Barzilai University Medical Center

94 Research Day 2020 Barzilai University Medical Center 68 CAN APOPTOTIC MARKERS PREDICT DISEASE COURSE OF PEDIATRIC ITP POPULATION? Sarina Levy-Mendelovich 1,2,3 , Shraga Aviner 4 , Nechama Sharon 5 , Hagit Miskin 6 , Joan Jacobovitch 7 , Gili Kenet 1,2,3 , Hagit Hauschner 3 and Nurit Rosenberg 1,2,3 . 1 Sackler Faculty of Medicine, Tel Aviv University, Israel; 2 The Israeli National Hemophilia Center and Thrombosis Unit, Sheba Medical Center, Tel Hashomer, Israel. 3 Amalia Biron Research Institute of Thrombosis and Hemostasis, Chaim Sheba Medical Center, Tel Hashomer, Israel. 4 Department of Pediatrics, Barzilai University Medical Center, Ashkelon and the Faculty of Health Sciences, Ben- Gurion University of the Negev, Beer Sheva, Israel. 5 Pediatric Hemato-oncology Unit, Laniado Hospital, Netanya, Israel. 6 Pediatric Hematoloy Unit, Shaare Zedek Medical Center, Jerusalem, Israel. 7 Schnider Pediatric Hospital, Petach tiqva, Israel and Sackler School of Medicine Tel Aviv University, Tel Aviv, Israel Background Pediatric patients with immune thrombocytopenia (ITP) are currently being treated with one of the first line treatments available, only 80-85% will enter durable remission end eventually cure, at one year. Currently none of the attempts to stratify patients on diagnosis have been successful. Hypothesis Different pathophysiology is responsible to non-chronic versus chronic pediatric ITP. Predicting the course of ITP on diagnosis will open the stage for stratification of the patients to receive different first line therapy, in an attempt to affect the disease course in patients currently defined as having chronic disease. Objectives In the current study, we examined whether there is a difference in the pathophysiologic mechanisms, namely the apoptotic markers presentation at diagnosis between the non-chronic and those who will turn to have chronic disease. Results Blood samples were collected from 42 patients with a clinical diagnosis of ITP presented to five pediatric departments in Israel, between the years 2010-2014. All blood samples were taken prior to treatment. We incubated patients' sera with washed platelets and compared the results between healthy controls, chronic and non-chronic ITP patients. Phosphatidylserine exposure and mitochondrial electrochemical potential were measured using Flow cytometry followed by a Human Apoptosis Array. This Array examines 43 apoptotic markers. We found increased expression of five apoptotic proteins namely: BIM, CD40, IGFBP2, P21 and SMAC on platelets incubated with sera of non-chronic pediatric ITP patients, compared to chronic ones' sera, on diagnosis. Conclusions Our data may help to understand the differences between patients with non-chronic vs. chronic course of disease. This data is one more step in the effort to stratify ITP patients at diagnosis to non-chronic and chronic ones at diagnosis. This, in turn, may enable us to tailor more specific therapy to these seemingly different clinical entities currently treated in the same way.