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Urinary Excretion of Degradation Products of Prostacyclin and Thromboxane Is Increased in Patients with Gestational Choriocarcinoma¹

Departments of Obstetrics and Gynecology [A. M. A.-T., R. O. Y.] and Children's Hospital [L. U. V.], University of Helsinki, SF-00290 Helsinki, Finland, and Department of Obstetrics and Gynecology, Catholic University Medical College, Kangnam St. Mary's Hospital, Seoul, Korea [J. K. J., S. J. K.]

Gestational choriocarcinoma metastasizes rapidly, in which process the vasoactive prostanoids may be significant. We therefore compared the urinary excretion of prostacyclin and thromboxane A₂ (TxA₂) metabolites in 19 women with gestational choriocarcinoma and 20 healthy age-matched women by assessing spot urine samples for 6-keto-prostaglandin F₁ (6-keto-PGF₁) and 2,3-dinor-6-keto-prostaglandin F₁ (2,3-dinor-6-keto-PGF₁) (degradation products of prostacyclin) as well as for thromboxane B₂ (TxB₂) and 2,3-dinor-TxB₂ (degradation products of TxA₂) by high-pressure liquid chromatography, followed by radioimmunoassay; the data were related to urinary creatinine concentration.

The urinary output of 6-keto-PGF₁ [29.56 ± 7.0 versus 25.08 ± 3.91 ng/mmol creatinine (SE)] in patients with choriocarcinoma was normal, but that of 2,3-dinor-6-keto-PGF₁ in cancer patients was higher than in controls (24.44 ± 5.20 versus 14.84 ± 1.94, P < 0.02), as was that of TxB₂ (22.72 ± 4.69 versus 9.69 ± 1.52, P < 0.001) and 2,3-dinor-TxB₂ (114.21 ± 30.81 versus 51.81 ± 10.40, P < 0.01). The ratio of net prostacyclin output (6-keto-PGF₁ plus 2,3-dinor-6-keto-PGF₁) to the net TxA₂ output (TxB₂ plus 2,3-dinor-TxB₂) in cancer patients [0.52 ± 0.1 (SE)] was lower (P < 0.03) than in the controls (0.83 ± 0.1), and in an inverse relation (r = -0.54, P < 0.05) to the scoring index of poor prognosis for the disease.

We conclude that the prostanoid excess in gestational trophoblastic disease, as evidenced for the first time in this study, may originate from choriocarcinoma cells, or may be a paraneoplastic phenomenon, and we conclude also that TxA₂ excess may contribute to the tumor growth and/or formation of metastases.

¹ This study was supported by grants from Research Council of the UpJohn Company, Kalamazoo, MI, and The Finnish Medical Foundation.

² To whom requests for reprints should be addressed.

Received 1/24/91. Accepted 5/30/91.