Thrombotic microangiopathy due to acquired complement factor I
deficiency in a male receiving interferon-beta treatment for multiple
sclerosis
Abstract
Interferon-beta, the most widely prescribed medication for multiple
sclerosis, is generally considered safe. Nevertheless, rarely 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
insufficient immunological studies have been unable to pin this
phenomenon down to a single pathophysiologic pathway. We report
thrombotic microangiopathy due to acquired complement factor I
deficiency in a male receiving interferon-beta treatment for multiple
sclerosis. After three years of starting the therapy, the 28-year-old
patient presented with malignant hypertension causing seizures, rapidly
progressive renal failure requiring hemodialysis, and hemolytic anemia.
Corticosteroid and plasma exchange sessions permitted hemolysis 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 two years. We
concluded that IFNβ treatment may cause complement factor I deficit,
which can lead to thrombotic microangiopathy and severe renal failure.