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Case Reports
. 2023 May;89(5):1682-1685.
doi: 10.1111/bcp.15631. Epub 2022 Dec 23.

Thrombotic microangiopathy due to acquired complement factor I deficiency in a male receiving interferon-beta treatment for multiple sclerosis

Sanda Mrabet  1 , Rihem Dahmane  1 , Boukadida Raja  1 , Asma Fradi  1 , Narjess Ben Aicha  1 , Wissal Sahtout  1 , Awatef Azzabi  1 , Yosra Guedri  1 , Dorsaf Zellama  1 , Abdellatif Achour  1 , Imen Sfar  2 , Rim Goucha  3 , Nihed Abdessayed  4 , Moncef Mokni  4
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Free article
Case Reports

Thrombotic microangiopathy due to acquired complement factor I deficiency in a male receiving interferon-beta treatment for multiple sclerosis

Sanda Mrabet et al. Br J Clin Pharmacol. 2023 May.
Free article

Abstract

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.

Keywords: alternative complement pathway; atypical haemolytic uremic syndrome; complement factor I; interferon-beta; multiple sclerosis; thrombotic microangiopathy.

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References

REFERENCES

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