Prostaglandin E2 (PG E2), urine

Clinical Significance:
Prostaglandins are fatty acids derived from arachidonic  acid metabolism.  They are closely related to the Thromboxanes and Leukotrienes.  Prostaglandin E2 is derived mainly from Prostaglandin H2, and is metabolized to Prostaglandin  F2a, A2, and Dihydroketo Prostaglandin E2.  Prostaglandin E2 is excreted directly into the urine.  Prostaglandin E2 is a potent vasodilator and also a stimulus for Renin release.  Prostaglandin E2 release is stimulated by cholinergic and alpha adrenergic agents.  Prostaglandin E2 potentiates the actions of Histamine and Bradykinin causing pain and accumulation of edema fluid.  It relaxes the circular muscle of the gut in opposition to Prostaglandin F2a, and also relaxes the lower esophageal sphincter.  Prostaglandin E2 also causes accumulation of water and electrolytes in the lumen of the gut by stimulating their secretion.  Elevated levels of Prostaglandin E2 have been detected in patients with the Watery Diarrhea Syndrome, neural crest tumors, pheochromocytomas, and other amine-peptide-secreting tumors. Prostaglandin E2 production and circulating levels are drastically suppressed by aspirin and indomethacin. 

Reference Range:
*Reported per liter basis. No reference intervals available for this test.

Urine Prostaglandin E2 is measured by direct EIA/ELISA.

Patient Preparation:
Patient should not be on aspirin, indomethacin, or anti-inflammatory medications, if possible, for at least 48 hours prior to collection of specimen.

Specimen Collection:
5-10mL of a random urine specimen should be collected and frozen immediately. Specimen must remain frozen prior to and during shipping. 24-hour urine collections are not acceptable. Rejection criteria include: room temperature, thawed or refrigerated specimens or 24-hour urine collections.

Shipping Instructions:
Ship specimens frozen in dry ice.

1. JS Redfern and M Feldman. Role of Endogenous Prostaglandins in Preventing Gastrointestinal Ulceration:  Induction of Ulcers by Antibodies to Prostaglandins.  Gastroenterology 96: 596, 1989.

2. J Balasch, V Arroyo, F Carmona, J Llach, W Jimenez, JC Pare, and JA Vanrell.  Severe Ovarian Hyperstimulation Syndrome:  Role of Peripheral Vasodilation.  Fertility and Sterility 56: 1077-1083, 1991.