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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.
Steroids induce resistance to neuromuscular blocking drugs. Betamethasone-induced resistance to vecuronium has been demonstrated in vitro, and a presynaptic site of interaction has been suggested. This study investigated whether atracurium is similarly affected. Rat phrenic nerve-hemidiaphragm preparations were bathed in a physiologic solution, and one-half were exposed to betamethasone (1 mumol/L). Dose responses were recorded for atracurium (8-13 mumol/L) and vecuronium (2-12 mumol/L) for control and betamethasone-treated preparations. In comparison to control, the betamethasone groups had significantly less depression of muscle contraction force at all concentrations of atracurium (P = 0.0004) and vecuronium (P = 0.002). The calculated ED50 (50% depression of muscle contraction force, expressed as mean +/- SEM) for atracurium was 8.83 +/- 0.62 mumol/L for controls and 11.19 +/- 0.54 mumol/L for betamethasone-treated preparations. The calculated ED50 for vecuronium was 4.72 +/- 0.41 mumol/L for controls and 6.84 +/- 0.66 mumol/L for betamethasone-treated preparations. Betamethasone therefore increased the ED50 for atracurium by 27% and vecuronium by 45%; however, the magnitudes of these differences were not significant (P = 0.74) between the neuromuscular blocking agents. These results indicate that betamethasone-induced resistance to nondepolarizing neuromuscular blockade affects both atracurium and vecuronium to similar degrees in vitro.
Betamethasone, betamethasone-17-valerate, betamethasone-17-benzoate, and betamethasone-17,21-diproprionate were investigated for their inhbitory action on glucose-beta-phosphate dehydrogenase (G-6-PDH) activity (pure enzyme from yeast, enzyme from human skin homogenate). Between these four compounds, marked differences were encountered which could not be attributed to the presence of an esterified or unesterified steroid. According to these data it does not seem to be justified to consider betamethasone esters simply as the transport forms of the topically inactive betamethasone but one must consider the betamethasone esters having biochemical actions of their own.
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.
Synthesis of plasma albumin was studied in perfused liver of normal and CCl4-intoxicated rats, using 14C-bicarbonate method. 1. In normal liver, albumin synthesis averaged 5.6 mg/hr/100 g body weight. 2. In CCl4-intoxicated liver, albumin synthesis decreased to 4.6 mg at acute stage, but restored to 5.1 mg at non-septal fibrotic stage. At septal fibrotic, cirrhotic and cirrhotic stage with ascites, the synthesis rate averaged 4.5 mg, 4.1 mg and 3.2 mg, respectively. From these results, it is inferred that albumin synthesis rate decreases in accordance with the progress of the liver injury. 3. Effect of betamethasone on plasma albumin synthesis in perfused rat liver was investigated. Albumin synthesis rate in normal liver averaged 5.4 mg, and after addition of betamethasone, the rate averaged 4.3 mg, 3.3 mg and 2.8 mg, respectively. The rate after addition of betamethasone increased to 7.3 mg, 5.5 mg and 4.5 mg, respectively. From these results obtained, it is inferred that betamethasone increases plasma albumin synthesis in both normal and CCl4-intoxicated liver. 4. In normal liver, actinomycin-D did not inhibit basal albumin synthesis, but inhibited the increase of albumin synthesis by betamethasone, when actinomycin-D was added together with betamethasone. From these facts, it is concluded that betamethasone is able to induce albumin synthesis.
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.
Because of premature labour, probability of fetal retardation, discrepance at term of delivery, Rh-incompatibility or EPH-gestosis 185 patients were hospitalized. 76 pregnant women received twice 1.5 ml Celestan Depot i.m. (4.5 betamethasone acetate and 6mg betamethasome dinatrium phosphate per injection) within an interval of 24 hours. It was necessary to maintain a tocolysis for at least 48 hours as a minimum after the first injection of Celestan Depot. The other 109 patients without treatment of glucocorticoids were considered as a controlgroup. We could show that antepartum application of betamethasone before the 38. week of gestation was associated with a reduction of RDS in our premature infants. Only one baby of the betamethasone-treated infants died of hyaline membrane disease during the first 7 days of life compared with 11 of the control group. In 11 patients patients amniocentesis was performed before the first injection of glucocorticoids and was repeated 2 to 7 days later. The amniotid fluid lecithin phosphorus concentration was determined. In the same period of pregnancy and the same iterval the lecithin phosphours level of amniotic fluid was analysed in 11 other patients who were not rreated with glucocorticoids. The difference between amniotic fluid lecithin phosphorus concentration in the first and second anslysis was found significant by a level of significance of alpha = 5%. There was no evidence of an influence of the therapy with Celestan Depot on this increase. The excretion of oestorgens in the urine of 24 hours was analysed in 22 gradidae before and 7 days after the treatment with betamethasone. The oestogen values of the day before application of betamethasone served as baseline figures. All patients showed a market fall in urinary oestrogens excretion, especially after the second day of therapy. After day 2 the values returned rapidly to baseline values. There were no differences between treated and control groups in Apgar scores at birth or in the incidence of icterus neonatroum (bilirubine level is greater that 10 mg% in the serum). The results of our study support the hypothesis that in humans glucocorticoid administration to the fetus accelerates lung maturation. Relatively brief intrauterine exposure of human infants to pharmacological doses of betamethasone was associated with a substantial reduction in the incidense of RDS.
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.
The influence of maternal corticosteroid administration on the cortisol concentration in fetal blood and amniotic fluid (AF) was studied in women receiving betamethasone for prevention of IRDS. Thirty-four pregnant women in danger of spontaneous or induced preterm delivery were treated with 12 mg. of betamethasone daily for 3 days. AF was obtained by amniocentesis on the day before and the day following the betamethasone treatment and by amniotomy at delivery; cord arterial and venous blood was taken at delivery. Corresponding samples were obtained from 17 pregnant control subjects. All samples were analyzed in duplicate for cortisol by radioimmunoassay. The basal AF cortisol level rose with gestational age. The AF cortisol concentration fell from the basal value of 24.5 +/- 1.8 to 5.4 +/- 0.4 ng. per milliliter 3 days after the start of treatment, and it remained low at delivery if the treatment-delivery time was less than 1 week. An almost significant positive correlation (r = 0.543) was found between the cortisol concentration in cord arterial blood and AF. The cortisol concentration in cord blood in the controls was 108.2 +/- 14.3 ng. per milliliter in the arteries and 106.4 +/- 18.6 ng. per milliliter in the vein. Also, the cord blood cortisol level was depressed in betamethasone had been given within one week before delivery. The multifactorial influence on cord blood cortisol level prevents interpretation of the results as support for the concept that the human fetal adrenal is involved in labor initiation. The duration of gestation was not altered by the betamethasone treatment. The analysis of cortisol in the easily accessible amniotic fluid is suggested for estimating the function of the fetal adrenal cortex.
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.
We studied the effect of maternal administration at various intervals of betamethasone, triiodothyronine (T3), or both, on fetal rat lung maturation. T3 alone did not enhance choline incorporation to phosphatidylcholine by 20-day fetal lung explants, or morphometric lung maturation. Betamethasone, and betamethasone plus T3, increased both of those parameters over control and T3 values. However, addition of T3 offered no advantage over administration of betamethasone alone. Significant enhancement of morphometric lung maturation was already present after only 24 h of exposure to beta-methasone, or to the combination of hormones. However, choline incorporation to phosphatidylcholine only increased significantly by 36 h of exposure to betamethasone with or without T3.
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.