Clinical pharmacokinetics of aspirin.
Aspirin is very rapidly absorbed from the gastrointestinal tract when administered as a solution, and somewhat more slowly when administered in tablets. It is rapidly hydrolyzed in the body to salicylic acid; the plasma concentration of the latter must be maintained within a relatively narrow range to obtain an adequate anti-inflammatory effect and to minimize systemic adverse effects. The two major pathways of salicylate elimination, i.e., formation of salicyluric acid and salicyl phenolic glucuronide, become saturated at relatively low body levels of the drug. Consequently, steady-state ("plateau") salicylate levels increase more than proportionately with increasing daily dose, and the time required to reach steady state increases with increasing daily dose. The renal clearance of salicylic acid increases markedly with increasing urine pH; antacids capable of increasing urine pH can therefore cause a pronounced lowering of steady-state salicylate concentrations under clinical conditions. There are pronounced intersubject differences in salicylate elimination kinetics; dosage must be individualized on the basis of plasma concentration and clinical response. The drug is readily transferred across the placenta and is only slowly eliminated by the newborn infant. The drug is also transferred from mother to nursing infant through the breast milk.
D000042:Absorption; D001241:Aspirin / Q000008:administration & dosage / Q000378:metabolism*; D001711:Biotransformation; D002648:Child; D005260:Female; D006801:Humans; D007231:Infant, Newborn; D007408:Intestinal Absorption; D007700:Kinetics; D008297:Male; D008431:Maternal-Fetal Exchange; D011247:Pregnancy; D012459:Salicylates / Q000097:blood
D012459:Salicylates; D001241:Aspirin