Dexamethasone in the post-partum treatment of HELLP syndrome. Effects of postpartum corticosteroids in patients with HELLP syndrome. Antepartum corticosteroids: disease stabilization in patients with the syndrome of hemolysis, elevated liver enzymes, and low platelets (HELLP) Postpartum corticosteroids: accelerated recovery from the syndrome of hemolysis, elevated liver enzymes, and low platelets (HELLP). 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. Dexamethasone compared with betamethasone for glucocorticoid treatment of postpartum HELLP syndrome. The effects of betamethasone treatment on clinical and laboratory features of pregnant women with HELLP syndrome. Dexamethasone treatment does not improve the outcome of women with HELLP syndrome: a double-blind, placebo-controlled, randomized clinical trial. [Maternal benefit of postpartum corticosteroid therapy in patients with HELLP (hemolysis elevated liver enzymes low platelets count) syndrome]. Idiopathic thrombocytopenic purpura in pregnancy: a randomized trial on the effect of antenatal low dose corticosteroids on neonatal platelet count. Betamethasone 17 valerate aerosol and disodium chromoglycate in severe childhood asthma.
To determine if the routine initiation of dexamethasone in patients with post-partum HELLP syndrome produces therapeutic benefits.
                The puerperal courses of 17 mothers who initially received dexamethasone after delivery were compared to 17 other mothers with HELLP syndrome who received no corticosteroids during the puerperium course. Treated patients immediately received 10 mg of dexamethasone post-partum (intravenously) followed 12 h later by 10 mg and 10 mg at 24 h post-partum, to a total of 30 mg.
                The steroid treated group had significant changes over time in platelet count. Relative to the control group the platelet count increased significantly by 30 h post-partum (P < 0.01). The blood pressure, urinary output, lactic dehydrogenase, aspartato aminotransferase and alanine aminotransferase values were not significantly different between the dexamethasone and control group at any time by 72 h post-partum.
                Parturients with HELLP syndrome who received a short course of post-partum dexamethasone therapy had an accelerated recovery from their platelet count, but not from their liver enzymes and blood pressure. To evaluate the effect of corticosteroid treatment on the postpartum recovery of parturients with HELLP syndrome.
                Thirty cases with HELLP syndrome were randomly assigned to a study or a control group, each including 15 patients. A total dose of 30 mg intravenous dexamethasone was given to the study group during the 36 h following the childbirth, while the control group did not receive any steroid medication. Arterial blood pressure, urine output, hematocrit ratio, platelet count, serum alanine and aspartate aminotransferases and uric acid levels were monitored during the first 48 h postpartum. The data were analyzed by unpaired t-test, chi2 or Fisher's exact tests.
                Before the treatment, no significant difference was observed between the two groups. The study group showed statistically significant improvement in mean arterial blood pressure, mean serum aspartate aminotransferase level, mean urine volume per hour and mean platelet count (P < 0.05). Length of hospitalization was also shorter in the study group (P < 0.01).
                Early postpartum high-dose corticosteroid treatment accelerates the recovery and shortens the hospitalization of the parturients with HELLP syndrome. Our purpose was to evaluate the impact of antepartum administration of corticosteroids on the course of the syndrome of hemolysis, elevated liver enzymes, and low platelets (HELLP) in pregnancies at 24 to 37 weeks' gestation.
                This prospective, randomized study was undertaken in 25 antepartum patients with atypical severe preeclampsia expressed as HELLP syndrome. Twelve pregnant women were randomized to receive double-dose dexamethasone (10 mg intravenously every 12 hours) until delivery, and 13 women were randomized to the control arm. Management and delivery decisions for all patients were based on a common protocol, with delivery undertaken for a deteriorating maternal or fetal condition.
                In the corticosteroid-treated group the maternal platelet count significantly increased (p = 0.006), whereas lactic dehydrogenase and alanine aminotransferase significantly decreased over time (p = 0.03 and p = 0.005) in comparison to the 13 women who did not receive corticosteroids. Maternal urinary output after entry into the study was significantly increased within hours after steroid administration versus the control group (p = 0.0006). The study entry-to-delivery interval (41 +/- 15 hours) was significantly longer in the group of steroid-treated women (p = 0.0068).
                Stabilization and significant improvement in the laboratory and clinical parameters associated with HELLP syndrome occurred in women who received high-dose antenatal corticosteroids, as measured by maternal platelet count, urinary output, lactic dehydrogenase, alanine aminotransferase, and postponement of delivery. We believe the findings of this investigation permit us to speculate that this therapeutic approach could enhance maternal-fetal care by postponing delivery of some previable fetuses, reduce the need for maternal transfusion of blood products, reduce neonatal morbidity or mortality from multiple systemic effects, and facilitate a safer transfer of the ill mother to a tertiary care site for optimal peripartal care. Because most morbidity and mortality associated with atypical preeclampsia and the syndrome of hemolysis, elevated liver enzymes, and low platelets is a postpartum phenomenon, we undertook this investigation to evaluate the use of high-dose corticosteroids to minimize maternal morbidity and accelerate postpartum recovery in patients with this form of severe preeclampsia.
