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Archivio digitale delle tesi discusse presso l’Università di Pisa

Tesi etd-11062025-092643


Tipo di tesi
Tesi di specializzazione (4 anni)
URN
etd-11062025-092643
Titolo
Coagulopatia in pazienti con patologia linfoproliferativa trattati con CAR-T: incidenza, fattori di rischio ed impatto clinico. Studio osservazionale, retrospettivo, monocentrico
Dipartimento
MEDICINA CLINICA E SPERIMENTALE
Corso di studi
EMATOLOGIA
Parole chiave
  • car-t
  • coagulopathy
  • dic
  • hemorrhagic and thrombotic risk.
Data inizio appello
21/11/2025
Consultabilità
Non consultabile
Data di rilascio
21/11/2028
Riassunto (Inglese)
Riassunto (Italiano)
The study retrospectively analyzed the incidence, risk factors, and clinical impact of coagulopathies, particularly disseminated intravascular coagulation (DIC), in patients with lymphoproliferative disorders treated with CAR-T cell therapy. It was found that CAR-T–associated coagulopathy represents a relatively uncommon but clinically significant toxicity, with an incidence of overt DIC of 5.5%.

The most relevant hemostatic abnormalities involved prothrombin time, fibrinogen, antithrombin III, platelet count, and hemoglobin, indicating a transient hemostatic dysfunction related to the systemic inflammatory response following CAR-T infusion.

Univariate analysis identified several predictive factors for overt DIC: younger age, diagnosis of B-cell acute lymphoblastic leukemia, presence of bulky disease, higher CAR-HEMATOTOX score, and shorter vein-to-vein times. In the post-infusion phase, DIC occurrence was associated with higher-grade cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS), higher interleukin-6 peaks, and greater CAR-T cell expansion. These findings suggest a central role of endothelial dysfunction induced by hyperinflammation.

The use of tocilizumab did not reach statistical significance, although a trend was observed toward an association between a higher number of administrations and an increased risk of inflammatory and neurological toxicities.

Future directions should focus on integrated prevention strategies combining early control of inflammation, particularly CRS, with endothelial-protective interventions.
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