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There is no clear first-line tocolytic agent. [6] [7] Current evidence suggests that first line treatment with β 2 agonists, calcium channel blockers, or NSAIDs to prolong pregnancy for up to 48 hours is the best course of action to allow time for glucocorticoid administration.
Women should speak to their doctor or healthcare professional before starting or stopping any medications while pregnant. [1] Drugs taken in pregnancy including over-the counter-medications, prescription medications, nutritional supplements, recreational drugs, and illicit drugs may cause harm to the mother or the unborn child.
Furosemide, sold under the brand name Lasix among others, is a loop diuretic medication used to treat edema due to heart failure, liver scarring, or kidney disease. [4] Furosemide may also be used for the treatment of high blood pressure. [4] It can be taken intravenously or orally. [4]
Contraindicated in pregnancy: Studies in animals or humans have demonstrated fetal abnormalities and/or there is positive evidence of human fetal risk based on adverse reaction data from investigational or marketing experience, and the risks involved in use of the drug in pregnant women clearly outweigh potential benefits.
Schedule 8 (S8) drugs and poisons, otherwise known as Controlled Drugs, are schedule 9 prohibited substances that are appropriate preparations for therapeutic use which have high potential for abuse and addiction. The possession of these medications without authority is the same as carrying a prohibited substance and is illegal.
Aliskiren (brand names Tekturna and Rasilez) is the first in a class of drugs called direct renin inhibitors.It is used for essential (primary) hypertension. [2] While used for high blood pressure, other better studied medications are typically recommended due to concerns of higher side effects and less evidence of benefit.
Acute fatty liver of pregnancy is a rare life-threatening complication of pregnancy that occurs in the third trimester or the immediate period after delivery. [1] It is thought to be caused by a disordered metabolism of fatty acids by mitochondria in the fetus, caused by long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency . [ 2 ]
Biological half-life is 10 to 20 hours, and steady-state concentrations are reached after four to five days after start of the treatment. [ 3 ] [ 9 ] Oxcarbazepine, for comparison, is also nearly completely absorbed from the gut, and peak plasma concentrations of licarbazepine are reached after 4.5 hours on average after oxcarbazepine intake.