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PubMed1981

Antenatal betamethasone and renal ammoniagenesis in the newborn.

As part of a double-blind clinical trial of antenatal betamethasone, we studied the effects of this drug on urinary ammonia excretion in 28 premature infants. Betamethasone was administered before 34 weeks of gestation according to dosage schedules which have been shown to alter the incidence of respiratory distress syndrome. Although glucocorticoids affect renal ammoniagenesis in adults, the antenatal betamethasone trial did not augment ammonia excretion measured during the first day of postnatal life. We speculate that precocious maturation of renal ammoniagenesis cannot be triggered by glucocorticoids during the gestational period studied.

Ammonia↗

PubMed1976

The effect of betamethasone on pressure-volume characteristics of nonfetal rat lungs.

Betamethasone was administered to rats for 28 days, and body weight, lung weight, and descending pressure-volume relations were measured in their excised lungs. In rats treated with corticosteroid, lung and body weights increased less rapidly than in control rats, but the ratio of lung wet weight to body weight and the per cent dry weight remained the same in both groups. The absolute lung volume was significantly greater at each pressure in the control rats; but when expressed per lung weight, the lungs of rats treated with corticosteroid held more air. When corrected for lung size, the only difference in the lung pressure-volume curves between groups existed at transpulmonary pressures of 0 and 5 cm H2O, where the lungs of the rats treated with betamethasone contained more volume, whether inflated with air or with saline. We concluded that betamethasone administered to nonfetal rats has little influence on the lung's pressure-volume characteristics, which cannot be ascribed to differences in lung size.

Animals↗

PubMed1994

Betamethasone activation of CTP:cholinephosphate cytidylyltransferase in vivo is lipid dependent.

Glucocorticoids increase surfactant phosphatidylcholine synthesis, in part, by stimulating the rate regulatory enzyme CTP:cholinephosphate cytidylyltransferase. This enzyme exists in mammalian lung cytosol as an active lipoprotein form (H-form) and an inactive apoprotein (L-form) species. We administered betamethasone to pregnant rats to examine the mechanisms for glucocorticoid stimulation of cytidylyltransferase activity in fetal lung. The hormone stimulated cytosolic activity threefold, and this effect was nearly abolished after lipid extraction. The addition of lipid extracts isolated from betamethasone-treated cytosolic preparations to L-form species increased enzyme activity to a greater extent than lipid extracts from control lungs. Further, the glucocorticoid increased the proportion of H-form activity from 34 to 55% of the total activity in the fetal lung cytosol. These changes were associated with a marked decrease in the activity of the L-form species. Analysis of the lipid composition of the H-form revealed that betamethasone increased the content of lipid activators, including phosphatidylglycerol and fatty acids. These observations provide evidence that glucocorticoid stimulation of CTP:cholinephosphate cytidylyltransferase in vivo is mediated by a conversion of the inactive form (L-form) to the active species (H-form). These studies further emphasize the critical role of lung lipids in mediating the glucocorticoid activation of this enzyme.

Animals↗

PubMed1983

Effect of salicylic acid on the activity of betamethasone-17,21-dipropionate in the treatment of erythematous squamous dermatoses.

Forty adult out-patients with erythematous squamous dermatoses of the scalp were treated in this 21-day double-blind study with an alcohol base lotion containing either 0.05% betamethasone-17,21-dipropionate, 2% salicylic acid, 0.05% betamethasone-17,21-dipropionate + 2% salicylic acid or their respective placebo. The four treatments were assigned randomly to the patients according to a 2 x 2 orthogonal factorial design. Changes in severity of redness, scaling, pruritus and size of lesions were evaluated. Since very few patients presented with excoriation and lichenification, these symptoms could not be ascertained. Results were assessed for significance by covariance analysis where initial status was used as regressor. A potentiation of the betamethasone-17,21-dipropionate activity by salicylic acid was observed for scaling. An additive effect was noted for redness and pruritus. According to the physician's global evaluation, patients treated with the combination drug showed a better evolution than those treated with placebo. The results suggest that addition of a keratolytic agent enhances the corticosteroid effect in the treatment of erythematous squamous dermatoses.

Administration, Topical↗

PubMedDate not supplied

Once-daily 0.1% mometasone furoate cream versus twice-daily 0.1% betamethasone valerate cream in the treatment of a variety of dermatoses.

