Intravenous prostaglandin E-1 reduces soluble vascular cell adhesion molecule-1 in peripheral arterial obstructive disease

Objectives Elevated levels of soluble (s) vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1, pointing to activation of cells involved in vascular inflammation, have been previously reported in p eripheral arterial obstructive disease (PAOD). We tested the hypothesis tha t intravenous prostaglandin E-1 (PGE(1)) treatment, which produces clinical benefits in this condition, might decrease such levels. Methods Ten subjects (age range 58 +/- 10 years, 6 male, 4 female) with cha racterized Fontaine stage IIa to IV PAOD (ankle/arm pressure index <0.96) w ere entered into a treatment protocol with twice daily intravenous infusion s of PGE(1) (alprostadil) at 120 mug per day, repeated for 10 consecutive d ays. Preinfusion and postinfusion plasma samples were stored for blind enzy me immunoassays of soluble adhesion molecules and the fibrinolytic marker t issue plasminogen activator, type-1 plasminogen-activator inhibitor, and D- dimer. Results Estimates of severity of pain at rest, consumption of analgesics, m agnitude of trophic lesions, remission to lower Fontaine stages, and favora ble changes in the venoarteriolar reflex documented significant beneficial effects of the treatment. Significant (P < .01) pretreatment and posttreatm ent reductions of in all soluble markers explored were found. Particularly, sVCAM-1 exhibited a significant decrease after each infusion, which was su stained at the last day of treatment (from 854 +/- 214 ng/mL to 775 +/- 215 ng/mL across the first infusion, from 773 +/- 146 ng/mL to 680 +/- 110 ng/ mL across the last infusion). Conclusion Thus a global decrease of vascular cell activation appears to oc cur as a result of PGE, administration and may contribute to the observed c linical benefits in PAOD.