ABSTRACT
A case of premature labor in a woman whose pregnancy was complicated by myasthenia gravis is presented. Ritodrine was given for tocolysis, and betamethasone was administered to accelerate fetal lung maturation. An acute, life-threatening exacerbation of muscular weakness requiring intubation and mechanical ventilation occurred. It appears that betamethasone initiated the respiratory crisis. It is apparent, however, that tocolytic agents currently being used in patients with premature labor (namely, beta-2-sympathomimetics and magnesium sulfate) also have the potential to produce severe exacerbations of weakness, and even respiratory arrest in patients with myasthenia gravis. Each must be used with extreme caution if prescribed for women with this disorder.
Subject(s)
Myasthenia Gravis/complications , Obstetric Labor, Premature/prevention & control , Pregnancy Complications , Respiratory Insufficiency/etiology , Adult , Betamethasone/adverse effects , Betamethasone/therapeutic use , Cholinesterase Inhibitors/adverse effects , Cholinesterase Inhibitors/therapeutic use , Female , Humans , Myasthenia Gravis/drug therapy , Obstetric Labor, Premature/chemically induced , Pregnancy , Pregnancy Complications/drug therapy , Ritodrine/adverse effects , Ritodrine/therapeutic useABSTRACT
In the first trimester of pregnancy, inactive renin in plasma rapidly increases (to 5 times the average concentration in plasma of nonpregnant controls), then declines slowly until midpregnancy, and falls quickly to the normal range after delivery. Inactive renin has the same large apparent molecular weight in pregnancy as in control plasma. Amniotic fluid contains very high levels of inactive renin; its mobility on Sephadex G-100 is the same as that of inactive plasma renin, but a lower molecular weight is indicated by the delayed elution of inactive renin of amniotic fluid from Sephacryl S-200. This anomalous behavior is probably responsible for the different estimates of molecular is probably responsible for the different estimates of molecular weight previously reported. The plasma concentration of active renin in pregnancy is modestly increased in the first trimester, declining gradually until term, and falling quickly after delivery. Although the increased PRA in early pregnancy involves an increase in active renin, increased angiotensinogen appears to play a more important part in sustaining the increased PRA of late pregnancy. The apparent molecular weight of te active renin in pregnancy plasma is larger than that in normal plasma. Gross changes in sodium intake during pregnancy result in changes in active and inactive renin concentrations parallel to those observed in nonpregnant controls. These responses suggest that the kidneys are an important source of the altered plasma renin in pregnancy, but do not exclude a contribution from other sources.