A randomized, investigator-blind, parallel-group trial was conducted to compare the safety and efficacy of 0.1% mometasone furoate cream applied once daily with that of 0.1% betamethasone valerate cream applied twice daily in patients (n = 69) with allergic contact dermatitis, atopic dermatitis and other steroid-responsive dermatoses. After 3 day's treatment improvement in conditions averaged 38.2% and 39.3%, respectively, in the mometasone and betamethasone treatment groups, and after 21 days average improvements were 93.6% and 96.5%, respectively. The physicians' global evaluation of overall change in disease status and the patients' evaluation of treatment also indicated that the two treatment regimens produced comparable, rapid and progressive improvements in the patients' conditions, and no local side-effects were reported. It is concluded that mometasone furoate was as effective as betamethasone valerate in the treatment of a variety of steroid-responsive dermatoses, although mometasone furoate was applied only half as frequently.

Administration, Cutaneous↗

PubMed1976

Betamethasone-I7, 2I-dipropionate ointment: an effective topical preparation in lichen ruber planus.

A clinical evaluation was carried out in 19 patients with lichen ruber planus to assess the effectiveness of 0.05% betamethasone-17,21-dipropionate ointment in the treatment of patients whose lesions had developed resistance to prolonged treatment with 0.1% betamethasone-17-valerate ointment. The new steroid ointment was substituted for the previous preparation and applied at the same frequency, once or twice daily, for 2 to 3 weeks. The results at the end of the betamethasone-17,21-dipropionate period were classified as better in 14 (73.7%) and equal in the remaining 5 patients.

Administration, Topical↗

PubMed1976

Local treatment of psoriasis of the scalp with clobetasol propionate and betamethasone-17,21-dipropionate: a double-blind comparison.

A double-blind evaluation was carried out in 40 patients with moderate to severe psoriasis of the scalp to assess the effectiveness of a 0.05% alcoholic solution of clobetasol propionate as compared with a 0.05% alcoholic solution of betamethasone-17,21-dipropionate. Patients were treated on a non-selective basis with a twice a day application for 2 weeks. When comparing the effects on the parameters scaling, induration, erythema and itching it was concluded that clobetasol propionate was superior to betamethasone-17,21-dipropionate as an antipsoriatic compound. Clobetasol propionate did not cause any side-effects, while 2 of the patients using betamethasone-17,21-dipropionate developed a forehead folliculitis during the second week of treatment.

Betamethasone↗

PubMed1981

Betamethasone and the rhesus fetus: effect on lung morphometry and connective tissue.

Pregnant rhesus monkeys (Macaca mulatta) at 67 to 85% of term pregnancy were treated with betamethasone for 3 days and then delivered by cesarean section. These treated fetuses had larger lung volumes (32.6 +/- 1.8 ml/kg of body weight) compared to gestational age-matched controls (22.9 +/- 3.2 ml/kg of body weight; P less than 0.025) but no alterations in surfactant properties as measured by amniotic fluid L/S ratios, alveolar deflation stability, or lung phosphatidylcholine. These findings suggest that betamethasone effects an increase in fetal lung volume by some method other than alteration in alveolar surfactant concentrations. Results also demonstrated an 11% increase in the collagen to elastin concentration in the treated fetuses as compared to the control animals (P less than 0.01), suggesting alterations in lung connective tissue. Morphometric studies done on the air-fixed inflated lung demonstrated a decrease in the number of alveoli per unit volume of lung among the treated animals (0.95 +/- 0.07 x 10(6)) compared to the control animals (1.19 +/- 0.08 x 10(6); P less than 0.025) and a reduction in the mean surface area of the lungs of the treated animals (506 +/- 10 cm2 per cm3) compared to the control animals (561 +/- 9 cm2 per cm3; P less than 0.005). These findings suggest that at least part of the increased maximal lung volumes is related to increased alveolar distensibility. Together, these pressure volume findings, biochemical studies, and morphometric analyses indicate that a major effect of betamethasone on the rhesus fetal lung is to alter lung connective tissue characteristics. Alterations in lung surfactant appear to be of less functional significance in this rhesus fetal model. The disparity between these findings and other animal studies might be due to differences in species, the preparation, or the method of glucocorticoid administration.

Animals↗

PubMed1984

Comparison of the effects of betamethasone and L-carnitine on dipalmitoylphosphatidylcholine content and phosphatidylcholine species composition in fetal rat lungs.

