In general, all effects of the antiinflammatory drugs are related to the inhibition of the arachidonic acid and inhibition of prostaglandins and tromboxans production. Two types of ciclo-oxygenasis (COX) exist, which are COX-1 and COX-2. COX-1 is a constitutional enzyme expressed in many sites, including platelets, and is involved in tecidual homeostasis. On the other hand, COX-2 is induced in inflammatory cells when they are activated, and it is considered as being the enzyme that produces the mediators of the inflammation. The action of antiinflammatory drugs is related to the inhibition of COX-2 and is probable that their undesirable effects are due mainly to the inhibition of COX-1. Maternal treatments with NSAIDs have been frequently associated, with the vasoconstriction of the fetal ductus arteriosus, lung arterial hypertension and inhibition of platelet aggregation. Alterations in hemostasis are some of the collateral effects produced by the indiscriminate use of NSAIDs, which induce to an unbalance in the prostaglandins and tromboxans liberation, that are reflected in the adhesiveness and platelet aggregation. The haemostatic alterations observed in neonates, caused by salicilates’s ingestion by the mother, are due to inhibition of the platelet aggregation and the decrease of the activity of the factor XII related to the clotting. Studies in mice revealed that corticoids’s use during the gestation can lead to abnormalities in fetal development, because of the alterations in the cellular differentiation.
antiinflammatory drugs; pregnancy; fetal alterations