317 Letters to the Editor trast, the rate of FXa inhibition by AT in the presence of heparin was reduced by GC in a concentration-dependent manner, 10 M GC com- pletely preventing the accelerating effect of heparin on FXa inhibition by AT. This result clearly indicates that GC binds to heparin with a high affinity thus preventing heparin binding to AT. The same mechanism, i.e the trapping of heparin by GC, can also be responsible for the inhibitory effect of GC on the heparin-dependent acceleration of thrombin inhibition by AT reported by de Cristofaro (8) and also observed by us (not shown). In conclusion, firstly, heparin cannot be used to localize the GPIb- binding site on thrombin since it also binds to GPIb, and secondly, the possible involvement of exosite 2 in thrombin interactions with GPIb remains to be further studied. Concerning the heparin-binding domain on GPIb, the observation that heparin did not inhibit the interaction between the sequence 269-287 of GPIb and thrombin exosite 1 (7) suggests that this sequence does not efficiently bind heparin and additionnal studies are now required to identify this heparin binding domain. M. Jandrot-Perrus 1 , K. J. Clemetson 1 , M.-C. Guillin, M.-C. Bouton From the Laboratoire de Recherche sur l’Hémostase et la Thrombose, Faculté Xavier Bichat, Paris, France; and 1 the Theodor Kocher Institut, University of Berne, Switzerland 1. Jamieson GA, Okumura T. Reduced thrombin binding and aggregation in Bernard-Soulier platelets. J Clin Invest 1978; 61: 861-4. 2. De Marco L, Mazzucato M, Masotti A, Fenton JW, Ruggeri ZM. Function of glycoprotein Ib alpha in platelet activation induced by alpha-thrombin. J Biol Chem 1991; 266: 23776-83. 3. Jandrot-Perrus M, Rendu F, Caen JP, Lévy-Toledano S, Guillin M-C. The common pathway for alpha- and gamma-thrombin-induced platelet activation is independent of GPIb: a study of Bernard-Soulier platelets. Br J Haematol 1990; 75: 385-92. 4. Jandrot-Perrus M, HuisseM-G, Krestnansky A, Bézeaud A, Guillin M-C. Effect of the hirudin carboxy-terminal peptide 54-65 on the interaction of thrombin with platelets. Thromb Haemost 1992; 18: 261-6. 5. Jandrot-Perrus M, Clemetson KJ, Huisse M-G, Guillin M-C. Thrombin interaction with platelet glycoprotein Ib: Effect of glycocalicin on thrombin specificity. Blood 1992; 80: 2781-6. 6. Bouton M-C, Jandrot-Perrus M, Bézeaud A, Guillin M-C. Late-fibrin(ogen) fragment E modulates human (-thrombin specificity. Eur J Biochem 1993; 215: 143-9. 7. Bouton M-C, Thurieau C, Guillin M-C, Jandrot-Perrus M. Characteristics of the interaction between thrombin exosite 1 and the sequence 269-287 of platelet glycoprotein Ib. Thromb Haemost 1998; 80: 310-5. 8. De Cristofaro R, de Candia E, Croce G, Morosetti R, Landolfi R. Binding of human alpha-thrombin to platelet GPIb: energetics and functional effects. Biochem J 1998; 332: 643-50. 9. Moroi M, Goetze A, Dubay E, Wu C, Hasitz M, Jamieson GA. Isolation of platelet glycocalicin by affinity chromatography on thrombin-sepharose. Thromb Res 1982; 28: 103-14. Received July 15, 1998 Accepted after revision November 4, 1998 Fig. 2 Glycocalicin competes with heparin for binding to antithrombin. Human FXa (25 nM) preincubated with buffer (open symbols) or GC (closed symbols) was incubated with human antithrombin, 75 nM in the absence of heparin (left panel) or 50 nM in the presence of heparin 3 mU/ml (right panel). At timed intervals, FXa activity was measured by the hydrolysis of its chromo- genic substrate, S-2765 (0.1 mM). Results are expressed as the ratio of FXa activity at a given time to FXa activity at time 0  100 Thromb Haemost 1999; 81: 317–8 Dear Sir, Autoimmune antiphospholipid antibodies with specificity towards  2 glycoprotein I ( 2 GPI) or prothrombin (II) are associated with thrombosis (1), but in rare occasions a hemorrhagic diathesis due to the occurrence of non-neutralising anti-II antibodies causing severe hypo- prothrombinemia (HPT) can be observed (2). Several authors have reported cases in children under age 17 years after viral infections with or without an associated underlying autoimmune disease (3, 4). Some of these cases with minor hemorrhagic diathesis resolved without therapy, but in other patients severe HPT caused hemorrhagic manifes- tations that required transfusion and/or corticosteroid treatment (2, 5). There are very few cases described in the literature presenting an acute hemorrhagic manifestation in adult patients (6, 7). The presence of anti- bodies that bind II without neutralising its coagulant activity leads to a rapid clearance of II antigen-antibody complexes from the circulation. Correspondence to: Prof. Luis O. Carreras, Hematología, Instituto Univer- sitario de Ciencias Biomédicas, Fundación Favaloro, Solís 453, (1078) Buenos Aires, Argentina – Tel.: 541 378 1145; FAX Number: 541 381 0323; E-mail: carreras@favaloro.edu.ar Downloaded by: University Library of Southern Denmark. Copyrighted material.