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1684 ABNORMAL PROSTAGLANDIN (PG) METABOLISM AND PLATELET FUNCTION IN CYSTIC FIBROSIS (CF) PATIENTS

Our previous studies (Lemen, et al. Am.Rev.Resp.Dis., 117:639-46, 1978) reported abnormal plasma PG concentrations in CF patients; but, the physiologic significance of these observations is unknown. We correlated plasma PGs to ADP induced platelet aggregation (PA) in 8 normal and 11 CF subjects. Platelet proaggregators (e.g. thromboxane (Tx)A2 as TxB2 and PGE2) and antiaggregators (PGI2 as 6-keto-F1α) were measured by radioimmunoassay. With parallelism between standards and plasma and with the within-sample coefficient of variation <9%, 6-keto-F1α was significantly (p <0.05) reduced in CF patients (X±SE 408 ± 105 pg/ml) compared to normal subjects (X± SE 708 ± 196 pg/ml). PGF2α was significantly (p <0.05) elevated in CF patients (X±SE, 282 ± 106 pg/ml compared to normal subjects (X±SE, 173 ± 65). TxB2 and PGE2 were not different in CF patients (X±SE, 327 ± 84 and 793 ± 239 pg/ml, respectively) compared to normal subjects (X±SE, 318 ± 92 and 995 ± 495 pg/ml, respectively). ADP induced PA was inhibited in 13/18 studies in CF patients. Platelet electronmicrographs showed decreased dense bodies/platelet profile in 4/8 studies, and PA correlated with dense bodies in 4/8 studies. PA was not correlated with drug therapy including antibiotics or vitamin E. We conclude that abnormal PG metabolism may result in abnormal platelet function in CF patients. Supported in part by grant HL 23773 and the Cystic Fibrosis Foundation.