Prostaglandin E2 (PGE2) is one of the most abundant prostanoid in the human body. In cells, arachidonic acid is transformed into PGE2 via cyclooxygenase 1 and 2 and terminal prostaglandin E synthases (PGES). PGE2 is produced in response to stress or cell injury. It is a potent mediator of inflammation in diseases such as rheumatoid arthritis and osteoarthritis.

PGE2 plays a central role inflammation, pyrexia, and pain sensation.PGE2 contributes to inflammation by increasing vascular permeability and thereby enhancing edema and leukocyte infiltration into tissues. In the central nervous system, PGE2 binds to prostaglandin receptor EP3 and increases body temperature. The binding of PGE2 to prostaglandin receptors EP1 and EP4 receptors increases the sensation of pain.  

PGE2 is a potent vasodilator that potentiates the actions of histamine and bradykinin and contributes to the formation of fever, edema and pain. It activates smooth muscles in the GI tract, causing contractions. It also stimulates secretion of water and electrolytes into the lumen of the gut. Elevated levels of Prostaglandin E2 have been detected in patients with the Watery Diarrhea Syndrome, neural crest tumors, and pheochromocytoma.

Prostaglandin E2 is excreted directly into the urine. The preferred specimen is a 24 hour collection of urine in a container without preservative. Reference value is 400-600 ng per 24 hours. 

Prostaglandin E2 levels are decreased by nonsteroidal anti-inflammatory drugs (NSAIDS). Patients should discontinue these medications for at least 48 hours prior to collection. 

References

Park JY, et al, Prostaglandin E2 synthesis and secretion: The role of PgE2 synthases, Clin Immunol, 2006;119(3):229-240. 

McCoy JM, et al, The role of prostaglandin E2 receptors in the pathogenesis of rheumatoid arthritis, J Clin Invest, 2002;110(5):651-658. 


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