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Vasculitis Associated with Biologic Use

While biologics have recently become potentially important interventions in vasculitis, especially medium and large vessel vasculitis, wherein rituximab is approved for granulomatosis with polyangitiitis and several agents (tocilizumab, abatacept) are under investigation for large vessel vasculitis.

The widespread use of existing biologics has sometimes been associated with the paradoxical development of biologics-induced autoimmune phenomena, including vasculitis.

A recent review of more than 200 vasculitis cases associated with biologic use has profiled the range of these unsual and rare events.  All of these were defined based on histopathology or meeting the ACR/Chapel Hill criteria.

Most of these were females (75%) with a mean age of 48 years and more than 50% had rheumatoid arthritis. Most of the biologics-associated vasculitis occured within  90 ± 31 days of starting the biologic.  

Review of the biologic-associated vasculitis events from the British Society of Rheumatology Register (BSRBR) showed the incidence rate to be 6/10,000 and 12/10,000 person-years for TNFi-associated and DMARD-associated vasculitis, respectively.  The adjusted risk ratio for TNFi- vasculitis was 1.13 (CI 95 % 0.51–2.49) compared to those on DMARDs.

Looking at several cohorts, the majority of cases were limited to cutaneous vasculitis, but a minority were shown to have systemic vasulitis, digital infarction, neurological disorder, or venous/arterial thromboembolism. Hemorrhagic alveolitis, episcleritis, and ANCA+ vasculitis have all been described.  

While these events were dominated by the TNF inhibitors, there have been no reports of certolizumab related vasculitis.

Drug discontinuation resulted in complete resolution in ~75 % of the cases. Steroid therapy, cyclophosphamide, rituximab or plasma exchange was rarely needed and only for the most severe cases.

Rarely are other biologics implicated in cutaneous vasculitis but has been seen with beta interferon and recombinant granulocyte colony-stimulating factor.

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Disclosures
The author has no conflicts of interest to disclose related to this subject