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PubMed1998

The role of betamethasone in the treatment of acute exudative pharyngitis.

OBJECTIVE: To compare betamethasone with placebo as an adjuvant to antibiotic therapy in the treatment of acute exudative pharyngitis. METHODS: The study was a randomized, doubled-blind, placebo-controlled, single-center, parallel, outpatient clinical trial. After consent was obtained, each patient was asked to rate his or her pain on a 10-cm numbered visual analog scale (VAS; 0-10). All of the patients received injectable benzathine penicillin. If allergic to penicillin, they were started on a 10-day course of polyenteric-coated erythromycin (PCE). Each patient was randomized to receive either i.m. betamethasone or i.m. placebo. All patients were contacted by telephone at 24 and 48 hours by one of the study investigators and asked to rate their pain based on another VAS. If their pain was not resolved by 48 hours, they were called again daily between the third and seventh days after the initial visit to determine the time of pain resolution. RESULTS: A total of 92 patients were enrolled in the study, with 46 randomized to receive placebo and 46 to receive betamethasone. Eight patients were excluded from the statistical analysis because of inability to obtain follow-up. Demographic comparison showed that gender distributions, ages, mean initial pain scores, mean times to the first and second follow-up calls, and treatment regimens were similar in the 2 groups. There were significantly better pain scores for the betamethasone group at first follow-up (p = 0.0005), at second follow-up (p = 0.004), and in number of hours until relief of pain (p = 0.004). When only those patients with a positive culture for a streptococcus species were analyzed, there also were significant reductions in pain score at the first (p = 0.006) and second (p = 0.02) follow-up visits. CONCLUSION: Pain relief was greater and more rapid in patients treated with betamethasone as an adjuvant therapy in acute exudative pharyngitis.

Acute Disease↗

PubMed2004

Efficacy of early systemic betamethasone or cyclosporin A after corneal alkali injury via inflammatory cytokine reduction.

PURPOSE: To evaluate the effects of early systemic administration of betamethasone or cyclosporin A (CsA) on inflammatory cytokine expression and corneal damage after alkali injury. METHODS: Sixty-five Wistar rat corneas injured with 1N NaOH were divided into three groups: untreated, betamethasone-treated and CsA-treated. Both agents were administered systemically and daily during the first 7 days after injury. Interleukin (IL)-1alpha, -6 and -8 concentrations in the injured corneas were measured with ELISA at 2, 4 and 7 days after injury. Corneal damage was evaluated by scoring clinical findings. RESULTS: In untreated injured corneas, IL-1alpha, -6 and -8 were markedly elevated during the 7-day period following injury. Both betamethasone and CsA significantly suppressed IL-1alpha and IL-8 at day 4. Only betamethasone significantly suppressed IL-6 at days 4 and 7. Both agents significantly reduced corneal opacity at day 4. CONCLUSION: Early systemic administration of betamethasone or CsA after alkali injury may be of benefit by suppressing inflammatory cytokine expression in the cornea.

Animals↗

PubMed2005

Betamethasone effects on fetal sheep cerebral blood flow are not dependent on maturation of cerebrovascular system and pituitary-adrenal axis.

Synthetic glucocorticoids are administered to pregnant women in premature labour to accelerate fetal lung maturation at a time when fetal cerebrovascular and endocrine systems are maturing. Exposure to glucocorticoids at 0.8-0.9 of gestation increases peripheral and cerebrovascular resistance (CVR) in fetal sheep. We examined whether the increase of CVR and its adverse effect on cerebral blood flow (CBF) depend on the current level of maturation of the pituitary-adrenal axis and the cerebrovascular system. Using fluorescent microspheres, regional CBF was measured in 11 brain regions before and 24 h and 48 h after the start of 3.3 microg kg(-1) h(-1) betamethasone (n = 8) or vehicle (n = 7) infusions to fetal sheep at 0.73 of gestation. Hypercapnic challenges were performed before and 24 h after the onset of betamethasone exposure to examine betamethasone effects on cerebrovascular reactivity. Betamethasone exposure decreased CBF by approximately 40% in all brain regions after 24 h of infusion (P < 0.05). The decline in CBF was mediated by a CVR increase of 111 +/- 16% in the cerebral cortex and 129 +/- 29% in subcortical regions (P < 0.05). Hypercapnic cerebral vasodilatation and associated increase in CBF were blunted (P < 0.05). Fetal CBF recovered after 48 h of betamethasone administration. There were no differences in glucocorticoid induced CBF and CVR changes compared with our previous findings at 0.87 of gestation. We conclude that the cerebrovascular effects of antenatal glucocorticoids are independent of cerebrovascular maturation and preparturient increase in activity of the fetal pituitary-adrenal axis.

