Following absorption into the blood stream, lisdexamfetamine is completely converted by red blood cells to dextroamphetamine and the amino acid L-lysine by hydrolysis via undetermined aminopeptidase enzymes. This is the rate-limiting step in the bioactivation of lisdexamfetamine. The elimination half-life of lisdexamfetamine is generally less than 1 hour. Due to the necessary conversion of lisdexamfetamine into dextroamphetamine, levels of dextroamphetamine with lisdexamfetamine peak about one hour later than with an equivalent dose of immediate-release dextroamphetamine. Presumably due to its rate-limited activation by red blood cells, intravenous administration of lisdexamfetamine shows greatly delayed time to peak and reduced peak levels compared to intravenous administration of an equivalent dose of dextroamphetamine. The pharmacokinetics of lisdexamfetamine are similar regardless of whether it is administered orally, intranasally, or intravenously. Hence, in contrast to dextroamphetamine, parenteral use does not enhance the subjective effects of lisdexamfetamine. Because of its behavior as a prodrug and its pharmacokinetic differences, lisdexamfetamine has a longer duration of therapeutic effect than immediate-release dextroamphetamine and shows reduced misuse potential.CYP2D6, dopamine β-hydroxylase (DBH), flavin-containing monooxygenase 3 (FMO3), butyrate-CoA ligase (XM-ligase), and glycine N-acyltransferase (GLYAT) are the enzymes known to metabolize amphetamine or its metabolites in humans. Amphetamine has a variety of excreted metabolic products, including 4-hydroxyamphetamine, 4-hydroxynorephedrine, 4-hydroxyphenylacetone, benzoic acid, hippuric acid, norephedrine, and phenylacetone. Among these metabolites, the active sympathomimetics are 4-hydroxyamphetamine, 4-hydroxynorephedrine, and norephedrine. The main metabolic pathways involve aromatic para-hydroxylation, aliphatic alpha- and beta-hydroxylation, N-oxidation, N-dealkylation, and deamination.
Clarkson published his series of three cases and named the syndrome after Poland in his article. Notable cases
TV presenter Jeremy Beadle (1948–2008) was known for having this condition. His Poland syndrome manifested itself in the form of his disproportionately small right hand. Olympic boxer Jérôme Thomas is also affected by Poland syndrome, as his left arm and hand are significantly shorter and smaller than his right. Thomas also lacks a left pectoral muscle. PGA Tour golfer Bryce Molder has Poland syndrome, with an absent left pectoral muscle and a small left hand. Several surgeries in his childhood repaired syndactyly on the left hand. Actor Ted Danson, famous for starring in the TV show Cheers, admitted he had the condition in 2000 to Orange Coast magazine and said that he was bullied as a child because of it. Formula One World Champion Fernando Alonso is affected by Poland syndrome; he is missing the right pectoral muscle. Cricketer Lewis Hatchett was born with Poland syndrome. Australian Paralympian Mathew Silcocks is affected by Poland syndrome. Hailey Dawson of Nevada (born 2010) has a missing right pectoral muscle and is missing three fingers on her right hand due to the condition. She has thrown out the ceremonial first pitch at all 30 Major League Baseball parks, using a 3D-printed robotic right hand fitted for her by engineers at the University of Nevada, Las Vegas. Actor Gary Burghoff, best known for the television series M*A*S*H, has Poland syndrome manifesting in brachydactyly on his left hand.