Immune thrombocytopenic purpura: autoimmune or immune complex disease?

To assess the pathogenic role of circulating immune complexes (CIC) in idiopathic thrombocytopenic purpura (ITP), 39 patients with ITP were compared to 17 patients with other forms of thrombocytopenia (hypersplenism (N = 12), impaired thrombopoiesis (3), thrombocytopenia of unknown origin (2)) and six nonthrombocytopenic subjects. In all patients, platelet mean life span (MLS), platelet associated IgG (PAIgG), as well as circulating anti-platelet antibodies and C1q binding activities were determined. In most cases, immune complex solubilization capacity (ICSC) and immune complex precipitation inhibition capacity (ICPIC) of sera were also assessed. All patients with ITP had a reduced platelet MLS, but PAIgG was elevated in only 16 out of 24 patients with chronic ITP, in six out of 10 patients with acute ITP and in four out of five patients with secondary ITP. In the group of patients with thrombocytopenia due to splenomegaly, seven out of 12 patients had elevated PAIgG while the platelet MLS was only slightly reduced. Of the 39 patients with ITP only one with secondary ITP had C1q binding material in his serum, as opposed to six out of 12 thrombocytopenic patients with splenomegaly. Whereas only three patients with ITP had abnormal immune-complex modulating capacities, such deviations were found in seven out of 12 patients with thrombocytopenia due to splenomegaly. We conclude that our data render the role of CIC in the pathogenesis of ITP very questionable.