Animals↗

PubMed1996

Antenatal betamethasone therapy augments nitric oxide-mediated relaxation of preterm ovine pulmonary veins.

Antenatal glucocorticoid therapy improves pulmonary function in preterm newborns. We have determined the effect of antenatal glucocorticoid therapy on nitric oxide-mediated relaxation in pulmonary vessels of preterm lambs. Ovine fetuses (126 days gestation; full term = 150 days) were injected with betamethasone (0.5 mg/kg body wt) or saline. After 48 h, lambs were delivered, ventilated for 3 h, and killed. Isolated fourth-generation pulmonary arteries (2-3 mm diameter) and veins (1.5-2 mm diameter) were suspended in organ chambers filled with modified Krebs-Ringer solution (95% O2-5% CO2) at 37 degrees C, and their isometric tension was recorded. During contractions to endothelin-1 or U-46619 (in the presence of indomethacin), acetylcholine and bradykinin induced endothelium-dependent nitro-L-arginine-inhibitable relaxation in arteries and veins. The relaxation was greater in veins of betamethasone-treated than in those of control lambs. Veins from lambs without endothelium treated with betamethasone were more sensitive to sodium nitroprusside than veins from controls. For arteries, there was no significant difference in relaxation between different groups. Relaxation induced by 8-bromoguanosine 3',5'-cyclic monophosphate was similar in arteries and veins of different groups. Radioimmunoassay showed that nitric oxide caused a greater increase in guanosine 3',5'-cyclic monophosphate in betamethasone-treated veins than in controls. These data suggest that antenatal betamethasone therapy augments nitric oxide-mediated relaxation of pulmonary veins of preterm lambs, probably by increasing soluble guanylate cyclase activity of vascular smooth muscle.

Animals↗

PubMed1998

A single dose of antenatal betamethasone enhances isoprenaline and prostaglandin E2-induced relaxation of preterm ovine pulmonary arteries.

Beta-adrenergic agonists and prostaglandin E2 (PGE2) play an important role in perinatal pulmonary circulation. We have determined the effect of antenatal glucocorticoid treatment on isoprenaline- and PGE2-mediated relaxation of pulmonary arteries of newborn preterm lambs. Ovine fetuses (121 days of gestation; term = 150 days) received a single intramuscular dose of betamethasone (0.5 mg/kg) or saline. Fifteen hours after the injection, the lambs were delivered, ventilated for 3 h, and sacrificed. The fourth-generation pulmonary arteries were dissected and cut into rings for study. In endothelin-1-preconstricted vessels, isoprenaline, PGE2, and forskolin (an activator of adenylyl cyclase) induced greater relaxations of pulmonary arteries of betamethasone-treated lambs than those of controls. 8-Bromo-cyclic adenosine monophosphate, a cell membrane permeable analogue of cyclic adenosine monophosphate, caused similar relaxation of all vessels. When stimulated with isoprenaline and PGE2, the adenylyl cyclase activity of crude membrane preparations of pulmonary arteries treated with betamethasone was greater than that of controls. These results show that single-dose antenatal betamethasone treatment enhances relaxation of pulmonary arteries of preterm lambs induced by isoprenaline and PGE2 and that an enhanced adenylyl cyclase activity contributes to the effect of betamethasone on pulmonary arteries of preterm lambs.

Adenylyl Cyclases↗

PubMed2003

Association of lipid peroxidation with antenatal betamethasone and oxygen radial disorders in preterm infants.

