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Abstracts of Poster Presentations Abstracts of Poster Presentations To view the full program, please visit the Congress website www.kenes.com/aps Downloaded from lup.sagepub.com at University Library Utrecht on March 17, 2015 loth ktertSic (Qn nsanAtiopuipdAMibocEes PFates 584 ANTIPHOSPHOLIPID ANTIBODIES IN PATIENTS WITH DEVELOPMENT OF ANTIPHOSDPHOLIPID-ANTIBODIES AND INTOLERANCE TO METALS IN THE ORAL CAVITY FACrOR V-INHIBITOR AFTER CIPROFLOXACIN IN TWO CASES H. Kucerova', J. Prochazkovat, I. Janatkova2, J. Bartova', T. Fucikova2 W.Miesbachl, J. Vogte, D. Peez3, B. Buehler', G. Asmelashl', 'Institute ofDental Research, 1st Medical Faculty, 2Institute ofClinical 1. Scharrerl Imnmunology andAllergology, General Faculty Hospital, Prague, 'J W.Goethe-University, Frankfurt, 25t. Vincenz Hospital, Mainz, Czech Republic 3Justus Liebig University, Frankfurt, Germany Dental alloys are not a physiological part of the organism. Metals can cause The development of factor V-inhibitor is very rare, especially in the production of autoantibodies in sensitive individuals as well as other combination with the antiphospholipid (aPL)-antibodies. The present paper undesired side effects. The aim of this presentation is to evaluate the describes two patients with factor V-inhibitor and aPL-antibodies after presence of antiphospholipid antibodies in sera of patients with oral trcatment with ciprofloxacin. Lupus anticoagulants (LA) were assayed discomfort and the occurrence of pathological galvanic currents in the oral according to the criteria of SSC of the ISTH, ACL by an ELISA, factor V- cavity. The patients were diagnosed by measurement of galvanic features inhibitor by the Bethesda method. with the device Odontologic accompanied by the modified method ofblastic Q.Oe.atirti 74 years old was treated with ciprofloxacin for a postoperative transfonnation for metals (Melisa) and by the anamnestic data. A group of septicemia with pneumonia. 4 days after start of treatment PT decreased and with galvanic currents and with diagnosed metal intolerance was a prolonged PTT was observed (PT: 13%, PTT > 120 sec). In addition. patients factor V-inhibitor (17,6 BU) and lupus anticoagulants could be detected. As compared to the group of patients with oral discomfort, with metal clinical correlation a massive muscle bleeding and anemia occurred intolerance and without galvanic currents. This study will present the (hemoglobin 6 g/dl). After terminating treatment with ciprofloxacin, factor importance of metal intolerance exaniinations in patients with V-inhibitor and lupus anticoagulants disappeared and the condition of the antiphospholipid antibodies. patient improved qickly. The study was supported by the Grant of the CzMH No.NK 6285-3. The other Datient, 85 years old was admitted to hospital due to a cerebral infarction. After improvenent of the neurological defects he was treated with ciprofloxacin foT 8 days for an urinary tract infection. Also 4 days after start of treatment, PT began to decrease to 12 % and aPTT was prolonged to 172 sec. In addition, factor V-inhibitor (1156 BU), lupus anticoagulants and anticardiolipin-antibodies could be detected. Factor V-activity could not be normalised even in dilutions up to 640 (Factor V-antigen was not reduced). The patient developed massive muscle and visceral bleedings and died from cardiovascular faihire. Thesc two cases demonstrate that treatment with ciprofloxacin can trigger the development of factor V inhibitor and antiphospholipid antibodies. In both cases ciprofloxacin was the only new taken medication. In one case there was a transient occurrence and normalisation after terminating treatment with ciprofloxavin. The other case ended with massive muscle and visceral bleedings and cardiovasculare failure. Probally the association of treatment with ciprofloxacin and development of factor V-inhibitor and antiphospholipid-antibodies is diagnosed to rarely. These two cases emphasize the necessity of a meticulous clatification of a prolonged PTT and drops of PT during and after treatinent with ciprofloxacin. AUTOIMMUNE ANTIPHOSPHOLIPID ANTIBODIES IMPAIR THE aPL AFFECTS PROTEIN C ACTIVATION IN VIVO INHIBITION OF ACTIVATED FACTOR X BY S.S. Pierangeli, X. Liu, R.G. Espinola, E.N, Harnis PROTEIN Z / PROTEIN Z DEPENDENT PROTEASE INHIBITOR Morehouse School ofMedicine, Atlanta, GA. USA L.C. Kordich2, G.J. R.R Forastiero', M.E. Martinuzzol, Broze3 Antiphospholipid (aPL) antibodies are associated with thrombosis, have 'Favaloro University, 2School ofExact and Natural Sciences, University of been shown to be thrombogenic in mice and to affect various phospholipid- Buenos Aires, Argentina, 3Washington University School ofMedicine, dependent hemostatic reactions in vitro. Studics have shown significant St. Louis, MO, USA inhibition