Serum from patients with heparin-associated thrombocytopenia deposited excess immunoglobulins on endothelial cells and stimulated tissue factor production, suggesting a mechanism for thrombosis.
Observational (n=27)
We studied the possibility that immune injury to endothelial cells may have a role in the development of thrombosis in some patients with heparin-associated thrombocytopenia. Serum samples from each of 27 patients who had this clinical diagnosis contained heparin-dependent platelet antibodies and deposited more than normal amounts of IgG, IgA, or IgM on endothelial cells, stimulating the production of tissue factor. Binding of immunoglobulins to endothelial cells was no longer detected when the patients were studied after heparin was withdrawn, but reappeared within several days upon reexposure to heparin in a patient who experienced a clinical recurrence. Binding of immunoglobulin to endothelial cells was partially reduced by the preadsorption of serum samples with heparin or heparan sulfate bound to Sepharose or by enzymatic cleavage of cell-bound heparan sulfate, and was augmented by the addition of heparan sulfate. Thus, serum from some patients with heparin-associated thrombocytopenia may contain antibodies that react with heparin bound to endothelial cells or with heparan sulfate synthesized by endothelial cells. Immune injury to both platelets and endothelial cells may play a part in the development of thrombosis in some patients after heparin therapy.
Cines et al. (Thu,) conducted a observational in Heparin-associated thrombocytopenia (n=27). Heparin-associated thrombocytopenia was evaluated on Deposition of IgG, IgA, or IgM on endothelial cells and stimulation of tissue factor production. Serum from patients with heparin-associated thrombocytopenia deposited excess immunoglobulins on endothelial cells and stimulated tissue factor production, suggesting a mechanism for thrombosis.