2003; baxter - Supplements - Haematologica

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92A. Huth-Kühne et al.patients with acquired haemophilia: modified Bonn-Malmö protocol. Haemophilia 2000;6:3027. Huth-Kühne A, Gebhardt A, Zimmermann R. New therapeuticoptions in acqiured hemophilia- the modifiedMalmö protocol. Haemophilia 2000;6:31228. Huth-Kühne A, Zimmermann R, Uhle C. Treatment withlong-term Ig-immunoadsorption and high-dose continuousfactor VIII in patients with acquired hemophilia andhemophiliacs with alloantibodies Thromb Haemost 1999;91 Suppl 1:277a[abstract].29. Kasper CK, Aledort LM, Counts RB. Proceedings. A moreuniform measurement of factor VIII inhibitors. ThrombDiath Haemorrh 1975;34:612.30. Monroe DM,Hoffman M, Oliver JA, Roberts HR. Plateletactivity of high-dose factor VIIa is independent of tissuefactor. Br J Haematol 1997;99:542-731. Chavin SI, Siegel DM; Rocco TA, Olson JP. Acute myocardialinfarction during treatment with an activated prothrombincomplex concentrate in a patient with factorVIII deficiency and a factor VIII inhibitor. Am J Med 1988;85:245-932. Lusher JM. Use of prothrombin complex concentrates inthe management of bleeding in hemophiliacs withinhibitors - benefits and limitations. Semin Hematol1994;31:49-52.33. Hough RE, Hampton KK, Preston FE, Channer KS,West J, Makris M. Recombinant VIIa concentrate inthe management of bleeding following prothrombincomplex concentrate-related myocardial in patientswith haemophilia and inhibitors. Br J Haematol 2000;111:974-9.34. Gallistl S, Cvirn G, Muntean W. Recombinant FactorVIIa Does not Induce Hypercoagulability In Vitro.ThrombHaemost 1999;81:245-9.35. Tagariello G, De Biasi E, Risato R, Radossi P, Davoli G,Traldi A. Recombinant FVIIa (NovoSeven) continuousinfusion and total hip replacement in patients withhaemophilia and high titre inhibitors to FVIII: experienceof two cases. Haemophilia 2000;6:581-3.36. Schulman S. Safety, efficacy and lessons from continuousinfusion with rFVIIa. Haemophilia 1998;4:564-737. Green D, Rademaker AW, Briet E. A prospective,randomizedtrial of prednisone and cyclophosphamide inthe treatment of patients with factor VIII autoantibodies.Thromb Haemost 1993; 70:753-7.38. Lottenberg R, Kentro TB, Kitchesn CS. Acquired haemophilia:a natural history study of 16 patients with factorVIII inhibitors receiving little or no therapy. Arch Int Med1987;147:1077-81.39. Morrison AE, Ludlam CA, Kessler C. Use of porcine factorVIII in the treatment of patients with acquired hemophilia.Blood 1993;81:1513-20.40. Lee EJ, Kueck B. Rituxan in the treatment of cold agglutinindisease. Blood 1998;92:3490-1.41. Karwal MW, Schlueter AJ, Zenk DW, Davis RT.Treatmentof Acquired Factor VIII Deficiency with Rituximab. Blood2001; 98 Suppl:2232a[abstract].42. Knöbl P, Derfler K, Korninger L, Kapiotis S, Jäger U,Maier-Dobersberger T, et al. Elimination of acquired factorVIII antibodies by extracorporal antibody-based IA (Ig-Therasorb®). Thromb Haemost 1995;74:1035-8.43. Du Moulin A. LDL Immunoapheresis Technique. In:Hypercholesterolemia in the Prevention of CoronaryHeart Disease. Gotto AM, Mancini M, Richter WO,Schwandt P, eds. Proceedings of the 2 nd InternationalSymposium in Munich, 1989. Basel, Switzerland: Karger,1990;170a[abstract].44. Derfler K, Swoboda K, Hirschl MM, Gottsauner-Wolf M,Steger G, Sunder-Plassmann G, et al. Comparison ofplasma separation and immunospecific LDL eliminationin severe hypercholesterolemia. Int J Artif Organs 1992;15:383-4.45. Richter WO, Jacob BG, Ritter MM, Sühler K, ViermeiselK, Schwandt P. Three year treatment of familial heterozygoushypercholesterolemia by extracorporal lowdensity lipoprotein IA with polyclonal apolipoprotein Bantibodies. Metabolism 1993;42:888-94.46. Derfler K, Druml W, Mayr W, Mühlbacher F, Jansen M,Sauter T, et al. Combination of IgG columns and IgG i.v.in the Downmodulation of Cytotoxic Anti-HLA Antibodiesand Autoantibodies. In: Congress of ImmunoglobulinsIntravenous – IgG i.v.: current status of clinicalapplication and research yopics. Lisbon, Portugal: BiotechGroup – Hyland Division; 1993. 15a[abstract].47. Dwyer JM. Manipulating the immune system withimmune globulin. N Engl J Med 1992;326:107-16.48. Gilles JG, Saint-Remy-JM. Healthy subjects produce bothanti-factor VIII and specific anti-idiotypic antibodies. JClin Invest 1994;94:1496-505.49. Gautier P, Sultan Y, Parquet-Gernez A, Meriane F,Guerois C, Derlon A. Detection and IgG subclass analysisof antibodies to FVIII in multitransfused hemophiliacsand healthy individuals. Haemophilia 1996; 2: 88-94.50. Dietrich G, Algiman M, Sultan Y. Origin of antiidiotypicactivity against anti-FVIII antibodies in pools of normalhuman immunoglobulin G, IVIG. Blood 1992;79:2946-51.51. Rossi F, Sultan Y, Kazatchkine MD. Antiidiotypes againstauto-antibodies and allo-antibodies to VIII:c (antihaemophilicfactor) are present in therapeutic polyspecificnormal immunoglobulins. Clin Exp Immunol 1988; 74:311-6.52. Green D, Kwaan HC. An acquired factor VIII inhibitorresponsive to high-dose γ globulin. Thromb Haemost1987;58:1005-7.53. Zimmermann R, Kommerell B, Harenberg J, Eich W,Rother K, Schimpf Kl. Intravenous IgG for patients withspontaneous inhibitor to Factor VIII. Lancet 1985;273-4.54. Zhiya Y, Lennon VA. Mechanism of intravenousimmune globulin therapy in antibody-mediated autoimmunediseases. N Engl J Med 1999;340:227-8.55. Masson PL. Elimination of infectious antigens andincrease of IgG catabolism as possible modes of IVIG. JAutoimmun 1993;6:638-9.56. Gilles JG, Desqueper B, Lenk H, Vermylen J, Saint-RemyJM. Neutralizing antiidiotypic antibodies to FVIIIinhibitors after desensitization in patients with haemophiliaA. J Clin Invest 1996;97:1382-8.haematologica vol. 88(supplement n. 12):september 2003
