Prostaglandins are fatty acids derived from arachidonic acid metabolism. They are closely related to the Thromboxanes and Leukotrienes. Prostaglandin D2 is derived mainly from Prostaglandin H2, and is metabolized to Dihydroketo Prostaglandin D2. Prostaglandin D2 is excreted directly into the urine. The sites of highest Prostaglandin D2 activity are the brain, spinal cord, intestines, and stomach. Prostaglandin D2 is the major Prostaglandin produced by uterine tissue. Prostaglandin D2 is a potent bronchoconstrictor, neuromodulator, and anti-antithrombin agent. It also stimulates the secretion of Pancreatic Glucagon. Prostaglandin D2 has been found to have an anti-metastatic effect on many malignant tumor cells. Prostaglandin D2 production and circulating levels are drastically suppressed by aspirin and indomethacin.
35 – 115 pg/ml
Prostaglandin D2 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. B Bennegard, M Halin, and L Hamberger. Luteotropic Effects of Prostaglandins I2 and D2 on Isolated Human Corpora Luteum. Fertility and Sterility 54: 459-464, 1990.