Prostaglandins are fatty acids derived from arachidonic acid metabolism. They are closely related to the Thromboxanes and Leukotrienes. Prostaglandin E1 is derived mainly from Prostaglandin H1, and is metabolized to Prostaglandin F1a. Prostaglandin E1 is excreted directly into the urine. Prostaglandin E1 relaxes the circular muscle of the gut in opposition to Prostaglandin F2a, and also relaxes the lower esophageal sphincter. Prostaglandin E1 reduces gastric secretion preventing the formation of ulcers. Prostaglandin E1 is also a potent inhibitor of platelet aggregation. Prostaglandin E1 stimulates accumulation of cyclic AMP and can stimulate thyroid activity in a manner similar to that of TSH. Elevated levels have been found in patients with tuberculosis, lung cancer, Medullary Carcinoma of the Thyroid, Carcinoid Syndrome, neuroblastomas, and the Watery Diarrhea Syndrome. Prostaglandin E1 production and circulating levels are drastically suppressed by aspirin and indomethacin.
250 – 500 pg/ml
Prostaglandin E1 is measured by EIA/ELISA following extraction of specimens.
Patient should not be on aspirin, indomethacin, or anti-inflammatory medications, if possible, for at least 48 hours prior to collection of specimen.
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.
For tumor/tissue and various fluids (i.e. CSF, peritoneal, synovial, etc.) contact the Institute for requirements and special handling.
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. MJ Dunn and EJ Zambraski. Renal Effects of Drugs that Inhibit Prostaglandin Synthesis. Kidney International 18: 609, 1980.