Immune Complexes in Thrombocytopenic Patients: Cause or Effect?
Article first published online: 12 MAR 2008
British Journal of Haematology
Volume 44, Issue 4, pages 645–654, April 1980
How to Cite
Trent, R. J., Clancy, R. L., Danis, V. and Basten, A. (1980), Immune Complexes in Thrombocytopenic Patients: Cause or Effect?. British Journal of Haematology, 44: 645–654. doi: 10.1111/j.1365-2141.1980.tb08719.x
- Issue published online: 12 MAR 2008
- Article first published online: 12 MAR 2008
- Received 9 April 1979; accepted for publication 29 August 1979
Summary. Immune complexes (ICs) in the serum of 43 patients with chronic idiopathic thrombocytopenic purpura (ITP) were measured by the C1q deviation assay during the active and inactive phases of the disease. An inverse relationship between platelet count and levels of ICs was demonstrated in all but one patient. To test whether this phenomenon was specific for chronic ITP, ICs were assayed in sera from two groups of control patients with thrombocytopenia. Group 1 had thrombocytopenia due to recognized immune mechanisms while group 2 had thrombocytopenia secondary to non-immune mechanisms. In both these groups the degree of thrombocytopenia proved to be inversely proportional to IC levels, which was similar to the pattern observed in chronic ITP. The specificity of the assay for detection of ICs was confirmed by demonstrating a positivity rate of 65% in sera of patients with systemic lupus erythematosus, a known IC disease. On analysis the ICs were shown to have molecular weights in excess of 500000 daltons and contain variable immunoglobulin classes. The findings implicate ICs in immune destruction of platelets both in chronic ITP (as has been suggested previously) and also in thrombocytopenia secondary to known immune mechanisms. In addition the association of ICs with non-immune thrombocytopenias is consistent with the hypothesis that platelets play an important role in clearance of ICs from the circulation, thereby protecting the vascular endothelium from damage.