A Rare Case of an Elderly Male with Progression to Chronic Myeloid Leukaemia Secondary to Chronic Lymphocytic Leukaemia.

Chronic lymphocytic leukaemia (CLL) is a lymphoproliferative disorder characterised by an accumulation of monoclonal B lymphocytes, with an increased risk of secondary cancers. The coexistence of CLL and chronic myeloid leukaemia (CML) is a rare phenomenon, with three main types being classified: CML preceding CLL, CLL preceding CML and simultaneous occurrence. The coexistence of these chronic leukaemias poses a complex clinical challenge, with the underlying mechanisms of their association remaining enigmatic. Here, we present a report of an elderly male with a long history of CLL, who was subsequently diagnosed with secondary CML. LEARNING POINTS: The development of chronic myeloid leukaemia (CML) subsequent to chronic lymphocytic leukaemia (CLL) is an uncommon occurrence, challenging conventional expectations of disease evolution in chronic leukaemia.Extensive and appropriate testing is necessary to promptly identify secondary CML in CLL patients.Targeted therapy with dasatinib, a tyrosine kinase inhibitor, may demonstrate efficacy in reducing leukocytosis and BCR-ABL1 levels in patients with coexisting CLL and CML.

Nivolumab-induced fatal myocarditis: A case report.

Key Clinical Message: Baseline assessment and interval monitoring with a careful history, clinical examination, laboratory work-up, and noninvasive imaging modalities may be beneficial for early detection of immune checkpoint inhibitor-associated side effects. Abstract: Previous reports of immune checkpoint inhibitors' cardiotoxic effects include pericarditis, myocarditis, myocardial infarction, ventricular dysfunction, vasculitis, and electrical abnormalities. The authors report a case of acute heart failure caused by nivolumab-induced cardiotoxicity in a middle-aged man with advanced esophageal carcinoma with no previous cardiac history or significant cardiovascular risk factors.

Platelets in chronic obstructive pulmonary disease: An update on pathophysiology and implications for antiplatelet therapy.

Platelets are essential mediators of inflammation and thrombosis. Chronic obstructive pulmonary disease (COPD) is a heterogeneous multisystem disease, causing significant morbidity and mortality worldwide. Recent evidence suggests that the lung is an important organ for platelet biogenesis. Cigarette smoking has been shown to induce platelet aggregation and decrease the capacity of mitochondrial electron transport system in platelets. Preclinical and clinical studies have suggested that platelets may contribute to the development of COPD through the breakdown of lung elastin by platelet factor 4, platelet activation and formation of platelet aggregates, and modulation of hypoxia signaling pathways. Recent large population studies have produced encouraging results indicating a potential role for aspirin in preventing exacerbations and delaying disease progression in patients with COPD. This review summarizes the information about the lung as an organ for platelet production, pathophysiological functions of platelets and platelet mediators in the development of COPD, and the most updated evidence on the utility of aspirin in patients with COPD.