iloprost and Takayasu-Arteritis

Topics: Academies and Institutes; Administration, Inhalation; Angioplasty, Balloon; Antihypertensive Agents; Asian People; Bone Morphogenetic Protein Receptors, Type II; Bosentan; Calcium Channel Blockers; Cardiology; Cooperative Behavior; Endothelin Receptor Antagonists; Female; Growth Differentiation Factor 2; Guidelines as Topic; Humans; Iloprost; Mutation; Phenylpropionates; Pulmonary Arterial Hypertension; Pulmonary Embolism; Pulmonary Medicine; Pyridazines; Takayasu Arteritis; Vasodilator Agents

Patients in an active stage of Takayasu arteritis are often complicated with thrombosis in the affected vessels. We investigated whether alteration of platelet sensitivity to prostacyclin is involved in platelet function in these patients. Twelve female patients in an active stage (48.3+/-11.8 years, mean+/-S.D.), diagnosed clinically by a persistently elevated erythrocyte sedimentation rate (>40 mm/h) with typical symptoms, along with 10 gender- and age-matched patients in an inactive stage and 12 control subjects were enrolled. Half-maximal concentration (EC(50)) for platelet aggregation to collagen was determined in the presence and absence of 1 nM iloprost, a stable prostacyclin analog. Sensitivity of platelets to prostacyclin was quantified by the ratio of EC(50) (R) in the presence of iloprost to that in its absence. Patients in an active stage exhibited enhanced platelet aggregation, as demonstrated by significantly lower EC(50) to collagen and increased plasma thromboxane B(2) concentration. However, R values in these patients were significantly higher (4.00+/-1.05; P<.001) than those in the inactive patients or controls (2.58+/-0.62 and 2.43+/-0.68, respectively), suggesting enhanced sensitivity to prostacyclin in patients with active disease. Plasma 6-keto-PGF1 alpha levels were lower in the active patients than those in other groups of subjects. We conclude that platelets in an active stage of TA may be sensitive not only to collagen but also to prostacyclin. The increase in sensitivity of the platelets to prostacyclin could be a compensatory mechanism against a decrease in the prostanoid production, presumably associated with endothelial dysfunction.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Blood Platelets; Case-Control Studies; Collagen; Epoprostenol; Female; Humans; Iloprost; Kinetics; Male; Middle Aged; Platelet Aggregation; Takayasu Arteritis; Thromboxane B2