INTRODUCTION: Premature infants are highly susceptible to 'oxygen radical diseases' (ORD), including bronchopulmonary dysplasia, intraventricular hemorrhage/white matter injury, retinopathy of prematurity, and necrotizing enterocolitis. The incidence of ORD is reduced following antenatal treatment with betamethasone. Oxidant-mediated injury is characterized at the cellular level by peroxidation of lipid membranes. This results in the generation of malondialdehyde (MDA), which can be quantified indirectly by measurement of thiobarbituric acid-reacting substances (TBARS). There is currently no effective way to quantify the risk for ORD. In this study, we analyzed the correlation of early urinary MDA and TBARS with prenatal betamethasone administration and with the development of ORD. METHODS: Preterm infants (<30 weeks gestation, n = 25) born at St. Peter's University Hospital were enrolled. Urine samples were collected during the first 10 days of life and stored at -70 degrees C for 0-21 days. TBARS were quantified by spectrophotometric assay, and malondialdehyde levels measured by HPLC. Subjects were screened for the subsequent development of ORD. Betamethasone administration was defined as one or more doses > or =24 h prior to delivery. RESULTS: Urinary MDA levels increased on days 2-3 and 5-10 relative to day 1 from birth. Maximal urinary MDA concentrations were significantly higher in the ORD group compared to controls, and there was a trend toward increased urinary TBARS in the presence of ORD. Infants receiving prenatal betamethasone demonstrated higher maximal urinary TBARS values during the first 10 days of life than control infants. The length of sample storage from 0 to 3 weeks at -70 degrees C did not significantly affect TBARS measurements. CONCLUSIONS: Elevated urinary MDA measurements in the first 10 days are correlated with the risk for ORD. Urinary TBARS concentrations, which are correlated with MDA measurements, can be quantified rapidly and are stable for short-term storage. Our findings suggest that urinary TBARS may be adaptable as a practical tool for assessing the risk for ORD in neonatal intensive care unit patients, allowing clinicians to optimize the use of preventive strategies. Antenatal betamethasone is associated with increased urinary TBARS in the first 10 days of life, indicating that the protective effects of corticosteroids are not mediated through reductions in oxidant-mediated lipid peroxidation.

Aging↗

PubMed1983

Long-term effects of betamethasone on blood pressure and hypothalamo-pituitary-adrenocortical function in spontaneously hypertensive and normotensive rats.

An enhanced hypothalamo-pituitary-adrenocortical (HPA) activity has been described during onset of elevated blood pressure in spontaneously hypertensive rats (SHR). An instability of the HPA axis could thus contribute to the development of hypertension in these animals. Glucocorticoid effects on blood pressure and HPA function were studied therefore in SHR and normotensive Wistar-Kyoto (WKY) and Wistar rats. Beginning at 4 weeks of age, the rats were treated with 0.1 and 0.5 microgram betamethasone per milliliter drinking water for 7 weeks. SHR and WKY responded with a significant elevation in average blood pressure. In SHR, mean blood pressure rose from 181.4 +/- 3.9 (mean +/- SEM) to 203.1 +/- 2.8 mm Hg in response to the lower dose of betamethasone and to 209.2 +/- 4.0 mm Hg in response to 0.5 microgram betamethasone per milliliter drinking water. In WKY, blood pressure increased from 134.4 +/- 3.3 to 148.2 +/- 3.0 and 157.9 +/- 4.5 mm Hg in response to the lower and higher dose of betamethasone, respectively. No significant effect was seen in Wistar rats, where the mean blood pressure values changed insignificantly from 133.8 +/- 2.1 to 136.3 +/- 3.2 and 135.6 +/- 2.4 mm Hg. Stress-induced secretion of corticosterone was significantly suppressed in a dose-dependent manner in all three strains. Stress-induced secretion of adrenocorticotropin was markedly reduced by 0.5 microgram betamethasone per milliliter in SHR and by both doses in WKY. No significant effect, however, was seen in Wistar rats. A predisposition to the hypertensiogenic actions of glucocorticoids was found therefore in SHR and WKY, but not in Wistar rats.

Animals↗

PubMedDate not supplied

Effect of antenatal betamethasone and dexamethasone administration on fetal heart rate variability in growth-retarded fetuses.

PURPOSE: To study the effect of betamethasone and dexamethasone on fetal heart rate in 55 growth-retarded fetuses. MATERIAL AND METHODS: Fifty-five fetuses with intrauterine growth retardation were exposed in utero to betamethasone (group 1, n = 32) or dexamethasone (group 2; n = 17). Six fetuses received both steroids alternatively at weekly intervals. Computerized cardiotocograms were recorded and analyzed retrospectively. Traces were obtained before, 1 day, 2 days and 4-7 days after treatment was started. RESULTS: One day after treatment was started, both steroids were associated with an initial increase in fetal heart rate variation that was higher with dexamethasone. Short-term variation was significantly decreased during the betamethasone course. All parameters returned to their pretreatment values within a week. CONCLUSION: Dexamethasone and betamethasone had similar effects compatible with a transient damping effect on fetal heart rate variability that reached significance only with betamethasone.

