Zusammenfassung
Hintergrund
Ziel der vorliegenden Studie war, Ex-vivo-Funktionsparameter bei der Transfusion pathogeninaktivierter Thrombozytenkonzentrate (TK) im Vergleich zu konventionellen TK im perioperativen Setting zu untersuchen.
Material und Methoden
Insgesamt 30 Patienten, bei denen postoperativ die Notwendigkeit zur Transfusion von 2 TK bestand, wurden in die Studie eingeschlossen. 15 Patienten erhielten konventionelle TK (konv. TK) und 15 Patienten erhielten pathogeninaktivierte TK (PI-TK). Alter, Volumen und Thrombozytengehalt der TK wurden erfasst. Vor (T0) und 30 min nach der Transfusion der TK (T1) wurden Blutproben für Thrombozytenfunktionsdiagnostik (MEA) entnommen. Der Anstieg der Thrombozytenkonzentration (Inkrement) und das korrigierte Inkrement (CCI) wurden zum Zeitpunkt T1 errechnet.
Ergebnisse
Weder an T0 noch an T1 wurden signifikante Gruppenunterschiede in den Ergebnissen der MEA oder in der konventionellen Gerinnungslaboranalyse beobachtet. Der Thrombozytengehalt pro TK war in den PI-TK signifikant höher [3,3 (3,1/3,5)×1011 Thrombozyten pro PI-TK vs. 3 (2,9/3)×1011 Thrombozyten pro konv. TK, p<0,001]. Das Inkrement (42±27×109/l vs. 69,4±29×109/l, p=0,013) war in der PI-TK Gruppe signifikant geringer als in der konventionellen TK-Gruppe.
Schlussfolgerung
Während die Ex-vivo-Funktionsparameter der Thrombozytenfunktion keine Gruppenunterschiede an T1 zeigten, fand sich nach PI-TK ein geringeres Inkrement im Vergleich zu konventionellen TK.
Abstract
Background
The aim of the present study was to assess ex-vivo function of pathogen-inactivated versus conventional platelet concentrates (PC) in the perioperative setting.
Material and methods
A total of 30 patients who underwent cardiac surgery and who postoperatively depended on the transfusion of two platelet concentrates were enrolled into this study. Of the patients 15 received conventional buffy coat PC (conv. PC) and 15 received pathogen-inactivated PC (PI-PC). Age, volume and platelet content of each PC were recorded. Before (T0) and 30 min after PC transfusion (T1), blood samples were taken and platelet function analyses (MEA) and conventional laboratory coagulation analyses were performed. The transfusion-associated increment of platelet concentration (increment) and the corrected count increment (CCI) were assessed at timepoint T1.
Results
There were no significant group differences between the groups in MEA analyses or conventional laboratory at T0 or T1. The platelet content per PC was significantly higher in the PI-PC group [3.3 (3.1/3.5)× 1011 platelets per PI-PC versus 3 (2.9/3)× 1011 platelets per conv. PC, p<0.001]. Platelet increment (42±27×109/l versus 69.4±29×109/l, p=0.013) was significantly lower in the PI-PC group.
Conclusion
Whereas ex-vivo analyses of platelet function did not show any group differences at T1, a significantly lower increment was seen in the pilot study after transfusion of PI-PC as compared to conventional PC.
Literatur
Apelseth TO, Bruserud O, Wentzel-Larsen T et al (2010) Therapeutic efficacy of platelet transfusion in Patients with acute leukemia: an evaluation of methods. Transfusion 50:766–775
Blajchman MA, Beckers EA, Dickmeiss E et al (2005) Bacterial detection of platelets: current problems and possible resolutions. Transfus Med Rev 19:259–272
Bundesärztekammer (2008) Querschnitts-Leitlinien zur Therapie mit Blutkomponenten und Plasmaderivaten. 4. Aufl. Deutscher Ärzteverlag, Köln
Bundesärztekammer (2010) Thrombozytenkonzentrate. In: Richtlinien zur Gewinnung von Blut und Blutbestandteilen und zur Anwendung von Blutprodukten (Hämotherapie). Deutscher Ärzteverlag, Köln, S 41ff
Burger R, Offergeld R (2008) Festlegung der Haltbarkeitsfrist von Thrombozytenkonzentraten mit dem Ziel der Reduktion lebensbedrohlicher septischer Transfusionsreaktionen durch bakterielle Kontamination. Bundesgesundheitsbl Gesundheitsforsch Gesundheitsschutz 12:1484
Cardinal DC, Flower RJ (1980) The electronic aggregometer: a novel device for assessing platelet behavior in blood. J Pharmacol Methods 3:135–158
Cauwenberghs S, Van Pampus E, Curvers J et al (2007) Hemostatic and signaling functions of transfused platelets. Transfus Med Rev 21:287–294
Daly PA, Schiffer CA, Aisner J et al (1980) Platelet transfusion therapy. One-hour posttransfusion increments are valuable in predicting the need for HLA-matched preparations. JAMA 243:435–438
Hanke AA, Roberg K, Monaca E et al (2010) Impact of platelet count on results obtained from Multiple Electrode Platelet Aggregometry (Multiplate™). Eur J Med Res 15:214–219
