Study of Autoantibodies Against Platelet GP IIb/IIIa and GP Ib/IX in Childhood Chronic Idiopathic Thrombocytopenic Purpura.
- Author:
Chanwook WOO
1
;
Junghwa LEE
;
Kwangchul LEE
;
Soonkyum KIM
Author Information
1. Department of Pediatrics, College of Medicine, Korea University, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Chronic Idiopathic Thrombocytopenic Purpura;
Autoantibody;
Glycoprotein IIb/IIIa complex;
Glycoprotein Ib/IX complex
- MeSH:
Antibodies;
Autoantibodies*;
Autoimmune Diseases;
Blood Platelets*;
Follow-Up Studies;
Glycoproteins;
Humans;
Immunoblotting;
Platelet Count;
Purpura, Thrombocytopenic, Idiopathic*
- From:Journal of the Korean Pediatric Society
2000;43(3):395-401
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Chronic idiopathic thrombocytopenic purpura (CITP) is an autoimmune disease caused by autoantibodies reacting to certain antigens, and platelet glycoprotein (GP) IIb/IIIa and GP Ib/IX complexes are thought to be some of those antigens. However, the clinical significance of anti-GP autoantibodies in CITP patients is unknown. In this study, we investigated the clinical correlation between the presence of circulating autoantibodies against GP IIb/IIIa and GP Ib/IX, and disease activity. MEHTODS: From December 1997 to June 1998, 20 CITP patients were enrolled in this study. Autoantibodies against GP IIb/IIIa and GP Ib/IX in patient's sera during treatment were detected by immunoblotting, and their platelet counts at the initial evaluation and 6 month follow-up were compared according to the presence or the absence of antibodies. RESULTS: Autoantibodies to GP antigens were found in 40% (8/20) of the patients. Seven patients were positive for GP IIb/IIIa; 4 for GP Ib/IX and 3 for both. GP autoantibody-positive patients had lower mean platelet counts than GP autoantibody-negative patients at initial evaluation (133,000/microliter vs 172,000/microliter, P>0.05) and at 6 month follow-up (154,000/microliter vs 192,000/microliter, P>0.05). Detection of GP autoantibodies related more with active disease than with remission at initial evaluation (45.5%(5/11) vs 33.3%(3/9), P>0.05) and at 6 month follow-up (50.0%(5/10) vs 30.0% (3/10), P>0.05). There was no detection of GP-specific antibodies in 3 splenectomized patients. CONCLUSION: It is hard to conclude on our data alone that the presence of GP autoantibodies correlates with disease status in CITP, although it seems to associate with lower platelet counts.
