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Treatment of myelodysplastic syndromes includes the administration of the hypomethylating agent decitabine. An early platelet response in decitabine-treated myelodysplastic syndrome patients is a predictor of overall survival. The effect of decitabine on megakaryocytes and the bone marrow, however, is understudied. We show that an early platelet increment was not detectable in healthy mice during decitabine treatment. Analyses of bone marrow sections revealed vessels with dilated lumina, decreased cellularity, but increased number of red blood cells and the presence of (pro)platelet-like particles. Taken together, decitabine treatment of healthy mice does not induce an early platelet increment, but affects the bone marrow. [ABSTRACT FROM AUTHOR]

The article discusses a 2022 study of the mechanics of the increased bleeding risk on mouse models of MYH9-related disease. It states that tranexamic acid treatment restored clot retraction in the presence of tPA, and reduced bleeding, with verification from mutant mice and patients' platelets with the mutation. Also noted is the possible lead of reduced platelets to increased bleeding tendency in patients with MYH9-related disease, with improved hemostatic function afforded by tranexamic acid.

The article presents a study which explores the reduced platelet forces underlie impaired hemostasis in mouse models of MYH9-related disease. It mentions that reduced platelet forces lead to an increased bleeding tendency in patients with MYH9-related disease, and treatment with tranexamic acid can improve the hemostatic function.