Clinical Pathologic Mismatch in a TNF-α Inhibitor-Associated Drug Reaction
August 2019 | Volume 18 | Issue 8 | Case Reports | 218 | Copyright © August 2019
Kathleen F. O’Brien MS,ª Rachel E. Maiman MD,B Christine A. DeWitt MDB
aGeorgetown University School of Medicine, Washington, DC, bMedstar Georgetown University Hospital, Department of Dermatology, Washington, DC
A 56-year-old Caucasian male with a history of chronic plaque psoriasis, primary sclerosing cholangitis status-post liver transplant on tacrolimus, and ulcerative colitis on infliximab developed a progressive erythematous eruption with associated fatigue, anorexia, myalgias, and arthralgias. On two separate occasions, his skin biopsy demonstrated a lichenoid interface dermatitis (LID). Despite multiple courses of oral prednisone, topical steroids, and a short course of hydroxychloroquine, his symptoms continued to relapse and remit. When a temporal association between increasing his infliximab dose and the global progression of his disease was identified, he was ultimately diagnosed with a TNF-α inhibitor-induced psoriasis flare.
Despite the patient’s long-standing history of psoriasis, a plausible psoriasis rebound reaction after systemic steroids was not strongly considered in light of his histopathology. Though lichenoid interface dermatitis is a commonly reported histologic finding in patients on TNF-α inhibitors, it has scarcely been reported in patients with psoriasiform eruptions clinically. J Drugs Dermatol. 2019;18(8):217-219.
There have been increasing reports of paradoxical inflammatory reactions induced by TNF-α inhibitors.1 Clinically, cutaneous reactions induced by TNF-α inhibitors are variable and have been described as lichenoid, psoriasiform, or a combination, though histopathology in all cases is overwhelmingly characterized by a lichenoid interface dermatitis (LID), a distinct inflammatory pattern characterized by keratinocyte damage along the basal layer of the epidermis.2 In other words, the clinical presentation in patients on TNF-α blocking agents may not correlate with the expected histopathologic pattern in its native disease form (eg, plaque psoriasis is characterized by a classic psoriasiform pattern and not a lichenoid or interface infiltrate).3,4 We herein describe a patient to illustrate this unique diagnostic challenge.
A CASE REPORT
A 56-year-old Caucasian male with a history of chronic plaque psoriasis, ulcerative colitis, and primary sclerosing cholangitis (PSC) 2 years status-post liver transplant presented with a progressive erythematous eruption of three months duration. His medications included infliximab, alprazolam, metoprolol, amlodipine, mirtazapine, and tacrolimus. There were no recent medication additions or dose adjustments. Given PSC remission post-transplant, he had been on increasing doses of infliximab, ranging 5-10 mg/kg, for management of ongoing ulcerative colitis. Two months prior, the eruption began on his hands and progressed to involve 50% of his body surface area (BSA). A pulsed 60mg prednisone taper resulted in complete resolution. Upon cessation, he experienced a rapid rebound of the dermatitis, prompting a second prednisone pulse with minimal improvement (Figure 1). Subsequent skin biopsy demonstrated an interface dermatitis with a diffuse perifollicular and perieccrine lymphocytic infiltrate (Figure 2). Anti-neutrophil antibodies (ANA) were negative and complement levels were normal. The working differential diagnosis included connective