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Autoantibodies against the platelet glycoproteins (GP) IIb/IIIa, Ia/IIa,
and IV and partial deficiency in GPIV in a patient with a bleeding disorder
and a defective platelet collagen interaction
JH Beer, M Rabaglio, P Berchtold, A von Felten, KJ Clemetson, DA Tsakiris, B Kehrel and S Brandenberger
Department of Medicine, University Hospital, Bern, Switzerland.
To evaluate the physiologic importance of the different collagen receptors
on platelets, we screened 806 patients admitted to the hospital because of
hemorrhagic diathesis for eventual laboratory evidence of a pathologic
platelet collagen interaction, and found 5 patients with an isolated
deficiency in collagen-induced platelet aggregation. Four of these five
patients had a partial defect, one had a complete defect. The structural
and functional analysis of the platelets from the patient with a complete
defect showed a deficiency in glycoprotein (GP) IV and autoantibodies
against GPIIb/IIIa, GPIa/IIa, and GPIV. Patient plasma had only a minimal
effect on normal control platelets and Naka-negative platelets. The
analyses of the defect in the patient and of the data in the literature
suggest that a single defect may not result in clinical bleeding
(GPIV-deficient patients do not bleed), but may become symptomatic in
combination with another defect such as the autoantibodies against
GPIa/IIa, GPIV, and/or GPIIb/IIIa, all of which are involved in platelet
collagen interactions (three of four of our immune thrombocytopenic purpura
patients with anti-GPIV and anti-GPIIb/IIIa autoantibodies had a bleeding
disorder). We hypothesize that it is the synergism of two abnormalities
that results in the defective function, a mechanism that is in agreement
with earlier studies on platelet collagen interaction that suggests that a
double defect in platelet collagen interactions is required to become
clinically apparent.
Volume 82,
Issue 3,
pp. 820-829,
08/01/1993
Copyright © 1993 by The American Society of Hematology
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