The mother-to-child HIV transmission debate.
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Biomedical subjects
Publications and source records attributed to J Anthony.
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OBJECTIVE: To compare the results of simultaneous opposite-arm and sequential same-arm intra-arterial validation of automated blood pressure monitors. DESIGN: Intra-arterial blood pressure measurements were compared with blood pressure measurements obtained using conventional sphygmomanometry and two automated blood pressure monitors (the Dinamap XL and the SpaceLabs Scout) using a methodology based on the protocol published by the Association for the Advancement of Medical Instrumentation (AAMI) for the intra-arterial validation of automated monitors. METHODS: Thirteen women with radial arterial lines were recruited from the obstetric intensive care unit at Groote Schuur Hospital, Cape Town. For each woman, intra-arterial blood pressure measurements were compared with those obtained by mercury sphygmomanometry and by using the two automated blood pressure monitors with both a sequential same-arm protocol and a simultaneous opposite-arm protocol. The mean and SD of the differences was calculated for each protocol and the results were compared using Student s t test. RESULTS: The differences between the 'means of the differences' for these two protocols never differed by more than 2 mmHg. For individuals the differences between data obtained using the two methodologies were up to 32 mmHg for mercury sphygmomanometry and 18 mmHg for the automated monitors. The differences between the SD of the differences were all less than 3 mmHg except for that of systolic blood pressure obtained by mercury sphygmomanometry, which was 7 mmHg CONCLUSIONS: The results of this study show that a sequential same-arm and a simultaneous opposite-arm comparison of intra-arterial and indirect blood pressure measurements yield similar results.
OBJECTIVE: To assess whether administration of dexamethasone in women with preterm premature rupture of membranes (PPROM) has an effect on the prevalence of maternal sepsis, neonatal respiratory distress syndrome (RDS), perinatal mortality and neonatal sepsis in a developing country. SETTING: Six public hospitals in South Africa that deal mainly with indigent women. METHOD: A multicentre, double-blind, placebo-controlled, randomised trial was performed on women with PPROM and fetuses of 28-34 weeks' gestation or clinically estimated fetal weight between 1,000 and 2,000 g if the gestational age was unknown. Women were randomised to receive either dexamethasone 24 mg intramuscularly or placebo in two divided doses 24 hours apart. All women received amoxycillin and metronidazole and were managed expectantly. Hexoprenaline was administered if contractions occurred within the first 24 hours after admission to the trial. OUTCOME MEASURES: The maternal outcome measures were clinical chorio-amnionitis and postpartum sepsis. The outcome measures for infants were perinatal death, RDS, mechanical ventilation, necrotising enterocolitis, and neonatal infection within 72 hours. RESULTS: One hundred and two women who delivered 105 babies were randomised to the dexamethasone group and 102 women who delivered 103 babies, to the placebo group. The groups were well balanced with regard to clinical features. There was a trend towards fewer perinatal deaths in the dexamethasone group: 4 compared with 10 (P = 0.16, odds ratio 0.37, 95% confidence intervals 0.09-1.34). A subanalysis of mothers who delivered more than 24 hours after admission to the study and their infants revealed a significant reduction in perinatal deaths; 1 death in the dexamethasone group and 7 in the placebo group, P = 0.047 (Fisher's exact test). No woman in either group developed severe sepsis, and the incidence of sepsis in the women did not differ significantly. Eleven infants in each group developed sepsis. CONCLUSION: This is the first randomised trial in women with PPROM to compare the effects of the use of corticosteroids with placebo, where all women received prophylactic antibiotics concomitantly with the corticosteroids. A trend towards an improved perinatal outcome was demonstrated in the women who received dexamethasone. There was no increased risk of infection in the women or their infants where dexamethasone was administered. Administration of corticosteroids to women with PPROM has more advantages than disadvantages in developing countries.
