thromboxane-b2 and Anorexia-Nervosa

We have previously demonstrated that platelets obtained from patients with anorexia nervosa or severe peripheral vascular disease are hyperaggregable. Since conventional heparins are known to activate platelets in vitro and occasionally induce thrombosis and consumptive thrombocytopenia in vivo, we have investigated the direct effect of a conventional heparin on platelets obtained from patients with anorexia nervosa or severe peripheral vascular disease. Heparin at therapeutic concentrations was found to induce platelet aggregation of such platelets in vitro. In contrast, a recently developed low molecular weight heparinoid (Org 10172), at therapeutic concentrations, had no effect on these hyperaggregable platelets. We conclude that: heparin may be potentially harmful to patients with hyperaggregable platelets; thrombocytopenia and thrombosis associated with heparin therapy may be mediated through a direct effect of heparin on platelets; it is unlikely that heparin induced thrombocytopenia is always mediated by classical immunological mechanisms, especially in patients with hyperaggregable platelets; and low molecular weight heparinoids may be safer anticoagulants in patients with platelet hyperaggregability.

Topics: Adolescent; Adult; Aged; Anorexia Nervosa; Blood Platelets; Chondroitin Sulfates; Collagen; Dermatan Sulfate; Epinephrine; Female; Glycosaminoglycans; Heparin; Heparitin Sulfate; Humans; Immunoglobulin G; In Vitro Techniques; Male; Middle Aged; Platelet Aggregation; Thrombocytopenia; Thromboembolism; Thromboxane B2; Vascular Diseases