Publications by authors named "M Cappellini"

Background: Beta-thalassemias (BTs) are characterized by deficient or absent synthesis of the beta-globin subunit, leading to anemia. Patient characteristics and treatment patterns in these patients may vary.

Objective: This retrospective study evaluated demographics, clinical characteristics, and treatment patterns in patients with transfusion-dependent BT (TDT) and non-transfusion-dependent BT (NTDT).

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Objectives: To estimate thresholds for defining meaningful within-patient improvement from baseline to weeks 13-24 and interpreting meaningfulness of between-group difference for the non-transfusion-dependent beta-thalassaemia patient-reported outcome (NTDT-PRO) tiredness/weakness (T/W) and shortness of breath (SoB) scores. A secondary objective was to determine the symptom severity threshold for the NTDT-PRO T/W domain to identify patients with symptomatic T/W.

Design: Pooled blinded data from the phase 2, double-blind, placebo-controlled, randomised BEYOND trial in NTDT (NCT03342404) were used.

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Metabolic requirements vary during development, and our understanding of how metabolic activity influences cell specialization is incomplete. Here, we describe a switch from glutamine catabolism to synthesis required for erythroid cell maturation. Glutamine synthetase (GS), one of the oldest functioning genes in evolution, is activated during erythroid maturation to detoxify ammonium generated from heme biosynthesis, which is up-regulated to support hemoglobin production.

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Anemia during acute inflammation is not well described in the literature. We aimed to study whether patients develop a transient hemoglobin decrease during an acute attack of recurrent pericarditis. We retrospectively analyzed patients with recurrent pericarditis.

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Article Synopsis
  • β-thalassemia and sickle cell disease are linked to a hypercoagulable state, increasing the risk of thrombosis and organ complications.
  • Factors like free heme, inflammation, and splenectomy, alongside the role of red blood cells, contribute to this thrombotic risk.
  • Understanding these mechanisms can help improve prevention and treatment strategies for managing thrombosis in patients with these blood disorders.
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