Extension of PT and APTT could be due to several factors. In this case we found a PT and APTT results are >120 seconds and >190 seconds of a 44 years old woman. After communication in ward was done we found that this patient has undergone plasmapheresis . There was also hipofibrinogenemia and increase of D Dimer. At a glance we may think of a DIC but but then we found that this patient has undergone plasmapheresis due to the primary disease i.e, Myasthenia Gravis. There was no bleeding nor thrombosis and no primary disease that could cause a DIC. The extension of PT and APTT in plasmapheresis in this patient due to heparin anticoagulant that was used during the plasmapheresis process, dilution effect of coagulation factors, coagulation activation and coagulation factors consumption. Hipofibrinogenemia occurred that also caused by dilution process and coagulation activity and consumption af coagulation factors during plasmapheresis. D Dimer also increased as a marker of coagulation activity and fibrinolysis as during plasmapheresis blood circulation exposed to outer surface so coagulation process activated. In this case we found anemia, leukocytosis-neutrofilia and trombositopenia. The patient already had anemia before plasmapheresis, which means anemia in this patient is anemia of chronic disease, that characteristic by mild and non progressive. (Hb rare below 9 mg/dl). The mechanism of anemia in chronic inflammation is due to decrease of iron release from its pool in RES, decrease of eritropoietin production and eritripoiesis pressure by cytokine due to macrophage and lymphocyte activated by the underlying disease. Neutrofilia could be occured as complication of infection during plasmapheresis. Trombositopenia caused by dilution effect and some platelet attached to apheresis circuit that could enhance coaguation activity.
Keywords : PT, APTT, Plasmapheresis, Heparin, Myasthenia Gravis.