부산대학교 도서관

Serotonin syndrome is a predictable consequence of excess serotonergic agonism of the central nervous system receptors as well as peripheral serotonergic receptors. The clinical manifestations of the syndrome range from barely noticeable to fatal features. In serotonin synthesis, ingested tryptophan crosses the blood–brain barrier and enters neurones where it is hydrolysed and decarboxylated to serotonin. The serotonin is stored in vesicles and released into the synaptic cleft with resultant depolarisation of the presynaptic neurones. Removal of serotonin from the cleft is via reuptake pumps and it is either repackaged or degraded by monoamine oxidase (MAO). Monoamine oxidase has two isoforms: MAO-A which metabolises serotonin, and MAO-B which metabolises catecholamines. Theoretically, damage to vascular endothelium is associated with a decrease in MAO-A activity, hence a reduction in the capacity to metabolise serotonin with a resultant increase in levels of serotonin. This lesson reports the case of serotonin syndrome in a 71-year-old man secondary to fluoxetine believed to be precipitated by radiation-induced vasculopathy.