OBJECTIVE: To elucidate the causes of cardiovascular hemorrhage associated with mediastinitis and to review recommendations for prevention and treatment. SUMMARY BACKGROUND DATA: Mediastinal debridement with immediate or early coverage using healthy, vascularized tissue has lead to greatly reduced morbidity and mortality for patients with mediastinitis. Myocardial hemorrhage has been anecdotally reported. PATIENTS AND METHODS: Over a 36-month period, 7 patients developed massive cardiovascular bleeding after undergoing debridement for poststernotomy mediastinitis. Causes included puncture or erosion by a sternal edge in three and tearing at the myocardial-sternal interface in four. RESULTS: Five patients survived and remain infection-free at an average of 24 months of follow-up. In these patients, ventricular defects were closed with pledgeted sutures and muscle transposition was used concomitantly to reinforce the repair. This involved a slide of the left pectoralis major muscle and turnover of the right pectoralis in three patients, bilateral sliding in one patient, and bilateral pectoralis and an omental flap in one patient who required additional coverage of the lower mediastinum. CONCLUSIONS: When a patient who has undergone mediastinal debridement shows evidence of significant bleeding, we recommend application of pressure for control of hemorrhage, expeditious return to an operating room with available cardiopulmonary bypass, and immediate muscle coverage with healthy, well-vascularized tissue. Finally, early sternectomy might largely prevent this life-threatening complication.
OBJECTIVE: To determine whether the administration of prophylactic intravenous magnesium sulphate reduces the occurrence of eclampsia in women with severe pre-eclampsia. DESIGN: Randomised controlled trial. SETTING: A tertiary referral obstetric unit. POPULATION: Eight hundred and twenty-two women with severe pre-eclampsia requiring termination of pregnancy by induction of labour or caesarean section. METHODS: The women were randomised to receive either placebo (saline) or magnesium sulphate intravenously. The investigators were blinded to the contents of the pre-mixed solutions. MAIN OUTCOME MEASURE: The occurrence of eclampsia in the two groups. RESULTS: The data of 699 women were evaluated. Fourteen were withdrawn after randomisation. The overall incidence of eclampsia was 1.8%. Of 345 women who received magnesium sulphate, one developed eclampsia (0.3%); in the placebo group, 11/340 women (3.2%) developed eclampsia (relative risk 0.09; 95% confidence interval 0.01-0.69; P = 0.003). CONCLUSION: The use of intravenous magnesium sulphate in the management of women with severe pre-eclampsia significantly reduced the development of eclampsia.
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OBJECTIVE: To establish the antihypertensive properties of intravenous nimodipine used to treat eclamptic patients. To assess the effects of intravenous nimodipine on oxygen delivery and consumption. DESIGN: A prospective observational study. SETTING: The Maternity Centre Obstetric Intensive Care Unit, Groote Schuur Hospital. PARTICIPANTS: Four unselected patients presenting with proteinuric hypertension and seizures. METHODS: Haemodynamic observations were obtained by a radial artery catheter and right heart catheterisation with a pulmonary artery flow directed thermodilution catheter. Observations were obtained prior to and after the administration of nimodipine. RESULTS: A significant reduction in mean arterial pressure occurred in all patients after administration of nimodipine. This was due to a significant reduction in systemic vascular resistance. Neither oxygen delivery to the tissues nor peripheral oxygen consumption changed significantly during nimodipine infusion. No adverse effects related to the use of nimodipine were documented. CONCLUSIONS: Nimodipine is an effective vasodilator. There may be a role for nimodipine as a single agent for the management of eclampsia.
Eclampsia is a leading cause of maternal mortality. The prevention of seizure activity in pre-eclampsia and recurrent seizures in eclamptic patients is an essential aspect of management. Many drugs with anticonvulsant properties have been used to treat patients with pre-eclampsia and eclampsia. Magnesium sulfate is a significantly better drug than either diazepam or phenytoin for preventing recurrent seizures in eclamptic patients. Magnesium sulfate has diverse cardiovascular and neurological effects and also alters calcium metabolism. Although the drug crosses the placenta and may affect the fetus, these effects are clinically small and fetal morbidity has been shown to be reduced in randomised studies comparing magnesium sulfate to either phenytoin or benzodiazepines. Dosage regimens of magnesium sulfate are empirical. Because adverse effects of this agent are related to toxicity, the establishment of greater efficacy by using higher dosage regimens needs to be tested against a greater risk of adverse effects. The most serious toxicity related to magnesium sulfate use is magnesium sulfate use is neuromuscular blockade that may result in respiratory arrest. Magnesium sulfate is now the drug choice for treating eclamptic patients. However, further studies are required to establish the role of this agent as a prophylactic agent in the prevention of eclampsia.
