Placental 11 beta hydroxysteroid dehydrogenase

                                                                                                                    

Women who have preeclampsia with severe features require hospitalization for careful monitoring. Treatment goals are fluid management, seizure prevention, lowering BP to prevent maternal end-organ damage, and expediting delivery based on disease severity and gestational age. 1 Excessive fluid administration can result in pulmonary edema and ascites, whereas too little fluid can exacerbate intravascular volume depletion and end-organ ischemia. Urine output should be maintained above 30 mL per hour, and a Foley catheter should be used to monitor urine output if MgSO 4 is administered. 28 Total intravenous intake should be less than 100 mL per hour, and total combined oral and intravenous fluids should be less than 125 mL per hour. 28

There is some evidence that CBS heterozygosity may interact with other risk factors to increase the risk of cardiovascular disease. Mandel et al. (1996) concluded that patients with concurrent homocystinuria due to CBS deficiency have an increased risk of thrombosis when they also have the factor V Leiden mutation ( ). They studied 7 unrelated consanguineous kindreds in which at least 1 member was homozygous for homocystinuria. Thrombosis (venous, arterial, or both) occurred in 6 of 11 patients with homocystinuria (aged to 8 years). All 6 also had the factor V Leiden mutation. One patient with prenatally diagnosed homocystinuria who was also heterozygous for factor V Leiden received warfarin therapy from birth and by the age of 18 months had not had thrombosis. Of 4 patients with homocystinuria who did not have factor V Leiden, none had thrombosis (aged 1 to 17 years). Three women who were heterozygous for both homocystinuria and factor V Leiden had recurrent fetal loss and placental infarctions.

Placental 11 beta hydroxysteroid dehydrogenase

placental 11 beta hydroxysteroid dehydrogenase

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