Demonstration of a platelet bypass mechanism in the clotting system using an acquired anticoagulant.
A lupus-type anticoagulant which causes strong inhibition of the partial thromboplastin time with kaolin (PTTK), the stypven time, and the thrombin generation tests has been investigated. All tests for platelet function were normal, as were all specific coagulation factor assays with the exception of a slightly reduced factor XI in this patient. A diethylaminoethyl-cellulose-immunoglobulin (DEAE-cellulose-IgG) fractionation of the patient's plasma produced two peaks containing inhibitory activity in the PTTK test. The first of these peaks had a cloudy appearance, suggesting the presence of immunoglobulin aggregates. Studies with IgG aggregates prepared from normal IgG and from the patient's IgG demonstrated that such aggregates were not the cause of inhibition. It was possible to neutralize the inhibitory activity of the purified IgG but not platelet-poor plasma (PPP) with a rabbit anti-IgG. The inhibition of the patient's PPP in the thrombin generation, the contact product, and the stypven time tests were corrected by the inclusion in the test system of platelets activated either by aggregation due to adenosine diphosphate (ADP) or formalin fixation and washing. These studies lend support to earlier findings that platelets interact at several sites in the coagulation cascade.
D000906:Antibodies / Q000302:isolation & purification; D001780:Blood Coagulation Tests; D001792:Blood Platelets / Q000276:immunology; D005260:Female; D006801:Humans; D007074:Immunoglobulin G; D008180:Lupus Erythematosus, Systemic / Q000097:blood*; D009500:Neutralization Tests; D010743:Phospholipids / Q000037:antagonists & inhibitors; D010974:Platelet Aggregation
D000906:Antibodies; D007074:Immunoglobulin G; D010743:Phospholipids