Clinical Significance:
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 13,14-dihydro-15-keto 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-
thrombin 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.
Reference Range:
18 – 268 ng/24hrs
Procedure:
Urine Prostaglandin D2 is measured by direct 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:
24 hours urine collection. Refrigerate during collection and mix well. Transfer 5 – 10 ml urine to
urine transport container and freeze immediately. Rejection criteria include: room temperature,
thawed or refrigerated specimens.
Shipping Instructions:
Ship specimens strictly frozen in dry ice.
References:
- 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. - 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.