European Medical Journal (Sep 2020)

Superficial Ulcerating Rheumatoid Necrobiosis Associated with Methotrexate Use in a Patient with Rheumatoid Arthritis

  • Austin Cusick,
  • Amandeep Goyal,
  • Ashley H. Merten,
  • Andrew Virata,
  • Rahul Sehgal,
  • Pankaj Bansal

DOI
https://doi.org/10.33590/emj/20-00066
Journal volume & issue
Vol. 5, no. 3
pp. 39 – 44

Abstract

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Methotrexate, a disease-modifying antirheumatic drug, is fundamental to limiting progression in several rheumatic diseases such as rheumatoid arthritis (RA). However, methotrexate is also associated with various significant adverse effects. Of note, there are several dermatologic manifestations attributed to methotrexate therapy. In particular, accelerated nodulosis and panniculitis are linked to methotrexate therapy in the current literature. The authors present the case of a 55-year-old Caucasian female with seropositive erosive RA who developed superficial ulcerating rheumatoid necrobiosis (SURN), secondary to methotrexate therapy. The patient’s treatment consisted of methotrexate discontinuation, topical clobetasol, and initiation of leflunomide as a replacement of methotrexate. Follow-up evaluation confirmed resolution of SURN over time and maintained low disease RA activity with leflunomide. Few cases describe SURN in the setting of RA and there are currently no cases published that suggest methotrexate’s possible role in SURN. Methotrexate-induced SURN is plausible in this case because of the correlation with therapy initiation and remission after therapy discontinuation. SURN has significant histological overlap with other methotrexate-induced dermatologic manifestations, allowing for a possible correlation. Most dermatological side effects of methotrexate are linked to a genetic predisposition of the HLA-DRB1 gene. Additionally, methotrexate’s mechanism of action for rheumatologic disease paradoxically stimulates adenosine-1 receptors and activates neutrophil chemotaxis and phagocytosis. Adenosine-1 receptor stimulation is hypothesised to be the source of rheumatoid-accelerated nodulosis and possibly SURN. Furthermore, the location of manifestation, genetic predisposition, and comorbid features in the patient all possibly have a role in this unique dermatological side effect.

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