Betamethasone↗

PubMed1983

Postnatal increase in airway surfactant in the premature rabbit exposed in utero to betamethasone.

In utero exposure to betamethasone on days 26 and 27 of gestation resulted in a significant increase in lung lavage phospholipid after 24 h of air breathing in rabbit pups delivered at 29 days of gestation. At 6 h of age, the proportion of type II epithelial cells in betamethasone-exposed newborns was nearly twice the saline-exposed control value. Phospholipid composition and pressure:volume analysis of compliance were both unaffected by betamethasone treatment. The betamethasone-associated increase in airway phospholipid content was observed only in female pups. These data support the conclusion that antenatal betamethasone treatment elicits an increase in airway phospholipid which is dependent on breathing and confined to the female newborn.

Animals↗

PubMed1993

Single dose versus two doses of betamethasone for lung maturation in preterm rabbits.

Most previous studies of induced lung maturation have used fetal exposures to multiple doses of hormones, and such treatments are associated with fetal growth retardation in rodents and rabbits. This study was designed to evaluate whether single-dose maternal corticosteroid treatments could induce lung maturation without causing fetal growth retardation. Lung maturation was evaluated in 27-d gestational age rabbits by measurements of lung function after preterm delivery and ventilation. Lung function was assessed by measurements of ventilatory requirements, responses to exogenous surfactant, measurements of the recovery of intravascular albumin in the lungs, and surfactant pool sizes. As demonstrated previously, 0.1 mg/kg betamethasone (1 mg = 2.13 mumol betamethasone) given 48 and 24 h before delivery caused both growth retardation (birth weight 20% lower than controls, p < 0.01) and lung maturation (improved compliance, decreased radiolabeled albumin recoveries) despite lower alveolar saturated phosphatidylcholine pool sizes (p < 0.05 versus controls). A single dose of 0.2 mg/kg betamethasone given 48 h before delivery had an equivalent effect on birth weight as the divided doses of 0.1 mg/kg betamethasone, with the only lung maturational effect being a decrease in recovery of labeled albumin in alveolar washes (p < 0.01). A single dose of 0.1 mg/kg betamethasone given 48 h before delivery decreased birth weight by 9.4% (p < 0.01 versus control) but had no effect on any of the lung maturation indicators. Fetal lung maturation caused by maternal corticosteroid is associated with global fetal growth retardation, and a single low dose of corticosteroid can cause growth retardation without inducing lung maturation.(ABSTRACT TRUNCATED AT 250 WORDS)

Albumins↗

PubMed1994

Effects of prenatal exposure to betamethasone and indomethacin on the glomerular filtration rate in the preterm infant.

The effects of gestational age (GA), body weight, and prenatal exposure to betamethasone and indomethacin on the glomerular filtration rate (GFR) on d 3 of life in preterm infants were studied. GFR measurements were performed in 147 preterm infants with a GA between 23.4 and 37.0 wk by means of the continuous inulin infusion technique. Mean GFR values increased significantly with GA (r = 0.60, p < 0.001) and with body weight (r = 0.44, p < 0.001). Multivariate analysis indicated that GA was the most important determinant for this increase. Prenatal exposure to indomethacin resulted in significantly lower GFR values (-0.15 +/- 0.03 mL/min, p < 0.001) at d 3 after birth. Prenatal administration of betamethasone and indomethacin significantly (p < 0.001) increased the GFR in comparison with exposure to indomethacin alone to levels not different than those seen in patients who were not prenatally exposed to betamethasone or indomethacin. GFR measurements were repeated in 40 preterm infants on d 10 after birth. During this 7-d period, a significant increase in GFR values (0.17 +/- 0.03 mL/min, p < 0.001) was detected. This postnatal increase in GFR values was independent of GA and was not influenced by prenatal exposure to betamethasone or indomethacin. We conclude that prenatal exposure to betamethasone or indomethacin exerts significant effects on the renal function of preterm infants in the first days of life.

Betamethasone↗

PubMed2005

Short-term (0-48 h) effects of maternal betamethasone administration on fetal heart rate and its variability.

