Nine months after starting her modified regimen, she returned to clinic with several new, well-demarcated, erythematous postauricular plaques. She was treated with topical corticosteroids for presumed seborrheic dermatitis. Over the course of two months, the lesions expanded to include well-demarcated, erythematous scaling plaques on her arms, trunk, scalp, and lower extremities (Figure 3a). Evaluation for fungal etiologies with KOH staining was negative. A diagnosis of adalimumab-induced psoriasis was favored, and she was started on secukinumab.
Within weeks of starting secukinumab, her psoriasis resolved despite remaining on adalimumab concurrently (Figure 3b). At this point, she had complications with insurance coverage and underwent numerous lapses in follow up visits, necessitating multiple medication changes (Figure 2). She later transitioned to secukinumab-only therapy but when her PG symptoms returned, secukinumab was discontinued and she was treated instead with a multidrug regimen of prednisone, cyclosporine, and mycophenolate mofetil.
When adalimumab (40 mg weekly) was approved by her insurance, it was restarted with the addition of methotrexate prophylactically to prevent another episode of adalimumabinduced psoriasis. With this combination, her PG symptoms went into remission without evidence of psoriasiform lesions for greater than one year to date (Figure 2).
When adalimumab (40 mg weekly) was approved by her insurance, it was restarted with the addition of methotrexate prophylactically to prevent another episode of adalimumabinduced psoriasis. With this combination, her PG symptoms went into remission without evidence of psoriasiform lesions for greater than one year to date (Figure 2).
DISCUSSION
Treatment of Pyoderma Gangrenosum
PG is a complex and multifactorial neutrophilic dermatosis requiring multi-drug therapy.4,5 It is estimated to occur in approximately 3 to 10 people per million per year.6 Although this disease is traditionally difficult to diagnose,7 recent diagnostic guidelines have been proposed.8,9 Currently, there are two randomized controlled trials (RCTs), multiple cohort studies , and limited open-label and case-control studies detailing treatment.10,11 In these, systemic steroids are most often used, followed by cyclosporine and biologics, with equivalent efficacy noted between prednisolone and cyclosporine.10
Infliximab, a TNF antagonist, is typically used in refractory cases of PG.10 Additional studies have documented PG remission with similar biologics, including adalimumab, etanercept, anakinra, and ustekinumab, but responses are often partial.12,13 In addition to partial response, TNF inhibitors can have unanticipated side effects, including paradoxical psoriasis. In fact, psoriasis is the third leading skin complication of anti-TNF therapy, behind xerosis and atopic dermatitis.14 And while there are over one hundred reported cases of TNF inhibitor-induced psoriasis,15 ours is the first to demonstrate this phenomenon in a PG patient.
Treatment of TNF-Inhibitor Induced Psoriasis
When TNF-inhibitor paradoxical reactions occur, the first step in management is commonly thought to be discontinuation of the offending agent. However, current literature provides conflicting data on this point. A recent review of anti-TNF-induced psoriasis recommends switching to a different agent or class of medications only in the setting of uncontrolled underlying disease.16 Another review of 222 cases of paradoxical psoriasis found that nearly 40% of patients continue therapy with either the same or a different TNF inhibitor and 74% of these patients achieve complete remission of their paradoxical psoriasis.17 As a result, in at least some cases of paradoxical psoriasis with controlled underlying disease, patients can seemingly tolerate the causative TNF inhibitor. Our case demonstrates that paradoxical psoriatic lesions can resolve in patients who continue the offending anti- TNF agent with the addition of a second immunosuppressive therapy, even in the setting of uncontrolled underlying disease.
Here we illustrated the efficacy of secukinumab and, subsequently, methotrexate as adjunct agents in treating TNFinhibitor- induced psoriasis. These treatments have yet to be
PG is a complex and multifactorial neutrophilic dermatosis requiring multi-drug therapy.4,5 It is estimated to occur in approximately 3 to 10 people per million per year.6 Although this disease is traditionally difficult to diagnose,7 recent diagnostic guidelines have been proposed.8,9 Currently, there are two randomized controlled trials (RCTs), multiple cohort studies , and limited open-label and case-control studies detailing treatment.10,11 In these, systemic steroids are most often used, followed by cyclosporine and biologics, with equivalent efficacy noted between prednisolone and cyclosporine.10
Infliximab, a TNF antagonist, is typically used in refractory cases of PG.10 Additional studies have documented PG remission with similar biologics, including adalimumab, etanercept, anakinra, and ustekinumab, but responses are often partial.12,13 In addition to partial response, TNF inhibitors can have unanticipated side effects, including paradoxical psoriasis. In fact, psoriasis is the third leading skin complication of anti-TNF therapy, behind xerosis and atopic dermatitis.14 And while there are over one hundred reported cases of TNF inhibitor-induced psoriasis,15 ours is the first to demonstrate this phenomenon in a PG patient.
Treatment of TNF-Inhibitor Induced Psoriasis
When TNF-inhibitor paradoxical reactions occur, the first step in management is commonly thought to be discontinuation of the offending agent. However, current literature provides conflicting data on this point. A recent review of anti-TNF-induced psoriasis recommends switching to a different agent or class of medications only in the setting of uncontrolled underlying disease.16 Another review of 222 cases of paradoxical psoriasis found that nearly 40% of patients continue therapy with either the same or a different TNF inhibitor and 74% of these patients achieve complete remission of their paradoxical psoriasis.17 As a result, in at least some cases of paradoxical psoriasis with controlled underlying disease, patients can seemingly tolerate the causative TNF inhibitor. Our case demonstrates that paradoxical psoriatic lesions can resolve in patients who continue the offending anti- TNF agent with the addition of a second immunosuppressive therapy, even in the setting of uncontrolled underlying disease.
Here we illustrated the efficacy of secukinumab and, subsequently, methotrexate as adjunct agents in treating TNFinhibitor- induced psoriasis. These treatments have yet to be
