Thrombotic microangiopathy in Interferon Beta treated multiple sclerosis patients: Review of literature and report of two new cases

Vosoughi, Reza; Marriott, James

doi:10.1016/j.msard.2013.12.007

Cited by 23 publications

(15 citation statements)

References 13 publications

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“…Cessation of interferon might resolve TMA in some patients, and PE has been effective in controlling TMA in other patients. Serious cases might require continuation of dialysis therapy [6][7][8][9]. Similar clinical courses have also been reported for tacrolimus in patients with organ transplantation [19,20].…”

Section: Case Reportsupporting

confidence: 58%

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

et al. 2016

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A 41-year-old man with a history of multiple sclerosis (MS) developed thrombotic microangiopathy after taking interferon b-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 b-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 b-1b, resulting in PRES in a patient with multiple sclerosis. We report this rare case and also review the literature.

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Section: Case Reportsupporting

confidence: 58%

“…Nevertheless, we concluded that his TMA have been triggered by interferon b-1b that was administered as a treatment for MS. Indeed, interferon b-1a has been shown to cause TMA [6][7][8][9]. The difference between interferon b-1a and interferon b-1b is the presence (1a) or absence (1b) of glycosylation.…”

Section: Case Reportmentioning

confidence: 99%

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

et al. 2016

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“…9 This is of particular relevance here because many cases of IFN-associated TMA have been reported using diverse terms including HUS, 7 thrombotic thrombocytopenic purpura (TTP), 35 or malignant hypertension, 35,36 each implying a different pathophysiological process. It is therefore an important first step to define the clinical syndrome through a center with expertise in the evaluation of this complex condition.…”

Section: Discussionmentioning

confidence: 99%

Type I interferon causes thrombotic microangiopathy by a dose-dependent toxic effect on the microvasculature

Kavanagh

McGlasson

Jury

et al. 2016

Blood

102

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Key Points• Type I IFN therapies can cause a dose-dependent TMA.• Recombinant type I IFN therapies should be stopped at the earliest opportunity in patients who develop TMA.Many drugs have been reported to cause thrombotic microangiopathy (TMA), yet evidence supporting a direct association is often weak. In particular, TMA has been reported in association with recombinant type I interferon (IFN) therapies, with recent concern regarding the use of IFN in multiple sclerosis patients. However, a causal association has yet to be demonstrated. Here, we adopt a combined clinical and experimental approach to provide evidence of such an association between type I IFN and TMA. We show that the clinical phenotype of cases referred to a national center is uniformly consistent with a direct dose-dependent drug-induced TMA. We then show that dosedependent microvascular disease is seen in a transgenic mouse model of IFN toxicity. This includes specific microvascular pathological changes seen in patient biopsies and is dependent on transcriptional activation of the IFN response through the type I interferon a/b receptor (IFNAR). Together our clinical and experimental findings provide evidence of a causal link between type I IFN and TMA. As such, recombinant type I IFN therapies should be stopped at the earliest stage in patients who develop this complication, with implications for risk mitigation. (Blood. 2016;128(24):2824-2833

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“…While an almost good safety profile is considered for IFN-β, an increasing number of reports have indicated some previously unknown adverse events, which may be potentially serious in some cases. Among these, thrombotic microangiopathy, arterial hypertension, Raynaud's phenomenon, livedo reticularis, capillary leak syndrome, pulmonary artery hypertension, and retinopathy warrant consideration (9)(10)(11)(12)(13)(14)(15)(16). There seems to be a common angiopathic mechanism involved in these more recent complications.…”

Section: Discussionmentioning

confidence: 99%

Intracerebral Hemorrhage in a Patient with Multiple Sclerosis Receiving Interferon Beta-1α

et al. 2016

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Interferon beta-1α (IFN β-1α) is one of the most widely used disease-modifying drugs, resulting in reduced annualized relapse rates and MRI activity in patients with multiple sclerosis (MS). Years of experience has indicated the relative safety of this class of medications in patients with MS. Despite its overall safety profile, an increasing number of reports have revealed serious adverse events in form of angiopathic complications in the preceding years. Herein, we present the case of a patient with chronic MS under treatment with IFN β-1α, presenting with intracerebral hemorrhage (ICH) without any other identifiable causes. The present report, along with various cases of bleeding in patients receiving IFN, indicates a possible association between IFN therapy and ICH.

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Thrombotic microangiopathy in Interferon Beta treated multiple sclerosis patients: Review of literature and report of two new cases

Cited by 23 publications

References 13 publications

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

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

Type I interferon causes thrombotic microangiopathy by a dose-dependent toxic effect on the microvasculature

Intracerebral Hemorrhage in a Patient with Multiple Sclerosis Receiving Interferon Beta-1α

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