy of betamethasone valerate.
The value of betamethasone valerate by inhalation in the prophylactic therapy of severe childhood asthma has been established. To determine whether the efficacy of this drug is due to a local or a systemic action a double-blind crossover study of 28 days' treatment with oral betamethasone valerate and 28 days' treatment with inhaled steroid was carried out in 10 asthmatic children. Daily doses used were 1 mg orally and 800 mug by inhalation. Nine patients had fewer symptoms, higher peak expiratory flow rates, and a lower bronchodilator requirement on inhaled than on oral therapy. Exercise-induced bronchoconstriction was diminished on inhaled therapy. Five children requested early termination of the oral therapy period because of unacceptable symptoms. Nine parents stated a preference for the period of inhaled therapy. It is concluded that betamethasone valerate is highly effective by inhalation but that a comparable oral dose has no appreciable clinical effect.