                Into this prospective, randomized study 40 parturients with the syndrome were recruited. The syndrome was defined by a clinical presentation consistent with a diagnosis of severe preeclampsia or eclampsia in addition to laboratory evidence of hemolysis, hepatic dysfunction, and thrombocytopenia. Immediately post partum 20 parturients assigned to the treatment group received four doses of intravenous dexamethasone at 12-hour intervals (10 mg, 10 mg, 5 mg, 5 mg) over 36 hours. Patients assigned to the control group received no corticosteroids. All study subjects were intensively monitored by mean arterial pressure and urinary output every 2 hours, hematocrit and platelet count every 6 hours and lactic dehydrogenase, aspartate aminotransferase, and alanine aminotransferase every 12 hours for the first 48 hours post partum.
                The steroid-treated group with the syndrome of hemolysis, elevated liver enzymes, and low platelets had significant changes over time in mean arterial pressure, urinary output, platelet count, lactic dehydrogenase and aspartate aminotransferase versus the control group with the syndrome. Relative to the control group, the mean arterial pressure became significantly decreased at 22 hours in the steroid-treated group (p < 0.03), urinary output increased significantly by 16 hours (p < 0.02), the platelet count increased significantly by 24 hours (p < 0.05), and both lactic dehydrogenase and aspartate aminotransferase decreased significantly by 36 hours (p < 0.04 and p < 0.05, respectively).
                In association with high-dose corticosteroid administration, parturients with the syndrome of hemolysis, elevated liver enzymes, and low platelets recovered from the disease process more rapidly than did control subjects, as measured by urinary output, mean arterial pressure, platelet count, lactic dehydrogenase, and aspartate aminotransferase. In this disease process, which has significant associated morbidity and mortality, especially in patients with advanced cases, high-dose corticosteroid therapy appears to significantly hasten recovery and lessen the severity of the disease post partum. We postulate that use of this therapeutic approach in properly selected patients could result in lessened overall maternal morbidity and mortality, shorter patient stays in recovery and intensive-care areas, and shorter overall hospitalization with reduced medical care costs. 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.
                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).
                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).
                Intravenously administered dexamethasone appears to be more effective than intramuscularly administered betamethasone for the antepartum treatment of mothers with HELLP syndrome. To compare the efficacy of dexamethasone and betamethasone to ameliorate the course of postpartum hemolysis, elevated liver enzymes, low platelets (HELLP) syndrome.
                A prospective, mixed randomized/non-randomized clinical investigation of patients with postpartum HELLP syndrome. Treatment with either dexamethasone or betamethasone was continued until there was evidence of disease recovery.
                Baseline characteristics of both the dexamethasone (n=18) and betamethasone (n=18) groups were similar. Although the time to discharge from the obstetrical recovery room was not statistically significant between groups, reduction in mean arterial blood pressure was more pronounced in the dexamethasone group as compared with the betamethasone group (-15.3+/-1.4 mmHg vs. -7.5+/-1.4 mmHg, respectively, P<0.01). Patients in the dexamethasone group required less antihypertensive treatment than the betamethasone group (6% vs. 50%, P=0.01) and also had a decreased need for readmission to the obstetrical recovery room (0% vs. 22%, P=0.03).
                This investigation supports the use of dexamethasone as the superior glucocorticoid to use for patients with postpartum HELLP syndrome. The present study aims to investigate the effects of betamethasone treatment on clinical outcome and laboratory data of pregnant women diagnosed with HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome.
                A prospective, randomized and placebo-controlled clinical trial was undertaken in a total of 60 pregnant women with HELLP syndrome who were treated at the perinatology department of the study center between January 2005 and February 2008. Betamethasone treatment (intramuscular injection of 12 mg in every 24 h) was given to 30 subjects while remaining 30 subjects received placebo. The treatment and control groups were compared in the aspects of clinical outcome and laboratory data.
                The alterations in platelet counts, alanine aminotransferase, aspartate aminotransferase and lactate dehydrogenase levels of women treated with betamethasone were statistically similar to those of the placebo group. Although there was a significant decrease in diastolic blood pressure values of control group (P = 0.04), alterations in systolic blood pressure values were statistically indifferent in both study groups. Hematological and metabolic complications occurred significantly less in women treated with betamethasone (P < 0.05). Interestingly, the percentage of women who received platelet transfusion was significantly higher in the control group (P < 0.005). No case of maternal mortality occurred.
                The betamethasone treatment has ended up with insignificant alterations in clinical outcomes and laboratory data of women with HELLP syndrome except beneficial effects on metabolic complications and need for platelet transfusion. Further investigation is required to assess the efficiency of betamethasone in management of HELLP syndrome. The purpose of this study was to determine the efficacy of dexamethasone for treatment of HELLP (hemolysis, elevated liver enzymes and low platelet count) syndrome.
