Cancer Risk for Fingolimod, Natalizumab, and Rituximab in Multiple Sclerosis Patients.


Journal

Annals of neurology
ISSN: 1531-8249
Titre abrégé: Ann Neurol
Pays: United States
ID NLM: 7707449

Informations de publication

Date de publication:
05 2020
Historique:
received: 22 08 2019
revised: 11 02 2020
accepted: 11 02 2020
pubmed: 15 2 2020
medline: 24 7 2020
entrez: 15 2 2020
Statut: ppublish

Résumé

Novel, highly effective disease-modifying therapies have revolutionized multiple sclerosis (MS) care. However, evidence from large comparative studies on important safety outcomes, such as cancer, is still lacking. In this nationwide register-based cohort study, we linked data from the Swedish MS register to the Swedish Cancer Register and other national health care and census registers. We included 4,187 first-ever initiations of rituximab, 1,620 of fingolimod, and 1,670 of natalizumab in 6,136 MS patients matched for age, sex, and location to 37,801 non-MS general population subjects. Primary outcome was time to first invasive cancer. We identified 78 invasive cancers among treated patients: rituximab 33 (incidence rate [IR] per 10,000 person-years = 34.4, 95% confidence interval [CI] = 23.7-48.3), fingolimod 28 (IR = 44.0, 95% CI = 29.2-63.5), and natalizumab 17 (IR = 26.0, 95% CI = 15.1-41.6). The general population IR was 31.0 (95% CI = 27.8-34.4). Adjusting for baseline characteristics, we found no difference in risk of invasive cancer between rituximab, natalizumab, and the general population but a possibly higher risk with fingolimod compared to the general population (hazard ratio [HR] = 1.53, 95% CI = 0.98-2.38) and rituximab (HR = 1.68, 95% CI = 1.00-2.84). In this first large comparative study of 3 highly effective MS disease-modifying therapies, no increased risk of invasive cancer was seen with rituximab and natalizumab, compared to the general population. However, there was a borderline-significant increased risk with fingolimod, compared to both the general population and rituximab. It was not possible to attribute this increased risk to any specific type of cancer, and further studies are warranted to validate these findings. ANN NEUROL 2020;87:688-699.

Identifiants

pubmed: 32056253
doi: 10.1002/ana.25701
doi:

Substances chimiques

Immunologic Factors 0
Natalizumab 0
Rituximab 4F4X42SYQ6
Fingolimod Hydrochloride G926EC510T

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

688-699

Informations de copyright

© 2020 The Authors. Annals of Neurology published by Wiley Periodicals, Inc. on behalf of American Neurological Association.

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Auteurs

Peter Alping (P)

Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden.
Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institute, Stockholm, Sweden.

Johan Askling (J)

Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institute, Stockholm, Sweden.

Joachim Burman (J)

Department of Neuroscience, Uppsala University, Uppsala, Sweden.

Katharina Fink (K)

Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden.
Academic Specialist Center, Stockholm Health Services, Stockholm, Sweden.

Anna Fogdell-Hahn (A)

Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden.

Martin Gunnarsson (M)

Department of Neurology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.

Jan Hillert (J)

Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden.
Department of Neurology, Karolinska University Hospital, Stockholm, Sweden.

Annette Langer-Gould (A)

Clinical and Translational Neuroscience, Southern California Permanente Medical Group, Kaiser Permanente, Pasadena, CA.

Jan Lycke (J)

Department of Clinical Neuroscience and Rehabilitation, University of Gothenburg, Gothenburg, Sweden.

Petra Nilsson (P)

Department of Clinical Sciences/Neurology, Lund University, Lund, Sweden.

Jonatan Salzer (J)

Department of Pharmacology and Clinical Neuroscience, Umeå University, Umeå, Sweden.

Anders Svenningsson (A)

Department of Clinical Sciences, Karolinska Institute, Danderyd Hospital, Stockholm, Sweden.

Magnus Vrethem (M)

Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.

Tomas Olsson (T)

Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden.
Academic Specialist Center, Stockholm Health Services, Stockholm, Sweden.

Fredrik Piehl (F)

Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden.
Academic Specialist Center, Stockholm Health Services, Stockholm, Sweden.

Thomas Frisell (T)

Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institute, Stockholm, Sweden.

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