Antepartum administration of L-carnitine to pregnant rats results in an increase of both total phospholipid (80 +/- 11 mg/g dry weight (dw); mean +/- SD) and dipalmitoylphosphatidylcholine (DPPC) content (7.7 +/- 2.1 mg/g dw) in fetal lungs as compared to controls (72 +/- 10 and 7.0 +/- 2.5 mg/g dw, respectively). On the other hand, no effect of L-carnitine could be demonstrated on the DPPC portion in the total phosphatidylcholine (PC) or on the portion of palmitic acid in the PC fatty acids. Betamethasone elevated the DPPC content in fetal lungs (8.1 +/- 2.0 versus 7.0 +/- 2.5 mg/g dw in the controls), while total phospholipid content remained unaffected (71 +/- 19 versus 72 +/- 10 mg/g dw). The portion of DPPC in the PC species increased significantly (p less than 0.01) from 27.6 +/- 4.5 in the fetal lungs of the control group to 34.2 +/- 3.3 in the lungs of the betamethasone-treated group, while the palmitic acid portion in the PC fatty acids was nearly unchanged (45.9 +/- 3.2 versus 43.9 +/- 2.6 in the controls). Further, after betamethasone treatment, a significant diminution (p less than 0.01) of the monoenic PC 32 species (palmitoyl-palmitoleyl PC and palmitoleyl-palmitoyl-PC) and the PC 34 species (consisting primarily of palmitoyl-oleoyl-PC) could be demonstrated both in absolute and relative terms. This is in agreement with a significant reduction of the portions of palmitoleic (p less than 0.01) and oleic (p less than 0.05) acids in the total PC fatty acids.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2005

Transient loss of the diurnal rhythms of fetal movements, heart rate, and its variation after maternal betamethasone administration.

Antenatal betamethasone administration to enhance fetal lung maturation is associated with transient reductions in fetal heart rate (FHR) variation, breathing, and body movements 2 d after the first dose (d 2). This study examines whether steroid administration affects the natural diurnal rhythms of fetal variables. Sixteen women at 27-32 wk of gestation received two doses of betamethasone 24 h apart. One-hour recordings of FHR, breathing, and body movements were made in the morning, afternoon, and evening of d 2, and again in the morning of d 3. Repeat recordings were obtained at 4-6 d later from 9/16 women. Maternal blood samples were obtained with each recording to determine ACTH and cortisol. No diurnal rhythm was present for FHR, FHR variation, breathing, and body movements on d 2. This resulted from suppression of the expected natural rise in body and breathing movements, and heart rate variation in the course of the day. Suppression of the diurnal rhythm of body movements depended on gestation (R = -0.89; p < 0.01). All variables showed diurnal rhythms 4-6 d later. Maternal ACTH and cortisol diurnal rhythms were completely suppressed on d 2. Four to six days later, the normal diurnal pattern was resumed, although absolute levels of ACTH and cortisol were still suppressed. We conclude that maternal betamethasone administration transiently abolishes the fetal diurnal rhythms of heart rate and its variation, breathing, and body movements.

Adrenocorticotropic Hormone↗

PubMed2006

The effects of maternal betamethasone administration on the intrauterine growth-restricted fetus.

Intrauterine growth restriction (IUGR) is associated with altered fetal cardiovascular function to ensure adequate perfusion of essential organs. IUGR fetuses are at risk of preterm delivery and so are likely to receive antenatal glucocorticoids to promote lung maturation. Because glucocorticoids alter vascular tone, we questioned whether such treatment may induce fetal cardiovascular alterations. Using pregnant sheep carrying twins, we induced IUGR at approximately 0.7 gestation by single umbilical artery ligation in one twin, using the other twin as a control. In each fetus, we monitored carotid blood flow and arterial blood gases. We administered 11.4 mg betamethasone (n = 5) or vehicle (n = 4) to the ewe on d 5 (BM1) and 6 (BM2) postsurgery. On d 7, fetal brains were collected for immunohistochemistry. In control fetuses, carotid blood flow decreased 3.5 h post-BM1 by 24% (P < 0.001), returning to baseline at 5.5 h. In IUGR fetuses, carotid flow decreased 2.5 h post-BM1 by 27% and then increased by 25% over baseline, peaking at 11 h (P < 0.001). Compared to control + saline, we observed a significant increase in oxidative damage (4-hydroxynonenal-positive cells) in the fetal hippocampus and subcallosal area of all treatment groups (IUGR + BM > IUGR + saline = control + BM). There was a significant correlation between carotid blood flow reperfusion after betamethasone and the number of 4-hydroxynonenal-positive cells in the cortex and hippocampus. These data suggest that antenatal betamethasone may induce brain injury in the IUGR fetus but not in the normally grown fetus.