Elevated fibronectin (Fn) concentrations in plasma from pregnant women have been suggested to be predictive for the development of pre-eclampsia. However, reported correlations between Fn concentration with gestational age or disease severity appear to be confounded by several variables. Our finding of degradation products of Fn in plasma from patients with severe pre-eclampsia led to a study of whether their presence could influence immunological and functional measurements of intact plasma Fn. Plasma samples (10 control pregnant and 10 severe pre-eclampsia patients) were studied for the presence of intact Fn and fragments by SDS-PAGE and Western blotting. Percentages of immunoreactive Fn fragmentation in control plasma (9.37 +/- 6.7%) and severe pre-eclampsia plasma (62.57 +/- 7.0%) were determined by densitometric scanning. Immunoassays by ELISA were performed on normal plasma samples and on purified Fn in the absence or presence of plasma digests of pure Fn. Artefactual underestimations of Fn concentration occurred in the presence of Fn fragments. The percentage underestimation increased with increasing digestion times (1 h, 46.52 +/- 3.69%; 3 h, 77.5 +/- 7.18%; 4 h, 100%) and with increasing concentrations of Fn digest products (1h) added to normal plasma samples (n = 10) (40 micrograms, 23 +/- 8.1%; 125 micrograms, 36.33 +/- 5.1%; 250 micrograms, 43.66 +/- 6.5%). The underestimation of Fn concentration in the presence of Fn fragments suggests that ELISAs for Fn may be unreliable and thus lose their predictive value in these patients. Opsonic activities of control pregnant and severe pre-eclamptic plasma were determined by gelatin-latex agglutination assay. The ratios of opsonic activity to Fn concentration in plasma from patients with pre-eclampsia were significantly lower than those of control pregnant plasma samples (p < 0.008). The impaired gelatin-latex agglutination of Fn in pre-eclamptic plasma suggests that Fn fragmentation could have biological sequelae in vivo.
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The objectives of this study were (1) To assess human umbilical cord vein endothelial cell (HUVEC) fibronectin (Fn) content and integrity in patients with preeclampsia and (2) to investigate the ability of Fn and Fn fragments (FnDP) to disrupt endothelial cell attachment to an Fn matrix through modulation of plasminogen activator activity. Intact Fn was released from normal cord veins, while Fn and FnDP (70 and 21 kd) were released from cord veins in culture from patients with severe preeclampsia. Factor VIII and Fn immunostaining of normal cord sections revealed endothelial integrity and low Fn content, while immunostaining of cord sections from patients with preeclampsia revealed a disrupted endothelium and high concentrations of Fn. Both intact Fn and FnDP isolated from patient plasma or prepared by plasmin digestion of pure Fn had no effect on chromium 51 release from HUVECs. These FnDP, but not intact Fn, stimulated HUVEC urokinase plasminogen activator production within 2 hours (p < 0.05) and caused a time- and concentration-dependent detachment and disruption of the HUVEC monolayers and HUVEC-mediated degradation of immobilized iodine 125-labeled Fn underneath the HUVEC monolayer (p < 0.02) after 2 hours. This 125I-labeled Fn release was enhanced by plasminogen and inhibited by aprotinin. Thus FnDP appear to cause endothelial cell disruption that may be due to plasmin generation in vitro.
In 87 patients (studied on average 1 year after their strokes) and 26 of their first-degree relatives, our specific aim was to assess the prevalence of the following stroke risk factors: hypofibrinolysis, familial hypofibrinolysis, high lipoprotein (a) level, and dyslipidemia. At least 2 months after their strokes (primarily ischemic), 87 patients had measures of lipids and lipoprotein (a); 69 and 67 patients had measures of basal and stimulated fibrinolytic activity, respectively, four new findings were as follows. (1) Hypofibrinolysis was common, with bottom decile-stimulated tissue plasminogen activator activity (the major stimulator of fibrinolysis) in 21% of stroke probands and in 30% of their first-degree relatives, versus 7% of 29 nomolipidemic control subjects (p = 0.09 and 0.026, respectively). (2) The hypofibrinolysis was mediated by top-decile levels of basal plasminogen activator inhibitor activity (the major inhibitor of fibrinolysis), which were observed in 20% of stroke probands and in 21% of their first-degree relatives, versus 8% of 175 nomolipidemic control subjects (p = 0.007 and 0.04, respectively). Mean (SD) basal plasminogen activator inhibitor activity and antigen level were higher in stroke probands (18 +/- 18 U/ml and 35 +/- 31 ng/ml, respectively) than in the 175 normolipemic control subjects (14 +/- 10 [p = 0.002], 28 +/- 34 [p = 0.016]). (3) Levels of basal tissue plasminogen activator antigen, a probable marker for atherosclerosis, were much higher in stroke probands than in the 175 normolipemic control subjects (15 +/- 7.3 ng/ml vs 7 +/- 3.8, p = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)