Natalizumab (Tysabry®) is a humanised monoclonal antibodies (MAb) which blocks alpha4beta1 integrin-mediated leukocyte migration; it is one among the plethora of pharmacological treatments against multiple sclerosis (MS) [1,2]. Some reports describe a relationship between clinical syndromes and administration of Mab, in particular on thyroid gland [3,4]. Therefore, only few data have been so far reported about cardiac involvement and MAb-therapy. We report here an unusual case of acute myocardial damage likely induced by taking Natalizumab, in an young woman in treatment for a relapsing–remitting (RR) MS.

Natalizumab treatment for multiple sclerosis inducing a toxic acute myocardial damage. Is there any relationship?

Fama', Fausto
Primo
Writing – Review & Editing
;
Dattola, Vincenzo
Conceptualization
;
Cicciu', Marco
Supervision
;
Buccafusca, Maria
Investigation
;
Russo, Margherita
Investigation
;
Dattilo, Giuseppe
Investigation
;
Di Bella, Gianluca
Ultimo
Validation
2016-01-01

Abstract

Natalizumab (Tysabry®) is a humanised monoclonal antibodies (MAb) which blocks alpha4beta1 integrin-mediated leukocyte migration; it is one among the plethora of pharmacological treatments against multiple sclerosis (MS) [1,2]. Some reports describe a relationship between clinical syndromes and administration of Mab, in particular on thyroid gland [3,4]. Therefore, only few data have been so far reported about cardiac involvement and MAb-therapy. We report here an unusual case of acute myocardial damage likely induced by taking Natalizumab, in an young woman in treatment for a relapsing–remitting (RR) MS.
2016
Inglese
STAMPA
Elsevier
206
March
127
128
2
https://www.internationaljournalofcardiology.com/article/S0167-5273(16)30071-7/fulltext
Internazionale
Esperti anonimi
Natalizumab, Toxic acute myocardial damage, Multiple sclerosis, Monoclonal antibodies.
no
info:eu-repo/semantics/article
Fama', Fausto; Dattola, Vincenzo; Cicciu', Marco; Buccafusca, Maria; Russo, Margherita; Lo Presti, Dario; Dattilo, Giuseppe; Di Bella, Gianluca...espandi
14.a Contributo in Rivista::14.a.1 Articolo su rivista
8
262
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11570/3085073
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