Animals↗

PubMed1981

Altered ontogenesis of muscarinic cholinergic receptor in mouse brain: effect of L-thyroxine and betamethasone.

The effects of L-T4 and betamethasone treatment of newborn mice on the development of the cholinergic muscarinic receptor in certain brain regions was studied using the potent labeled muscarinic antagonist [3H]4-N-methyl-piperidyl benzilate. Treatment with both L-T4 and betamethasone caused an accelerated accumulation of muscarinic receptors in the cortex 16 days post partum, with a subsequent reduction in level at 30 days. In the cerebellum and caudate putamen, only betamethasone caused a similar early accumulation of muscarinic receptors, while the later effect, namely a reduction in the level at 30 days, was seen with both hormones in these two regions as well as in the hippocampus. The results can explain some behavioral effects observed in other studies after treatment with these hormones.

Aging↗

PubMed2004

Efficacy and systemic tolerability of mometasone furoate and betamethasone sodium phosphate.

This study evaluates the efficacy and systemic tolerability of licensed doses of mometasone furoate (Nasonex) and betamethasone sodium phosphate (Betnesol) in allergic chronic rhinosinusitis patients. It also assesses the diagnostic accuracy of morning salivary cortisol (MSC) concentrations to screen for adrenal suppression in these patients. Forty-eight patients were prospectively randomized to two treatment limbs. Symptom scores and adrenal function assessments were performed immediately prior to commencement and at the end of treatment. One (4 per cent) mometasone furoate and 14 (58 per cent) betamethasone sodium phosphate patients developed biochemical evidence of adrenal suppression. There were statistically significant (p < 0.005) reductions in symptom scores following treatment, but no significant difference (p > 0.05) between the drug groups regarding post-treatment symptom scores. As a screening tool for iatrogenic adrenal suppression, MSC had a sensitivity of 100 per cent and a specificity of 97 per cent. This study demonstrates the high risk of developing adrenal suppression secondary to betamethasone sodium phosphate therapy. The salivary cortisol assay is an accurate tool for monitoring adrenal function and is ideally suited to the out-patient setting.

Adolescent↗

PubMed1998

The effects of Betamethasone on white blood cells during pregnancy with PPROM.

OBJECTIVE: To determine the effects of Betamethasone injections on maternal white blood cell counts. STUDY DESIGN: Thirteen pregnant women without fever or clinical infection and with premature rupture of the membranes at less than 34 weeks gestation were studied. No subject had labor during the week of study. Daily complete blood counts were done before and on days one and two after two 12 mg intramuscular injections of Betamethasone given 24 hours apart. RESULTS: The steroid injections produced a significant increase in total white counts from 9.8 +/- 5.0 to 14.2 +/- 0.7 x 10(3) cells/cc. There was a significant increase in polymorphonucleocytes and a decrease in lymphocytes and monocytes. CONCLUSION: The use of Betamethasone injections to mature fetal lungs results in a leukocytosis, but total white cell counts remain less than 20 x 10(3) cells/cc.

Adolescent↗

PubMed1987

Effect of betamethasone treatment on luteal lifespan and the LH response to GnRH in dairy cows.

Betamethasone (a synthetic glucocorticoid, 15 mg) was administered i.m. twice daily for 10 days to 4 regularly cycling dairy cows, beginning on Day 10 of the oestrous cycle. Luteal function, monitored by plasma progesterone, was extended by 7, 9, 19 and 20 days, respectively. Luteal function in the next cycle was normal. Endogenous cortisol values were suppressed for 14, 13, 34 and 27 days, respectively. Pituitary responsiveness to 20 micrograms GnRH was assessed by LH measurement on Days -1, +3 and +7 relative to the start of betamethasone treatment. There was a progressive decrease in peak LH concentrations after each GnRH challenge compared to control cows. Hourly measurements of PGF-2 alpha metabolite during the expected period of luteolysis failed to reveal normal increases. It is suggested that betamethasone caused prolonged luteal function, either by directly inhibiting PGF-2 alpha release, or by suppressing pituitary stimulation of follicular growth and hence lowering oestradiol concentrations, since it is known that PGF-2 alpha and oestradiol act synergistically to cause luteolysis.

