Successful Management of Anti-TNF-Induced Psoriasis despite Continuation of Therapy in a Pyoderma Gangrenosum Patient

AbstractPyoderma gangrenosum (PG) is a rare, inflammatory neutrophil-mediated disorder that is hard to treat. PG generally arises at sites of minor trauma. Its etiology is mostly unknown, T cell activation, abnormal neutrophil migration, and tumor necrosis factor (TNF), and interleukin (IL)-17 signaling seems to play key roles in pathogenesis. In spite of their beneficial efficacy in psoriasis, TNF inhibitors, have been connected in paradoxical anti-TNF-induced psoriasis. The present case discussed the effectiveness of adjunct treatment, in the particular induction and preservation of remission from anti-TNF-induced psoriasis.

Case ReportA 67-year-old female with refractory PG treated with TNF inhibitors, who unexpectedly developed psoriasis. An interleukin-17 inhibitor, was further added to her regimen, ensuing in successful treatment of her psoriasis. She had a history of severe, deteriorating PG requiring multi-drug therapy, with an ulcer at the site of a current skin biopsy.

In these, systemic steroids are most frequently used, followed by cyclosporine and biologics, with equal efficacy noted between prednisolone and cyclosporine.Nine months after starting her altered regimen, she was treated with topical corticosteroids for presumed seborrheic dermatitis. After completing the course of two months, the lesions extended to include well-demarcated, erythematous scaling plaques on her arms, trunk, scalp, and lower extremities. Assessment for fungal etiologies with KOH staining was negative.

She was put under treatment with a multidrug regimen of cyclosporine and prednisone.

ConclusionIn few cases of paradoxical psoriasis with precise underlying disease, patients can apparently abide the causal TNF inhibitor. Paradoxical skin reactions should be measured when new cutaneous lesions appear in a patient with no earlier immuno-mediated long-lasting skin condition or as a changed morphology of an already prevailing skin disease.

Suggested reading1.    Kirkham B, Mease PJ, Nash P, et al. AB0945 Secukinumab efficacy in patients with active psoriatic arthritis: pooled analysis of four phase 3 trials by prior anti-tnf therapy and concomitant methotrexate use. Ann Rheum Dis. 2018;77(Suppl 2):1597.2.    Farhangian ME, Feldman SR. Immunogenicity of biologic treatments for psoriasis: therapeutic consequences and the potential value of concomitant methotrexate. Am J ClinDermatol. 2015;16(4):285-294.3.    Yiu ZZ, Griffiths CE. Interleukin 17-A inhibition in the treatment of psoriasis. Expert Rev ClinImmunol. 2016;12(1):1-4.4.    Krstic A, Mojsilovic S, Jovcic G, Bugarski D. The potential of interleukin-17 to mediate hematopoietic response. Immunol Res. 2012;52(1-2):34-41.5.    Ye P, Rodriguez FH, Kanaly S, et al. Requirement of interleukin 17 receptor signaling for lung Cxc chemokine and granulocyte colony-stimulating factor expression, neutrophil recruitment, and host defense. Int J ClinExp Med. 2001;194(4):519-528.6.    Marzano AV, Fanoni D, Antiga E, et al. Expression of cytokines, chemokines and other effector molecules in two prototypic autoinflammatory skin diseases, pyoderma gangrenosum and Sweets syndrome. ClinExpImmunol. 2014;178(1):48-56.