Background: The landscape of first-line treatment for acute myeloid leukemia (AML) patients ineligible for intensive chemotherapy has changed remarkably after venetoclax approval. Accumulating real-world data further apprises us with more knowledgeable use. To assess the efficacy and safety challenges in the real-life setting of the combination of hypomethylated agent (HMA) and venetoclax, we conducted a multi-center retrospective study. Methods: Forty adult AML patients treated with the combination of HMA and venetoclax as a first-line treatment after full approval (2020) were included. To confirm VIALE-A results, this group was compared to a historical cohort of 17 chemotherapy-ineligible AML patients treated with HMA monotherapy before 2020. Results: The combination of HMA-venetoclax achieved a composite complete response rate of 86.8% (p < 0.001), median overall survival, and event-free survival of 33.8 and 19.7 months, respectively, in a median follow-up of 17.8 months (p_os < 0.001, HR = 0.276, CI: 0.132–0.575, p_EFS = 0.004, HR = 0.367, CI: 0.174–0.773). High rates of neutropenia (90%) and consequent infection rates (57.5%) were noted. Only 55% of our patients received antifungal prophylaxis, as its use remains controversial, and invasive fungal infections were presented in 7.5%. Conclusions: Evidently, venetoclax-HMA yields high response rates and profound survival benefits in real life and has changed our approach to alternative chemotherapy options.

Platelet satellitism (PS) is an in vitro phenomenon of platelets adhering around white blood cells, especially in blood samples anticoagulated with K3EDTA. This, in some cases, can lead to spurious thrombocytopenia, without platelet dysfunction or bleeding events. Diagnosis is made by peripheral blood smear examination. The potential mechanism for PS remains largely unknown; however, it possibly involves the formation of IgG antibodies against the platelet glycoprotein receptor IIb/IIIa (GPIIb/IIIa). PS has been observed in various medical conditions, including infectious, autoimmune, and lymphoproliferative disorders, without an obvious causative relationship. Here, we describe a case of PS in a patient who presented with infection in the setting of underlying Immune Thombocytopenic Purpura and Multiple Sclerosis.