Biologic therapies associated with development of palmoplantar pustulosis and palmoplantar pustular psoriasis: a systematic review.

BACKGROUND: Palmoplantar pustulosis (PPP) and palmoplantar pustular psoriasis (PPPP) are chronic inflammatory skin conditions characterized by eruptions of sterile pustules on the palms and/or soles. Biologic use has been associated with PPP and PPPP development in the literature. OBJECTIVES: To identify PPP and PPPP associated with biologics and summarize reported treatments and outcomes. METHODS: We systematically searched in MEDLINE and Embase for articles that reported PPP or PPPP during biologic treatment. After a full-text review, 53 studies were included for analysis. RESULTS: We identified 155 patients with PPP/PPPP onset during biologic treatment, with a mean age of 44.1 years and a female preponderance (71.6%). The most frequently reported biologics were adalimumab (43.9%) and infliximab (33.3%). IL-17 inhibitors, secukinumab (7.6%) and brodalumab (1.5%), were reported only in association with PPPP. Overall, 58.8% of patients had complete remission (CR) in 3.6 months and 23.5% had partial remission (PR) in 3.7 months. The most common treatments that led to CR were topical corticosteroids (n = 16) and biologic switching (n = 8). CONCLUSIONS: Clinicians should anticipate PPP or PPPP as potential drug reactions to biologics such as adalimumab and infliximab. Large-scale studies are required to confirm our findings and further explore the pathogenesis for biologic-associated PPP and PPPP.

A Systematic Review Characterizing Psoriatic Arthritis Onset and Exacerbation in Patients Receiving Biologic Therapy.

BACKGROUND: While biologic therapies revolutionized treatment of immune-mediated inflammatory diseases (IMIDs), some adverse effects have been noted. This includes the development and exacerbation of PsA in patients on biologic agents, however the outcomes were not extensively explored. OBJECTIVE: To perform a systematic review to characterize the outcomes of PsA onset or exacerbation secondary to biologic use. METHODS: MEDLINE and EMBASE search conducted on March 23, 2021 resulted in 18 studies comprised of 64 patients. RESULTS: Of the 64 patients, 57 (89.1%) experienced new-onset PsA and 7 (10.9%) experienced exacerbation of preexisting PsA following exposure to a biologic; most commonly a TNF-α inhibitor (42.2%, n = 27/64) and IL-12/23 inhibitors (39.1%, n = 25/64). The mean durations of biologic use before PsA onset and exacerbation were 14.8 months and 5.2 months, respectively. Twenty-four patients (44.4%) subsequently switched to an alternate biologic without further reports of PsA-related adverse events. All 64 patients reported a specific treatment for PsA; most commonly discontinuation of the associated biologic agent (32.8%, n = 21/64). Complete resolution of PsA was reported in 35.9% (n = 23/64) of cases, of which 91.3% (n = 21/23) resulted after discontinuation of biologic. CONCLUSION: Although we characterized outcomes of PsA induction and exacerbation secondary to biologic use, large-scale studies are required.

Onset of Pyoderma Gangrenosum in Patients on Biologic Therapies: A Systematic Review.

OBJECTIVE: To summarize clinical outcomes of paradoxical pyoderma gangrenosum (PG) onset in patients on biologic therapy. METHODS: The authors conducted MEDLINE and EMBASE searches using PRISMA guidelines to include 57 patients (23 reports). RESULTS: Of the included patients, 71.9% (n = 41/57) noted PG onset after initiating rituximab, 21.1% (n = 12/57) noted tumor necrosis factor α (TNF-α) inhibitors, 5.3% (n = 3/57) reported interleukin 17A inhibitors, and 1.8% (n = 1/57) reported cytotoxic T-lymphocyte-associated protein 4 antibodies. The majority of patients (94.3%) discontinued biologic use. The most common medications used to resolve rituximab-associated PG were intravenous immunoglobulins, oral corticosteroids, and antibiotics, with an average resolution time of 3.3 months. Complete resolution of PG in TNF-α-associated cases occurred within an average of 2.2 months after switching to another TNF-α inhibitor (n = 1), an interleukin 12/23 inhibitor (n = 2), or treatment with systemic corticosteroids and cyclosporine (n = 3), systemic corticosteroids alone (n = 1), or cyclosporine alone (n = 1). CONCLUSIONS: Further investigations are warranted to determine whether PG onset is associated with underlying comorbidities, the use of biologic agents, or a synergistic effect. Nevertheless, PG may develop in patients on rituximab or TNF-α inhibitors, suggesting the need to monitor and treat such adverse effects.

Drugs associated with development of porokeratosis: A systematic review.

Porokeratosis is a rare disorder characterized by atrophic macules or patches, with a well-defined ridge-like hyperkeratotic border called cornoid lamella. Although the exact pathogenesis is unknown, drug associated cases have recently been reported in the literature. As such, we systematically reviewed and identified drugs associated with drug-induced porokeratosis, their resultant effects, and whether there was a casual relationship between the use of a drug and the development of porokeratosis. We searched for articles which reported drug-induced porokeratosis in MEDLINE and Embase in June 2020. After full-text review, 25 studies were included for analysis. We identified 26 patients with drug-induced porokeratosis. The most common therapies associated with development of porokeratosis is biologic use, phototherapy, and radiotherapy. The most common clinical variants were the disseminated superficial or actinic types (60%), which occurred in psoriasis patients undergoing phototherapy, and eruptive disseminated type (24%) which occurred in the context of biologic therapies. The Naranjo score ranged from possible to probable for the identified treatments. Clinicians should consider drug reactions as possible triggering events for porokeratosis, especially for patients taking biologics, phototherapy, and radiotherapy. Large-scale studies are required to confirm our findings and further explore the pathogenesis for drug-induced porokeratosis.