Thrombotic microangiopathy caused by interferon β-1b for multiple sclerosis: a case report

Abstract

A 41-year-old man with a history of multiple sclerosis (MS) developed thrombotic microangiopathy after taking interferon β-1b for 10 years. Although the relapse of his MS was well controlled under normal blood pressure, he had persistent nausea, anorexia, gait disturbance and visual disorder 1 month before admission. He showed lethargy and high blood pressure (180/102 mmHg). Laboratory test results revealed anemia and thrombocytopenia, elevated LDH and renal dysfunction. Urinary dipstick showed a 2+ result for proteinuria and 3+ for hematuria. Schizocyte were present and haptoglobin decreased, and we diagnosed him with possible thrombotic microangiopathy (TMA). Magnetic resonance image indicated posterior reversible encephalopathy syndrome (PRES), which could be accelerated by TMA. After discontinuing interferon β-1b, high dose intravenous methylpredonisolone, anti-hypertension therapy and plasma exchange was started. Because a mild decrease in ADAMTS13 activity and absence of ADAMTS 13 inhibitor could not cause thrombotic thrombocytopenic purpura, plasma exchange was stopped. The patient's renal function recovered and PRES resolved, and he was discharged with slightly decrease of visual acuity. We suggest that his TMA was likely caused by interferon β-1b, resulting in PRES in a patient with multiple sclerosis. We report this rare case and also review the literature.

Keywords: Interferon; Multiple sclerosis; Thrombotic microangiopathy.

Fig. 1

Fluid attenuated inversion recovery (FLAIR) magnetic resonance imaging. Bilateral hyperintense subcortical white matter lesions were observed in a predominantly posterior distribution on admission (a). Those lesions were resolved after 12 days (b), suggesting posterior reversible encephalopathy syndrome (PRES)

Fig. 2

Clinical course