[Acquired Inhibitors in Non-Hemophiliacs]review paperAcquired factor VIII and factorIX inhibitors: a survey of ItalianHemophilia CentersFRANCESCO BAUDO, GIANNI MOSTARDA,haematologica 2003; 88(suppl. n. 12):93-99http://www.haematologica.org/free/immunotolerance2001.pdfFRANCESCO DE CATALDO, WRITING COMMITTEEContributing hemophilia centers: Bari, Schiavon M; Bergamo,Finazzi G; Bologna, De Rosa V; Bolzano, Billio A; CastefrancoVeneto, Tagariello G; Catania, Musso R; Catanzaro, Santoro R;Firenze, Linari S; Milano Niguarda, Mostarda G; Milano Policlinico,Santagostino E; Palermo, Caracciolo C; Parma, TagliaferriAR; Pavia, Gamba G; Perugia, Berrettini M; Pescara, Dragani A;Reggio Emilia, Ghirarduzzi A; Roma, Mazzucconi G; Torino,Schinco P; Verona, Franchini M; Vicenza, Castaman G.Objective. To evaluate the clinical problems relatedto the acquired hemophilia syndrome.Study design. Data collected from the ItalianAcquired Hemophilia Register.Results. Ninety-six cases were registered, 95 withanti-factor VIII and 1 with anti-factor IX. Forty-fivecases (46.8%) were idiopathic, 51 (53.2%) associatedwith different clinical conditions. The overallfollow-up is 7 years (range 1-20). In 31 patients(32.2%) bleeding occurred during or after an intervention.A prolonged activated partial thromboplastintime (aPTT) was present in all the patients inwhom the test was carried out but the inhibitor wasidentified on the occasion of a bleed. Twenty-threepatients did not require treatment for bleeding; 66patients received different therapies and in 58patients bleeding was controlled. An anamnesticresponse occurred in 8 cases unrelated to pregnancy.Sixty-five of the ninety patients evaluable forresponse to the initial anti-hemorrhagic therapy arealso evaluable for the effect of the immunosuppressivetherapy used to suppress the inhibitor. The finalresults of induction therapy are 52 (80% ) completeremissions, 6 (9.3%) partial remissions and 7(10.7%) treatment failures. The majority of thepatients who achieved complete remission receivedsteroids. A 2nd remission was obtained in 10/11patients who relapsed with combined therapy. Theoverall mortality was 16.6%.Correspondence: Francesco Baudo, MD, Thrombosis and HemostasisUnit, Niguarda Hospital, p.za Ospedale Maggiore 3,20162 Milan, Italy. Phone: international +39.02.64442970,Fax: international +39.02.66103898. E-mail:md9821@mclink.itConclusions. Correct evaluation of coagulationscreening tests, in particular the prothrombin time,is mandatory. At present combined immunosuppressivetherapy seems to be a reasonable choice forthe treatment of cases unrelated to pregnancy.©2003, Ferrata Storti FoundationKey words: acquired FVIII and FIX inhibitors; survey ofItalian Hemophilia Centers.Acquired hemophilia is a clinical syndromecharacterized by the sudden onset of bleeding,which may be either spontaneous oroccur after surgery or trauma and is usuallysevere (87% of the cases), in patients with a negativefamily or personal history of hemophilia.The depletion of factor VIII (FVIII), and muchless frequently of factor IX (FIX), is immunemediatedby specific autoantibodies. The incidencereported in the literature varies between 1to 4 cases per million/population per year. 1,2 Theincidence increases with age (median age 60-67years) with an equal sex distribution except inthe younger group because of the relation topregnancy. Acquired hemophilia is commonlyassociated with autoimmune (systemic lupuserythematosus, rheumatoid arthritis, asthma)and neoplastic diseases, hypersensitivity to drugsand pregnancy but in 50% of the cases the conditionis idiopathic. 3-5 Common sites of bleedingare the skin (large ecchymoses), the mucosae(epistaxis, gengivorrhagia, metrorrhagia), themuscles and the retro-peritoneum (hematomata);hemarthroses are very rare. The bleeding canarise spontaneously or after a procedure (positioningof an intravenous catheter, surgery,intramuscular injections). If the bleeding occursin critical sites compression problems mayensue. The severity of the bleeding is not proportionallyrelated to the inhibitor titer. 6 Thereported mortality related to bleeding is 8-22%. 2-5The majority of deaths occur within the firstfew weeks after presentation.haematologica vol. 88(supplement n. 12):september 2003
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