Animals↗

PubMed2004

[Effects of cyclosporin A or betamethasone on experimental murine toxocariasis].

The effects of administration of either cyclosporin A or betamethasone 15 days before or 45 days after experimental infection with Toxocara canis on mice had been studied. The dynamics of IgG antibody production, employing an enzyme-linked immunosorbent assay, was studied 60 and 90 days after mice infection by Toxocara canis. In the 90th day after infection all surviving mice were sacrificed and the tissue trapped larvae recovered by acid digestion in the muscles, lungs, liver and brain. A significative delay in the production of IgG antibodies anti-Toxocara was observed in all the mice treated with cyclosporin A or betamethasone 15 days before infection. On the other side, mice treated with cyclosporine 15 days before infection, but not with betamethasone, showed a significative higher number of trapped Toxocara canis larvae in the examined tissues.

Animals↗

PubMed1977

Functional activity of the hypothalamo-pituitary complex in the rat after betamethasone treatment.

The precise nature of the impairment of hypothalamo-pituitary-adrenocortical (HPA) activity which follows prolonged corticosteroid treatment is not yet understood. To study this problem, hypothalamic corticotrophin releasing hormone (CRH) content, pituitary ACTH content and the functional capacity of adenohypophysial tissue in vitro were measured in rats after treatment with betamethasone. The content of CRH and ACTH in the hypothalamus and pituitary gland respectively were markedly reduced. After stopping the treatment the hormone concentrations in both structures returned to normal with the rise in the hypothalamus preceding that in the pituitary gland. Adenohypophysial tissue from betamethasone-treated rats incubated with hypothalamic extracts from control animals showed a considerable reduction in its ability to synthesize and release ACTH. However, corticotrophin release was impaired in adenohypophyses removed from untreated rats and incubated with betamethasone but synthesis was not affected. The physiological significance and the possible clinical relevance of the results are discussed.

Adrenal Glands↗

PubMed1999

Developmental expression of and effect of betamethasone on the messenger ribonucleic acid levels for peptide growth factors in the baboon fetal adrenal gland.

In the present study, we determined whether expression of the messenger ribonucleic acids (mRNAs) for insulin-like growth factor-II (IGF-II), and its principal IGF type-1 receptor and IGF-binding protein-2 (IGFBP-2), as well as basic fibroblast growth factor (bFGF), was developmentally regulated in the baboon fetal adrenal gland. In the second phase of this study, fetal pituitary ACTH was suppressed by the administration of betamethasone to determine the possible effect on the mRNA levels for those factors, i.e. IGF-II and IGFBP-2, shown to be expressed at high levels in the adrenal late in fetal development. Adrenals were obtained from fetuses delivered via Cesarean section on days 60 (early), 100 (mid), and 165 (late) of gestation (term=184 days) from untreated baboons and on day 165 from baboons in which betamethasone was administered to the fetus, or to fetus and mother, every other day between days 150 and 164 of gestation. Although the mRNA levels of IGF-II in the fetal adrenal were similar at early, mid and late gestation, IGF type-1 receptor mRNA levels were approximately 2- to 3-fold greater (P<0.01) at mid than at early or late gestation. In contrast, there was an increase (P<0.001) in fetal adrenal IGFBP-2 and bFGF mRNA levels in late gestation. Although fetal adrenal weights and width of the zone of definitive/transitional cells exhibiting immunocytochemical staining for Delta(5)-3beta-hydroxysteroid dehydrogenase (3beta-HSD) were markedly suppressed (P<0.01) by the administration of betamethasone, IGF-II and IGFBP-2 mRNA expression was not decreased. In summary, very different patterns of mRNA levels for IGF-II, IGF type-1 receptor, IGFBP-2 and bFGF were exhibited in the developing baboon fetal adrenal gland, which may reflect functionally important differences in their respective cellular localization within the cortex, as well as a divergence in the functional development of the fetal, transitional and definitive zones of the baboon fetal adrenal cortex.

Adrenal Glands↗