Shinta Oktya Wardhani is an MD Trainee in Hematology and Medical Oncology at Hasan Sadikin Hospital, Padjadjaran University and has special interest in apheresis and other hematology and oncology research with a 3rd Best Poster Presentation Award from Indonesian Society of Medical Oncology in ROICAM 6 Conference in Jakarta on 23-26 August 2018 and 2nd Best Oral Presentation in Regional Conference of Internal Medicine (Trigonum SUDEMA) in Malang on July 2018. She also become an author and co-author of some publication including “correlation between soluble urokinase plasminogen activator receptor with CD-4 T lymphocyte and WHO clinical staging of HIV infection”.
Hyperleukocytosis is defined as total leukemic blood cell count greater than 50x109 L or 100x109 L. Critical hyperleukocytosis can cause leukostasis, a poorly understood and life-threatening complication. The incidence of hyperleukocytosis and leukostasis differs among various types of leukemia. Leukapheresis is known to be a rapid and safe procedure to reduce leucocyte (leukoreduction) and early mortality in patients with hyperleukocytosis leukemia. The aim of our study is to investigate the correlation of hematologic parameter before leukapheresis to the degree of leukoreduction. We retrospectively analyzed 42 patients with hyperleukocytosis leukemia with and without clinical sign of leukostasis. Paired t-test showed that there were significant leukoreduction (p<0.001), decrease of neutrophils (<0.001) and also platelets (p<0.001) after leukapheresis. The result of bivariant analysis indicated that all haematologic parameters before leukapheresis, hemoglobin (r=0.364; p=0.009), leukocyte (r=-0.397; p=0.005), platelets (r=-0.385; p=0.006), haematocrit (r=0.512; <0.001), lymphocyte (r=0.408; p=0.004) and neutrophil (r=- 0.300; p=0.027) correlate with leukocyte reduction. This result was similar to Jin Y-study, who found that only leukocyte and haematocrit had an influence on collection efficiencies (rate of leukocyte depletion). In conclusion leukapheresis is effective in reducing leucocyte and neutrophil, but also platelets. Hematological parameters before leukapheresis significantly correlate with the degree of leukoreduction.
E Tjønnfjord took his Degree at Odense University Hospital, Denmark. He has worked in the field of hematology with a special interest in the benign hematology.He is now starting a PhD focusing on the treatment of ITP and how to improve it.
Introduction: Immune thrombocytopenia (ITP) is characterized by immune mediated destruction of platelets and suboptimal production. RITP was a randomized placebo-controlled trial in which ITP patients who failed to achieve adequate response to steroids were randomized to receive rituximab or placebo plus standards of care (Ghanima et al. Lancet 2015; 385:1653-61). Study end points were treatment failure (splenectomy or meeting criteria for splenectomy), response rates and duration of response with a follow-up of 18 months. Apart from longer duration of response in the rituximab arm, the study showed no significant differences and the other outcomes. Objective: To provide long-term rates of splenectomy, death and duration of response based on extended open follow-up after completion of the RITP study. Methods: Platelet counts, splenectomy status, ITP medication and death were retrospectively collected. Response was defined as platelet count of >30X109/L or atleast a doubling of the platelet count from baseline without administration of any platelet increasing therapy except stable or decreasing doses of prednisone or prednisolone during the past 4 weeks; or > 100X109/L for complete response (CR) after week 4 from first study drug administration. Relapse was defined as platelet count <30X109/L or reinstitution of ITP medication. The study was approved by the ethics committees in Norway and Tunisia. Results: Extended follow-up data were acquired from 90 of 109 patients participating in RITP. Median duration of follow-up from randomization to last observation was 72 months (IQR 62-82). Overall 35 patients underwent splenectomy (13 in the rituximab; 22 in the placebo arm) with a trend towards longer time to splenectomy in the rituximab arm (p=0.11) (figure 1). Eleven patients (10%) died during the extended followup: 5 in the rituximab and 6 in the placebo arms. Seventy-six of 109 patients achieved response (40 in the rituximab; 36 in the placebo arms) including complete response (28 in the rituximab; 21 in the placebo arms) during the RITP study. Figure 2 shows probability of first relapse in responding patients. Median duration of response was 8.2 (5.2-16.7) after response and 17 (8-34) months after CR, in the rituximab arm and 1.8 (1.3-3.7) and 11 (4.5- not reached) months respectively in the placebo arm. Not statistically significant (p=0.09). During the extended follow-up, 2 more patients in the rituximab arm relapsed after achieving response and 4 after achieving CR. Conclusion: To our knowledge, the data provided here represent the longest single study follow-up reported on the effect of rituximab in ITP. Although, rituximab seemed to yield longer duration of OR and CR, the effect was clearly transient and the two curves cross after 34 months. Around 20% of patients in both arms are still responders at 6 years. Interestingly a trend towards lower splenectomy rate was found in rituximab treated patients. The retrospective collection of data in the follow-up represents a limitation of this study. In the future, efforts should be made to augment the initial response to rituximab and to prolong the duration of response, as our ongoing prolong study (NCT03010202) will look at.