Hanke AA, Dellweg C, Kienbaum P et al (2010) Effects of desmopressin on platelet function under conditions of hypothermia and acidosis: an in vitro study using multiple electrode aggregometry. Anaesthesia 65:688–691
Innerhofer P, Kienast J (2010) Principles of perioperative coagulopathy. Best Pract Res Clin Anaesthesiol 24:1–14
Jacobs MR, Palavecino E, Yomtovian R (2001) Don’t bug me: the problem of bacterial contamination of blood components – challenges and solutions. Transfusion 41:1331–1334
Jámbor C, Weber C, Beesel K van et al (2008) In vitro platelet function of platelet concentrates transfused to high risk cardiac surgery Patients as determined bedside by the multiplate impedance aggregometry. Eur J Anaesthesiol 25:6AP2-1 (Abstr)
Jansen GA, Van Vliet HH, Vermeij H et al (2004) Functional characteristics of photochemically treated platelets. Transfusion 44:313–319
Kluter H, Dorges L, Maass E et al (1996) In-vivo evaluation of random donor platelet concentrates from pooled buffy coats. Ann Hematol 73:85–89
McCullough J, Vesole DH, Benjamin RJ et al (2004) Therapeutic efficacy and safety of platelets treated with a photochemical process for pathogen inactivation: the SPRINT Trial. Blood 104:1534–1541
Ness P, Braine H, King K et al (2001) Single-donor platelets reduce the risk of septic platelet transfusion reactions. Transfusion 41:857–861
Palavecino EL, Yomtovian RA, Jacobs MR (2006) Detecting bacterial contamination in platelet products. Clin Lab 52:443–456
Picker SM, Schneider V, Oustianskaia L et al (2009) Cell viability during platelet storage in correlation to cellular metabolism after different pathogen reduction technologies. Transfusion 49:2311–2318
Pineda A, McCullough J, Benjamin RJ et al (2006) Pathogen inactivation of platelets with a photochemical treatment with amotosalen HCl and ultraviolet light: process used in the SPRINT trial. Transfusion 46:562–571
Rood IG, Pettersson A, Savelkoul PH et al (2010) Development of a reverse transcription-polymerase chain reaction assay for eubacterial RNA detection in platelet concentrates. Transfusion 50:1352–1358
Schrezenmeier H, Walther-Wenke G, Muller TH et al (2007) Bacterial contamination of platelet concentrates: results of a prospective multicenter study comparing pooled whole blood-derived platelets and apheresis platelets. Transfusion 47:644–652
Sohngen D, Schneider W (1991) Thrombocyte transfusion: clinical aspects, follow-up and complications. Klin Wochenschr 69:379–386
Toth O, Calatzis A, Penz S et al (2006) Multiple electrode aggregometry: a new device to measure platelet aggregation in whole blood. Thromb Haemost 96:781–788
Tynngard N (2009) Preparation, storage and quality control of platelet concentrates. Transfus Apher Sci 41:97–104
Van Rhenen D, Gulliksson H, Cazenave JP et al (2003) Transfusion of pooled buffy coat platelet components prepared with photochemical pathogen inactivation treatment: the euroSPRITE trial. Blood 101:2426–2433
Weber CF, Dietrich W, Spannagl M et al (2010) A point-of-care assessment of the effects of desmopressin on impaired platelet function using multiple electrode whole-blood aggregometry in Patients after cardiac surgery. Anesth Analg 110:702–707
Weber CF, Schneider AC, Kirschning T et al (2009) Therapeutic options for perioperatively acquired platelet dysfunctions. Anaesthesist 58:931–940
Wollowitz S (2001) Fundamentals of the psoralen-based Helinx technology for inactivation of infectious pathogens and leukocytes in platelets and plasma. Semin Hematol 38:4–11
Yomtovian R (2004) Bacterial contamination of blood: lessons from the past and road map for the future. Transfusion 44:450–460
Interessenskonflikt
Der korrespondierende Autor gibt an, dass für ihn kein Interessenkonflikt besteht. Die Untersuchung wurde aus dem Forschungsetat der Klinik für Anästhesiologie, Intensivmedizin und Schmerztherapie finanziert. R. Henschler und M. M. Müller erhielten Forschungsunterstützung für eine andere Studie durch die Firma CERUS
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Weber, C., Meininger, D., Byhahn, C. et al. Konventionelle vs. pathogeninaktivierte Thrombozytenkonzentrate bei perioperativer Koagulopathie. Chirurg 82, 348–358 (2011). https://doi.org/10.1007/s00104-010-2023-2
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DOI: https://doi.org/10.1007/s00104-010-2023-2
Schlüsselwörter
- Perioperative Koagulopathie
- Thrombozytenkonzentrate
- Pathogeninaktivierung
- Thrombozytenzahl
- Multiple Elektrodenaggregometrie