The short-term (0-48 h) effects of maternal betamethasone administration on computerized fetal heart rate (FHR) parameters were studied in 36 pregnancies at increased risk for preterm delivery. FHR was recorded for 90 min immediately before the start of betamethasone treatment and again at 6-h intervals during the next 48 h. Multiple linear regression models were used to assess the possible effects on FHR parameters of gestational age, time of day, clinical indication for treatment, and use of tocolytic drugs. Within 12 h after the start of treatment, significant increases occurred in FHR accelerations, and short- and long-term FHR variability (36%, 28%, and 22%, respectively), whereas basal FHR showed a 5% decrease. FHR variability was decreased by 10% at 42-48 h. The observed changes were more pronounced in older (29-33 wk of gestation) compared with younger fetuses (25-28 wk of gestation). Decelerations occurred only in 4 out of 11 compromised fetuses during betamethasone therapy. We conclude that there are significant changes in FHR parameters during the first 48 h after betamethasone administration. These changes are transient in normal fetuses. However, the compromised fetus may be adversely affected by betamethasone.

Betamethasone↗

PubMed2006

Cognition- and anxiety-related behavior, synaptophysin and MAP2 immunoreactivity in the adult rat treated with a single course of antenatal betamethasone.

We investigated the effects of a single course of antenatal betamethasone on cognition- and anxiety-related behavior and synaptophysin and microtubule-associated protein 2 (MAP2) immunoreactivity in the adult rat hippocampus. On d 20 of gestation, pregnant rats were injected with either 1) 170 microg/kg body weight of betamethasone ("clinically equivalent dose," equivalent to 12 mg twice, 24 h apart); 2) half this dose; or 3) vehicle. Cognition- and anxiety-related behavior of the offspring was analyzed at an age of 5 mo using the Morris water maze, object recognition task, and open field test. Subsequently, synaptophysin and MAP2 immunoreactivity were measured in the hippocampus. We report no detrimental effects of antenatal betamethasone on cognition- and anxiety-related behavior and synaptophysin immunoreactivity in the adult rat. On the other hand, MAP2 immunoreactivity was decreased by betamethasone in males, suggesting a permanent impairment in the hippocampus. Interestingly, the lower dose appears to have less influence in terms of growth restriction, known to be associated with an increased risk of disease in adulthood. Further research might elucidate whether the betamethasone effect on hippocampal neurons persists later in life and could affect the aging process increasing the risk for neuropathology of the adult.

Animals↗

PubMed1986

Methimazole, but not betamethasone, prevents 131I treatment-induced rises in thyrotropin receptor autoantibodies in hyperthyroid Graves' disease.

The effects of methimazole or betamethasone therapy on the TSH receptor antibody response to radioiodine therapy were compared in a prospective randomized study of 60 patients with hyperthyroidism due to Graves' disease. The patients were followed for 1 yr after treatment with 131I. Twenty-three patients received 131I alone, 17 were treated with methimazole for 2 months before and 3 months after 131I therapy, and 20 patients were treated with betamethasone for 3 weeks before and 4 weeks after 131I therapy. 131I induced a transient rise in the mean serum level of TSH receptor autoantibodies, measured as TSH binding inhibitory immunoglobulin (TBII), but in patients receiving methimazole treatment, no such rise occurred. In the betamethasone-treated patients, TBII increased similarly to that in patients treated with 131I alone. In addition, in patients given betamethasone, there was an early decrease in total serum immunoglobulin G, which persisted throughout the follow-up period. In the other 2 groups, no changes in total immunoglobulin G were found. The results demonstrate that in hyperthyroid Graves' disease, TBII production is influenced by therapy. Methimazole abolished the 131I-induced increase in TBII, whereas betamethasone did not have such an inhibitory effect.

Adult↗

PubMed1994

Antenatal betamethasone-dose-effects on fetal rat lung morphology and surfactant.

