ABSTRACTS VOORDRACHTEN WETENSCHAPSDAG SFG 2012 for the need of admittance on the ICU postoperative after bariatric surgery. Bariatric surgery is not a criterion to be admitted to an ICU poster operatively. Provided there is attention for pulmonary problems on the wards, it is safe for these patients to bypass the ICU, as major complications do not happen directly postoperatively. Basic pulmonary support on the wards could be done by providing supplemental oxygen, regular control of breathing frequency and pulse oximetry as suggested by other authors. Patients with a haemorrhagic diathesis were more frequently admitted to the ICU on the basis of reintervention in a later stage with major actions on the ICU. Sunitinib Associated Thrombocytopenia: Not always what it seems. Arjan Albersen1 , Joyce Schilders2 Paul Hamberg2 1 , Leendert Porcelijn3 , Hanneke Zuetenhorst2 the Netherlands 3 , Tjin Njo1 , Department of clinical chemistry and hematology, Sint Franciscus Gasthuis, Rotterdam 2 The Netherlands department of internal medicine, Sint Franciscus Gasthuis, Rotterdam, Sanquin diagnostic services, amsterdam, the Netherlands. INTRODUCTION: Sunitinib is an oral treatment for metastatic renal cell carcinoma (RCC) which is known to cause thrombocytopenia as an adverse affect. Thrombocytopenia may lead to dose reduction or therapy termination. Pseudothrombocytopenia (PTCP) is an in vitro anticoagulant-induced agglutination of platelets by antiplatelet autoantibodies resulting in a falsely low reported platelet count. This occurs commonly, but not exclusively, in EDTA-anticoagulated blood. The target antigen is the platelet membrane glycoprotein (GP) IIb/IIIa complex. Antiplatelet autoantibodies react with hidden antigens on platelet GPIIb/IIIa which are exposed due to the Ca2+ chelating effect of EDTA. Furthermore, pre-supplementation of vacutainers with aminoglycosides (amikacin) can prevent EDTA-dependent PTCP. CASE REPORT: A 63 year old male patient with metastatic clear-cell RCC, undergoing sunitinib treatment, was admitted at the emergency department with nausea and fatigue. No bleeding symptoms were observed. Platelet counts in EDTA- and citrate-anticoagulated blood samples were 19x10e9/l and 8x10e9/l, respectively. Due to the apparent severe thrombocytopenia the patient was transfused with three units of platelets. One hour post-transfusion platelet counts were 43x109/l and 21x109/l in EDTA and citrate, respectively. A heparin blood sample revealed a platelet count of 88x109/l confirming PTCP. RESULTS: Laboratory investigation revealed that vitro platelet clumping was most abundant in citrate- (11x10e9/l) followed by EDTA- (15x10e9/l) and heparin (114x10e9/l) anticoagulated blood samples. This effect was partially reversible after placing blood samples at 37 °C. No clumping was observed in blood smears obtained directly from capillary blood samples, substantiating an in vitro phenomenon. Pre-supplementation with amikacin in citrate-, EDTA- and heparin vacutainers did not reduce in vitro platelet agglutination. Blood collection at 37 °C diminished, but did not eliminate, in vitro agglutination in all three anticoagulants. The indirect platelet immunofluorescence test (iPIFT) revealed strong platelet reactive IgM antibodies (IgG negative) whereas the monoclonal antibody specific immobilisation of platelet antigens (MAIPA, IgM and IgG conjugate) was negative for the GPIIb/IIIa, -Ib/IX and -V. An iPIFT with Glanzmann (GPIIb/IIIa negative) donor platelets also showed positive IgM antibody reactions, confirming the negative GPIIb/IIIa MAIPA. Sixteen days after discontinuing sunitinib, no PTCP and no platelet reactive antibodies could be detected. 105 WETENSCHAPPELIJK jaarverslag 2012 Pagina 104
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