LITERATURE UPDATE Bone marrow aspirate showing two megakaryocytes (Wright’s stain).
Recent advances in the management of immune thrombocytopenic purpura (ITP): A comprehensive review. Madkhali MA. Medicine (Baltimore). 2024 Jan 19; 103 (3): e36936.
doi: 10.1097/MD.0000000000036936.
Autoimmune disorders place a substantial burden on the healthcare system all over the world affecting almost 3% to 8% of the population. Immune thrombocytopenic purpura (ITP), also known as idiopathic thrombocytopenic purpura, is a blood disorder in which the body’s immune system destroys platelets, leading to low platelet counts in the blood (peripheral blood platelet count <150 × 109/L). Although the pathophysiology of ITP is not fully understood, it is believed to result from a complex interplay between hereditary and environmental variables. Certain factors, such as a low platelet count, history of bleeding, and certain comorbidities can increase the risk of severe bleeding in patients with ITP. Corticosteroids, intravenous immunoglobulin (IVIG), immunosuppressants, rituximab, and thrombopoietin receptor agonists (TPO-RAs) are some of the advanced treatments for ITP. Although these therapies may be successful, they also carry the risk of negative effects. Recently, significant advancements have been made in the understanding and treatment of ITP. There is still much to learn about the disease, and new, more effective treatments are needed. This review offers a comprehensive assessment of recent advancements in
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ITP management, with a focus on active research projects, novel therapeutic targets, new treatment modalities, and areas of uncertainty and unmet needs. According to research, it is crucial to develop individualised treatment plans for ITP patients based on their age, platelet count, risk of bleeding, and comorbidities. The article also looks at how future developments in gene editing, bispecific antibody therapies, and cellular therapy may completely change the treatment of ITP.
Platelet-associated biomarkers in nonalcoholic steatohepatitis: Insights from a female cohort with obesity. Duran-Bertran J, Rusu EC, Barrientos- Riosalido A et al. Eur J Clin Invest. 2024 Mar; 54 (3): e14123. doi: 10.1111/eci.14123.
There is a lack of non-invasive diagnostic methods for non-alcoholic steatohepatitis (NASH), the severe condition of metabolic dysfunction- associated steatotic liver disease (MASLD). Platelet activation, evaluated through certain related parameters, is associated with liver disease and inflammation, but previous results are inconclusive. This study aims to investigate the potential utility of platelet-related indices as non-invasive diagnostic markers for the detection and prediction of MASLD, focusing on NASH.
The authors found that mean platelet volume (MPV), plateletcrit (PCT) and platelet distribution width (PDW) were increased in the severe and morbidly obese (SMO) group compared to the
normal weight (NW) group. They found decreased levels of MPV in steatosis and NASH patients. MPV and PCT values were decreased in the presence of mild liver inflammation. Platelet count (PLA) and PCT values were lower in the presence of ballooning. They obtained an area under the ROC curve of 0.84 using MPV and three other variables to predict MASLD. Some platelet-related indices vary depending on liver condition. Here, the authors reported decreased MPV in MASLD presence. Moreover, they presented for the first time a predictive model using MPV, ALT levels and the presence of diabetes mellitus and metabolic syndrome to predict MASLD in obese women. Also, MPV is closely related to early liver inflammation in NASH, and PLA and PCT are related to hepatic ballooning. These indices could be widely used for the early detection of NASH since they are usually determined in routine laboratory tests.
Platelet mass cytometry reveals dysregulation of prothrombotic pathways in essential thrombocythemia. Dill V, Kirmes K, Han J et al. Platelets. 2024 Dec; 35 (1): 2358244.
doi: 10.1080/09537104.2024.2358244.
Thromboembolic events are common in patients with essential thrombocythemia (ET). However, the pathophysiological mechanisms underlying the increased thrombotic risk remain to be determined. Here, the authors perform the first phenotypical characterisation of platelet expression using single-cell mass cytometry in six ET patients and six age- and sex-matched healthy individuals. A large panel of 18 transmembrane
regulators of platelet function and activation were analysed, at baseline and after ex-vivo stimulation with thrombin receptor-activating peptide (TRAP). The authors detected a significant overexpression of the activation marker CD62P (p-Selectin) (P=0.049) and the collagen receptor GPVI (P=0.044) in non-stimulated ET platelets. In contrast, ET platelets had a lower expression of the integrin subunits of the fibrinogen receptor GPIIb/IIIa CD41 (P=0.036) and CD61 (P=0.044) and of the von Willebrand factor receptor CD42b (P=0.044).
Using the FlowSOM algorithm, the authors identified two subclusters of ET platelets with a prothrombotic expression profile, one of them (cluster 3) significantly over-represented in ET
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