Pregnant rats received betamethasone 0.02, 0.05, 0.10, or 0.20 mg/kg body weight/day or saline (controls) for three days before delivery of fetuses at day 19 of gestation. Dose related effects on morphology, dipalmitoyl phosphatidylcholine content, and phosphatidylcholine species composition of the fetal lungs were evaluated. Injection of 0.02 and 0.05 mg/kg body weight betamethasone resulted in cellular differentiation of some cells, but the increase in dipalmitoyl phosphatidylcholine content was not significant. Dosages of either 0.10 or 0.20 mg/kg body weight resulted in markedly accelerated organ differentiation, complete cytodifferentiation of type II cells, and markedly increased numbers of lamellar bodies per alveolar type II cell. Compared to the controls, maternal administration of 0.10 or 0.20 mg/kg betamethasone caused significant increases of both fetal lung dipalmitoyl phosphatidylcholine content, and the fraction of dipalmitoyl phosphatidylcholine of total phosphatidylcholine. None of the parameters differed between the groups that were treated with 0.10 or 0.20 mg/kg body weight betamethasone respectively. Diminution of lung DNA content was significant after treatment with betamethasone in doses of 0.05, 0.10, and 0.20 mg/kg body weight. The results of the present study suggest that maternal treatment with lower doses than those in common usage may be successful in prevention of respiratory distress syndrome, and that higher dosages do not confer any additional advantage.

1,2-Dipalmitoylphosphatidylcholine↗

PubMed2004

Blood pressure at 6 years of age after prenatal exposure to betamethasone: follow-up results of a randomized, controlled trial.

OBJECTIVE: To determine whether prenatal exposure to betamethasone for the prevention of neonatal respiratory distress syndrome (RDS) alters blood pressure in childhood. DESIGN: Prospective follow-up study of a randomized, double-blind, placebo-controlled trial. SETTING: National Women's Hospital (Auckland, New Zealand). PARTICIPANTS: Two hundred twenty-three 6-year-old children of mothers who presented with unplanned premature labor and took part in a randomized, controlled trial of prenatal betamethasone therapy for the prevention of neonatal RDS. INTERVENTION: Mothers received 2 doses of betamethasone (12 mg) or placebo, administered through intramuscular injection, 24 hours apart. MAIN OUTCOME MEASURES: Systolic and diastolic blood pressure at 6 years of age. RESULTS: Children exposed prenatally to betamethasone (n = 121) did not differ in systolic or diastolic blood pressure from children exposed to placebo (n = 102) (mean difference: systolic: -1.6 mm Hg; 95% confidence interval: -4.1 to 0.8 mm Hg; diastolic: -0.3 mm Hg; 95% confidence interval: -2.5 to 1.8 mm Hg). CONCLUSION: Prenatal exposure to betamethasone for prevention of neonatal RDS does not alter blood pressure at 6 years of age.

Betamethasone↗

PubMed1978

Effects of low calcium and low phosphorus diets on the duodenal absorption of calcium in betamethasone-treated chicks.

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.

Animals↗

PubMed2006

Effects of antenatal betamethasone on maternal and fetoplacental matrix metalloproteinases 2 and 9 activities in human singleton pregnancies.

BACKGROUND: A single course of antenatal betamethasone is administered to women at risk of preterm labor to advance fetal lung maturation. Matrix metalloproteinases (MMPs) are collagen-degrading enzymes that remodel extracellular matrix components during lung development. We tested the hypothesis that the effects of betamethasone on fetal lung maturation involve changes in MMP activity. METHODS: We conducted a prospective, observational pilot study of three groups of singleton pregnancies. Group 1 (n = 21) was composed of women who were antenatally treated with a single course of betamethasone and who delivered < 37 weeks of gestation, group 2 (n = 7) was composed of matched untreated women who delivered < 37 weeks of gestation, and group 3 (n = 15) was composed of untreated women who delivered > 37 weeks of gestation. Maternal blood, mixed cord blood, and placental samples were collected at the time of delivery for MMP-2 and MMP-9 activity and tissue inhibitor of metalloproteinases (TIMP)-1 and -2 levels. RESULTS: MMP-2 activity was significantly higher in the maternal, placental, and fetal compartments in group 1 compared with group 2 (p < .05). TIMP-2 levels were lower in groups 1 and 2 compared with group 3. Maternal TIMP-2 levels were higher (p < 0.003), whereas fetal TIMP-1 (p < .01) and MMP-9 to TIMP-1 ratios (p < .05) were lower when delivery was delayed more than 2 weeks following betamethasone treatment. CONCLUSION: We conclude that elevated MMP-2 activity in the maternal and fetoplacental compartments may suggest a mechanism, in part, for betamethasone-induced fetal lung maturation.

Adult↗