Thrombotic microangiopathy due to acquired complement factor I deficiency in a male receiving interferon-beta treatment for multiple sclerosis.
alternative complement pathway
atypical haemolytic uremic syndrome
complement factor I
interferon-beta
multiple sclerosis
thrombotic microangiopathy
Journal
British journal of clinical pharmacology
ISSN: 1365-2125
Titre abrégé: Br J Clin Pharmacol
Pays: England
ID NLM: 7503323
Informations de publication
Date de publication:
05 2023
05 2023
Historique:
revised:
20
11
2022
received:
13
07
2022
accepted:
29
11
2022
medline:
14
4
2023
pubmed:
9
12
2022
entrez:
8
12
2022
Statut:
ppublish
Résumé
Interferon-beta (IFNβ), the most widely prescribed medication for multiple sclerosis, is generally considered safe. Nevertheless, rare serious and/or life-threatening side effects have been reported such as thrombotic microangiopathy. A few mechanisms have been proposed to explain how interferon causes thrombotic microangiopathy, but immunological studies have been unable to pin this phenomenon down to a single pathophysiologic pathway. The aim of this article was to report a new mechanism explaining Interferon beta related thrombotic microangiopathy. We report thrombotic microangiopathy in a 28-year-old male receiving interferon-beta treatment for multiple sclerosis. After three years of starting interferon beta therapy, the patient presented with malignant hypertension causing seizures, rapidly progressive renal failure requiring haemodialysis and haemolytic anaemia. Corticosteroid and plasma exchange sessions permitted haemolysis control. Nonetheless, the patient remained hemodialysis-dependent. Exploration of the complement system found a complement factor I deficiency whose activity normalized at the control carried out after 2 years. IFNβ treatment may cause complement factor I deficit, which can lead to thrombotic microangiopathy and severe renal failure.
Substances chimiques
Interferon-beta
77238-31-4
Types de publication
Case Reports
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1682-1685Informations de copyright
© 2022 British Pharmacological Society.
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