Investigations of the lupus-like inhibitor by-passing activity of platelets.
Plasmas from ten patients with a lupus or lupus-like inhibitor were investigated. In each case the partial thromboplastin time with kaolin (PTTK) was prolonged and failed to correct on the addition of an equal volume of normal plasma. Activated control platelets corrected the inhibitory effect in the PTTK or thrombin generation time (TGT) in every instance. Activated autologous platelets were as effective as control platelets and may thus explain why bleeding is rarely associated with the lupus inhibitor. Experiments using platelets or plasma from patients congenitally deficient in a single clotting factor or normal washed platelets resuspended in deficient plasma indicated that the inhibitor by-passing activity is platelet and not plasma derived. Platelet fractionation studies suggested that this activity is localised at the platelet membrane.
D001778:Blood Coagulation Disorders; D001779:Blood Coagulation Factors / Q000037:antagonists & inhibitors*; D001792:Blood Platelets / Q000502:physiology*; D006801:Humans; D066298:In Vitro Techniques; D016682:Lupus Coagulation Inhibitor; D008180:Lupus Erythematosus, Systemic; D010314:Partial Thromboplastin Time; D010979:Platelet Function Tests
D001779:Blood Coagulation Factors; D016682:Lupus Coagulation Inhibitor