                A prospective, double-blind clinical trial was conducted among 132 women with HELLP syndrome who were assigned randomly to treatment or placebo groups. Pregnant women in the experimental group received 10-mg doses of dexamethasone intravenously every 12 hours until delivery and 3 additional doses after delivery. Puerperal women received 3 10-mg doses of dexamethasone after delivery. The same schedule was used in the placebo group. The main outcome variable was the duration of hospitalization. In addition, we evaluated treatment effects on the time to recovery of laboratory and clinical parameters and on frequency of complications.
                The mean duration of hospitalization of patients who received dexamethasone therapy was shorter than in the placebo group (6.5 vs 8.2 days), but this difference was not statistically significant (P = .37). No significant differences were found in the time to recovery of platelet counts (hazard ratio, 1.2; 95% CI, 0.8-1.8), lactate dehydrogenase (hazard ratio, 0.9; 95% CI, 0.5-1.5), aspartate aminotransferase (hazard ratio, 0.6; 95% CI, 0.4-1.1) and to the development of complications. The results were found in both pregnant and puerperal women.
                The results of this investigation do not support the use of dexamethasone for treatment of HELLP syndrome. Our purpose was to assess the effects of corticotherapy prescribed after delivery on the kinetic of biological parameters of HELLP syndrome (hemolysis elevated liver enzymes low platelets count). Twenty patients in whom pregnancy was complicated by antepartum or postpartum Hellp Syndrome, were randomised to receive, after delivery, either 12 mg of Dexamethasone every 12 hours for two doses (Group C, n=10), or a placebo (Group T, n=10). Biological parameters of the Hellp syndrome were analysed just before the first bolus of either treatment (H0), then after 24, 36, 48 and 72 hours. The corticotherapy was more efficient than placebo, in the correction of the biological parameters of the hellp syndrome. It permitted a rapid correction of the thrombopenia (from the 24th hour) but its effect on hemolysis marker was later (from the 36th hour). The kinetic of the hepatic cytolysis marker was not modified by corticotherapy. Finally, the administration of corticosteroids does not reduce maternal morbidity related to HELLP Syndrome. To determine the efficacy of antenatal low dose oral betamethasone in preventing neonatal thrombocytopenia and/or bleeding in infants of mothers with idiopathic thrombocytopenic purpura (ITP).
                Hospital department of obstetrics and gynaecology, referral centre.
                41 pregnancies in 38 women were randomized. The results of 13 pregnancies were considered non-assessable. The final analysis involved 14 in the betamethasone group and 14 in the non-treatment group. All fulfilled the criteria for ITP.
                The treated group received 1.5 mg betamethasone orally per day, from day 259 till day 273 and 1 mg from day 273 till delivery.
                Effects of treatment were assessed in terms of maternal platelet counts after the first trimester and neonatal platelet counts at birth and the first week of life and neonatal bleeding episodes.
                There were no significant differences in neonatal platelet counts at birth. Two infants in the betamethasone group and one in the untreated group had a severe thrombocytopenia either at birth or during the first week of life (less than 50 x 10(9)/l). Seven infants in the betamethasone group and six in the non-treatment group had a mild thrombocytopenia. The overall frequency of neonatal thrombocytopenia was similar: 64% in the betamethasone group and 57% in the untreated group (95% CI of the true difference: -43.5% to +29.5%). There was also no significant difference in neonatal bleeding episodes.
                Low-dose betamethasone in pregnant women with ITP does not prevent thrombocytopenia or bleeding in their newborn infants. Eleven children with severe perennial asthma and a poor clinical response to disodium cromoglycate were studied in a 4-month, double blind trial involving 1 month's treatment with placebo, disodium cromoglycate, betamethasone 17 valerate, and both drugs combined according to a predetermined random design. Each drug apparently reduced symptoms and improved daily peak flow and fortnightly spirometric measurements compared with placebo, but the improvement after betamethasone 17 valerate was greater in part because of the way this group of patients was selected. There did not appear to be any additional benefit when both drugs were used together. Betamethasone 17 valerate was not compared with beclomethasone diproprionate aerosol and there is no reason to believe it may be superior. Corticosteroid aerosols have potential hazards which may prove to equal those of long-term systemic steroids, but they offer the prospect of satisfactory control of symptoms without the risk of growth suppression in children with severe asthma. Disodium cromoglycate remains the drug of choice in severe childhood asthma and the use of corticosteroid aerosols should be confined to those children who fail to respond satisfactorily to disodium cromoglycate.
There was no clear evidence of any effect of corticosteroids on substantive clinical outcomes. Those receiving steroids showed significantly greater improvement in platelet counts which was greater for those receiving dexamethasone than those receiving betamethasone. There is to date insufficient evidence of benefits in terms of substantive clinical outcomes to support the routine use of steroids for the management of HELLP. The use of corticosteroids may be justified in clinical situations in which increased rate of recovery in platelet count is considered clinically worthwhile.