Summary Thrombocytopenia has been identified as a common complication of severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2) infection in the general population. In an attempt to determine the impact of coronavirus disease 2019 (COVID‐19) in patients with immune thrombocytopenia (ITP), a retrospective single‐centre study was performed. Thrombocytosis was observed in patients with chronic ITP after SARS‐CoV‐2 infection, frequently needing treatment adjustment or even discontinuation of therapy. Relapses and newly diagnosed cases showed a fast response after initial treatment compared to ITP. Reduced immune activity due to lymphopenia during COVID‐19 could explain this paradoxical effect, although further studies are needed.

Summary The COVID‐19 pandemic has dramatically challenged care for cancer patients, especially those with active treatment who represent a vulnerable population for SARS‐CoV‐2 infection. Aggressive lymphoid neoplasms, such as diffuse large B cell lymphoma and high‐grade B cell lymphoma, need to be treated without delay in order to get the best disease outcome. Because of that, our clinical practice was changed to minimise the risk of SARS‐CoV‐2 infection while continuing haematological treatment. In this report, we analyse the management of front‐line therapy in 18 patients during the COVID‐19 outbreak, as well as the results of the implemented measures in their outcome.

Loss of sialic acid from the carbohydrate side chains of platelet glycoproteins can affect platelet clearance, a proposed mechanism involved in the etiopathogenesis of immune thrombocytopaenia (ITP). We aimed to assess whether changes in platelet glycosylation in patients with ITP affected platelet counts, function, and apoptosis. This observational, prospective, and transversal study included 82 patients with chronic primary ITP and 115 healthy controls. We measured platelet activation markers and assayed platelet glycosylation and caspase activity, analysing samples using flow cytometry. Platelets from patients with ITP with a platelet count <30 × 103/µL presented less sialic acid. Levels of α1,6-fucose (a glycan residue that can directly regulate antibody-dependent cellular cytotoxicity) and α-mannose (which can be recognised by mannose-binding-lectin and activate the complement pathway) were increased in the platelets from these patients. Platelet surface exposure of other glycoside residues due to sialic acid loss inversely correlated with platelet count and the ability to be activated. Moreover, loss of sialic acid induced the ingestion of platelets by human hepatome HepG2 cells. Changes in glycoside composition of glycoproteins on the platelets’ surface impaired their functional capacity and increased their apoptosis. These changes in platelet glycoside residues appeared to be related to ITP severity.

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