British journal of clinical pharmacology · 2022
Thrombotic microangiopathy due to acquired complement factor I deficiency in a male receiving interferon-beta treatment for multiple sclerosis.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Mrabet Sanda, Dahmane Rihem, Raja Boukadida, Fradi Asma, Aicha Narjess Ben, Sahtout Wissal, Azzabi Awatef, Guedri Yosra, Zellama Dorsaf, Achour Abdellatif, Sfar Imen, Goucha Rim, Abdessayed Nihed, Mokni Moncef
Аннотация
AIMS: 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.
METHODS: We report thrombotic microangiopathy in a 28-year-old male receiving interferon-beta treatment for multiple sclerosis.
RESULTS: 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.
CONCLUSION: IFNβ treatment may cause complement factor I deficit, which can lead to thrombotic microangiopathy and severe renal failure.
METHODS: We report thrombotic microangiopathy in a 28-year-old male receiving interferon-beta treatment for multiple sclerosis.
RESULTS: 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.
CONCLUSION: IFNβ treatment may cause complement factor I deficit, which can lead to thrombotic microangiopathy and severe renal failure.