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:
250 – 400 pg/ml
Procedure:
Prostaglandin E2 is measured by EIA/ELISA following extraction of specimens.
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:
3 ml serum or EDTA plasma should be collected and separated as soon as possible. Freeze specimen immediately after separation. Minimum specimen size is 1 ml.
Special Specimens:
For tumor/tissue and various fluids (i.e. CSF, peritoneal, synovial, etc.) contact the Institute for requirements and special handling.
Shipping Instructions:
Ship specimens frozen in dry ice.
References:
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.