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.
Up to 175 ng/g Creatinine
Urine Prostaglandin D2 is measured by direct EIA/ELISA.
Patient should not be on aspirin, indomethacin, or anti-inflammatory medications, if possible, for at least 48 hours prior to collection of specimen.
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.
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 Prosta-glandins. 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.