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Re: Terbutaline LawyersFrom: viv souter (vsouter@yahoo.com)Fri Nov 19 20:39:56 2004
Hi Terry Thanks for your response.... and reassurance! I can't hear it enough. The management of preterm labour is so controversial and while as a pregnant mother you want to do everything to prevent preterm birth, you also don't want to do anything to harm your baby. We need more studies, including longterm follow up studies of tocolytics. Viv Terrence.Jones@kp.org wrote: With Your genetics background, You've developed a sensitivity for mechanisms outside that attributable to therapeutic response. But keep in mind, with Human data, the potential confounders; when magnitude of effefct is marginal. It's a matter of distinguishing whether intrauterine or extrauterine environment is better/worse. If intrauterine, then what Rx option(s)? In the presence of certain conditions, beta agonist might be more toxic than magnesium or, perhaps, no Rx at all. As the indication for Terb is PTL, the population studied will demonstrate heterogeneity WRT deciduitis, amnionitis (as etiology). The cytotkine mediated damage to CNS, in such cases (infection/sepsis) , may be exaggerated by ischemia/hypoxia; upon reperfusion and secondary neuronal loss. (Which can be 'chronic', 'acute' or both.) In glutamate predominant centers (Putamen, Perirolandic cortex, Int capsule, caudate, thalamus) the enhaced blood flow secondary to beta-agonist, during reperfusion, might enhance glutamate excitotoxicity. Magnesium, OTOH, might mediate in a protective fashion via secondary effects on NMDA. The fetal CNS receptor does not down-regulate to beta-agonist (at least in murine model), so risk remains along with exposure. OTOH, If there's no cytotkine or ischemic (perfusion) insult... In terms of alpha-R dysmodulation (Kreider/Slotkin '04) - 10 mg/kg seems a bit high, even for a rat? And their (Durham) postnatal data (pyramidal, purkinje, hippocampus) appears restricted to females? (In the absence of infection as potential co-contributing factor to CNS morbidity, beta-agonist effects on alveolar surfactant production might even reduce pulmonary morbidity. In thrombophilic mediated vaso-occlusive disease, at least within the cerebral circulation, it reduces thrombogenesis via at least one of Virchow's triad (flow). This may not be the case with Nifedipine - which may also have adverse effects on placental perfusion thru a variety of mechanisms in susceptible Patients.) That rats on high doses of terbutaline show suspicious CNS developmental changes is not in question. What is in question is the extrapolation to outcomes in Humans, with a variety of underlying causes for the condition (PTL), and a variety of causes for CNS sensitization toward injury. Behind the confounders lie: either the truth, or the plaintiff's bar. Even a Kiwi like Peter Gluckman (Liggins Inst) will give us that measure of understanding. (So long as it doesn't compromise the care of the neonate...) "To everything there is a season" - and to the seasons, there's Vivaldi. tj (PS - haven't used Terb for over 10 yrs, more due to receptor down-reg (in the myometrium), than toxicity concerns in fetal CNS. OTOH, haven't used Atosiban, either!)
-- viv souter <vsouter@yahoo.com> Sent by: ob-gyn-l@obgyn.net 11/18/2004 11:47 AM Please respond to ob-gyn-l
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