of conversion of protein C into activated protein C (APC) by aPL in vitro, indicating that aPL may impair an important anticoagulant PZ is the cofactor for the inhibition of factor Xa (FXa) by ZPI in thc mechanism. However, no studies have examined whether aPL antibodies presence of phospholipids (PL) and calcium (Ca). Recent data suggests that affect the activation of protein C in vivo. If confinned in vivo, aPL- defects in PZ/ZPI may increase the thrombotic risk in subjects carrying mediated inhibition of prolein C activation might explain thrombogenic other prothrombotic traits. Low plasma PZ levels were found in association mechanisms of aPL. This study addressed that question and examined how with aPL. In this study we tested whether aPL could impair the FXa infusions of APC affect aPL-mediated enhanced thrombus formation in a inhibition by PZ/ZPI. Purified IgGs from 25 aPL patients (19 with and 6 mouse model of venous thrombosis. CDI mice in groups of eighteen were without APS) wcre evaluated in a FXa inhibition assay usinig purified either injected i.p. twice with 500 jig of hunman affinity purified aPL or IgG components. PZ (2.5ug/ml), ZPI (4ug/ml), Hepes/saline/BSA (lmg/ml) control (lgG-NHS). Seventy-two hours aftcr the first injection, the surgical buffer, and Ca (5mM) with or without IgGs (1.75mg/ml) and with or procedure to expose the femoral vein of treated and control mice and to without beta2-glycoprotein I (b2GPI) (100ug/mI) were constructed at RT. examine dynamics of thrombus formation was carried out in anesthetized Then PL (2OuM) and FXa (250ng/ml) were added. At 5 min, samples were animals. Mean thrombus area was determined as described (Circ 1999; diluted 25-fold and assayed for remaining FXa activity (rFXa). Without 99:1997) and a sample of blood was obtained to detennine anticardiolipin b2GPI and IgGs, rFXa was 2%. Adding b2GPI to the mixture, rPXa was (aCL) levels by ELISA. Subsequently, one group of nine mice treated with slightly higher (10%). IgGs from 2 normal subjects did not inhibit the effect aPL and one treated with IgG-NHS were infused intravenously with 0.1 ml FXa and did not enhance the effect of b2GPI (rEXa, 10% and APC (16ILg/ml) in stenle saline-dextrose solution, while the animals still of PZ/ZPI on under anesthesia. The remaining animals were infused with 0.1 ml sterile 11%). However, IgGs from most patients with aPL decreased the FXa saline solution. Thirty minutes later, a second thrombus was induced in each inhibition by PZ/ZPI when b2GPI is present (rFXa, 10-29% n=9, 30-50% animal and its arca (in micrometes square) determined and compared to n=l 1, and >50% n=5). Only one IgG-aPL showed a significant effect on values obtained before the i.v. infusions. Mean aCL titer of aPI-treated PZ/ZPI in the absence of b2GPI (rFXa 19%). These data suggest that some animals was 92 +/- 28 GPL units. Mean trhombus size in aPL-treated mice aPL impair the FXa inactivation by PZ/ZPI and thus may contribute to was significantly larger when compared to IgG-NHS-treated mice (4719+/- thrombosis in the APS. Ongoing studies may provide firther information. 1609 vs 1162 =/- 454 ). Infusions of APC decreased significantly the thrombus size of of aPL-treated mice (from 4719 +/- 1609 to 624 +/- 392, 88% decrease). As expected, a decrease in thrombus size in IgG-NHS- treated mice was also observed after the infusion of APC (from 1162 +/- 454 to 470 +/-252), but the decrease was significantly lower than in aPL-treated mice. Neither thrombus size nor aCL titers were affected by saline infusions in aPL or IgG-NHS-treated mice. The data clearly indicate for the first time, that aPL antibodies affect protein C activation in vivo and this may explain, at least in part their procoagulant and thrombogenic properties. i- A-ndd20 1011.9106120ML246K Downloaded from lup.sagepub.com at University Library Utrecht on March 17, 2015 10Ctliir anixQs anAhqtdpdhrloldes P*rPWFset*m 585 CHARACTERIZATION OF IMMUNOGLOBULIN-BOUND ANTICARDIOLIPIN ANTIBODIES IN SERUM SAMPLES OF 'NATIVE'BETA2GLYCOPROTEIN I FROM PLASMA (ISOLATED PATIENTS WITH CHRONIC HEPAT[TIS C INFECTION UNDER MILD CONDITIONS) Z. Mondher, Z. Yusr, L. Lilia, A. Ilhem, S. Maryarn, M. Sondes B.L. Myones', S. Majumdarl, L.I. Fedorova', J.D. Morrisett', A.Y. Volgin' Immunology Department, La Rabta, Tunis, Tunisia 'Department ofPediatrics, 2Department ofMedicine, Baylor College of Infectious agents have been implicated in the induction of antiphospholipid USA Medicine, Houston, TX, antibodies particularly chronic hepatitis C virus which was linked to extra 'Native' beta2GPI was previously isolated from plasma under mild liepatic autoimmune phenomena. Objectives: to study the prevalence of conditions by sequential purification on heparin-Sepharose (hepS), high- antiphospholipid
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