Complement activation contributes to platelet destruction in immune thrombocytopenia (ITP). However, there has been very little data describing serum complement levels in ITP patients, and no data describing a possible relation to disease characteristics. A study at the 2019 American Society of Hematology annual meeting in Orlando .
In this exclusive Ƶ video, , of the Cleveland Clinic, an ITP expert not involved with the study, discusses the research.
Following is a transcript of his remarks:
Complement is, when an antibody binds to a cell, it often, so-called "fixes complement," so the complement will then bind to the antibody and to the cell and do cellular damage and accelerate cellular clearance. Complement is very important in many diseases, classically things like PNH and atypical hemolytic uremic syndrome. It's not been studied that much in ITP, although it's been known for 30 or 40 years that some of the ITP antibodies fix complement onto platelets.
This actually looked carefully at levels of complement in a large cohort of ITP patients. I think there were 104 patients or so, and they looked at complement 4, which is one of the complement proteins, C4. They looked at C3 and they looked at something called CH50, which is a test for total hemolytic complement present in the blood. As complement gets consumed in an inflammatory disease, the C3 levels may drop. The C4 levels may drop, and the CH50 becomes abnormal. Basically that's what they looked at in this cohort of patients.
The bottom line is that I believe more than half of the patients had at least one abnormality in one of the complement tests, C3, C4, or CH50. The C4, I think, was the lowest, went the low most often. I remember C3 actually tended to be actually not low in patients particularly who had undergone splenectomy for their ITP. Without going into too much detail on specific complement measurements, which I don't think is that important, I think what is important is this abstract provided evidence for complement activation and consumption in a fair number of patients with ITP suggesting that complement may contribute to the pathogenesis of ITP and the low platelet counts that these patients experience.