Paradoxical Psoriasis Induced by Anti-TNFα Treatment: Evaluation of Disease-Specific Clinical and Genetic Markers

Bucalo, Agostino; Rega, Federica; Zangrilli, Arianna; Silvestri, Valentina; Valentini, Virginia; Scafetta, Giorgia; Marraffa, Federica; Grassi, Sara; Rogante, Elena; Piccolo, Arianna; Cucchiara, Salvatore; Viola, Franca; Bianchi, Luca; Ottini, Laura; Richetta, Antonio Giovanni

doi:10.3390/ijms21217873

Cited by 23 publications

(15 citation statements)

References 54 publications

(110 reference statements)

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“…Surprisingly, TNFα inhibition can cause de novo disease or reactivation of inflammatory disease, such as psoriasis, arthritis, colitis, uveitis, etc. [ 318 ].…”

Section: Discussionmentioning

confidence: 99%

Harnessing Tumor Necrosis Factor Alpha to Achieve Effective Cancer Immunotherapy

Mercogliano

Bruni

Mauro

et al. 2021

Cancers

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Tumor necrosis factor alpha (TNFα) is a pleiotropic cytokine known to have contradictory roles in oncoimmunology. Indeed, TNFα has a central role in the onset of the immune response, inducing both activation and the effector function of macrophages, dendritic cells, natural killer (NK) cells, and B and T lymphocytes. Within the tumor microenvironment, however, TNFα is one of the main mediators of cancer-related inflammation. It is involved in the recruitment and differentiation of immune suppressor cells, leading to evasion of tumor immune surveillance. These characteristics turn TNFα into an attractive target to overcome therapy resistance and tackle cancer. This review focuses on the diverse molecular mechanisms that place TNFα as a source of resistance to immunotherapy such as monoclonal antibodies against cancer cells or immune checkpoints and adoptive cell therapy. We also expose the benefits of TNFα blocking strategies in combination with immunotherapy to improve the antitumor effect and prevent or treat adverse immune-related effects.

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“…Surprisingly, TNFα inhibition can cause de novo disease or reactivation of inflammatory disease, such as psoriasis, arthritis, colitis, uveitis, etc. [ 318 ].…”

Section: Discussionmentioning

confidence: 99%

Harnessing Tumor Necrosis Factor Alpha to Achieve Effective Cancer Immunotherapy

Mercogliano

Bruni

Mauro

et al. 2021

Cancers

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“…126 More recently, enrichment in a polymorphism in TNF-a (rs1799964) was found in patients with paradoxical psoriasis with TNFi compared to those without in a small cohort of 53 patients with IBD. 127 Further study to validate these findings is needed, but genetic variants may have an expanded role in future selection of early therapies.…”

Section: Predictors Of Adverse Events With Inflammatory Bowel Disease Therapymentioning

confidence: 99%

Approach to the Management of Recently Diagnosed Inflammatory Bowel Disease Patients: A User’s Guide for Adult and Pediatric Gastroenterologists

et al. 2021

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Inflammatory bowel diseases (IBDs), including Crohn's disease and ulcerative colitis, are chronic, progressive, immune-mediated diseases of adults and children that have no cure. IBD can cause significant morbidity and lead to complications such as strictures, fistulas, infections, and cancer. In children, IBD can also result in growth impairment and pubertal delays. IBD is highly heterogenous, with severity ranging from mild to severe and symptoms ranging from mild to debilitating. Delay in IBD diagnosis, especially in Crohn's disease, is common and associated with adverse outcomes. Early diagnosis and prompt institution of treatment are the cornerstones for improving outcomes and maximizing health. Early diagnosis requires a low threshold of suspicion and red flags to guide early specialist referral at the primary provider level. Although the armamentarium of IBD medications is growing, many patients will not respond to treatment, and the selection of first-line therapy is critical. Risk stratification of disease severity, based on clinical, demographic, and serologic markers, can help guide selection of first-line therapy. Clinical decision support tools, genomics, and other biomarkers of response to therapy and risk of adverse events are the future of personalized medicine. After starting appropriate therapy, it is important to confirm remission using objective end points (treat to target) with continued control of inflammation with adjustment of therapy using surrogate biomarkers (tight control). Lastly, IBD therapy extends far beyond medications, and other aspects of the overall health and wellbeing of the patient are critical. These include preventive health, nutrition, and psychobehavioral support addressing patients' concerns around complementary therapy and medication adherence, prevention of disability, and ensuring open communication.

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“…28 to have increased risk of paradoxical psoriasis. 29 Other genes implicated in the development of paradoxical psoriasis include FBXL19, CTLA4, TAP1, and SLC12A8. 30 These genetic polymorphisms may also predict treatment response to topical therapies and help delineate why ustekinumab may be effective for the concomitant treatment of both IBD and TNFα inhibitor-induced psoriasis.…”

Section: Discussionmentioning

confidence: 99%

Paradoxical psoriasis in pediatric patients: A systematic review

Cyrenne

Parpia

Sibbald

2021

Pediatric Dermatology

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Background: Paradoxical psoriasis occurs in pediatric patients following treatment with biologic agents. These presentations are not well described, and optimal treatment strategies have not been established. Objective:To describe the reported rates, demographic characteristics, clinical presentation, and treatment options for TNFα inhibitor-induced psoriasis.Methods: Systematic review of published cases and cohort studies of paradoxical psoriasis induced by biologic agents, with specific reference to TNFα inhibitors. Results:We identified 4564 pediatric patients treated with TNFα inhibitors, of whom 210 (4.6%) developed paradoxical psoriasis. Infliximab was the drug most likely to induce psoriasis (8.3%), followed by adalimumab (3.3%). Individual-level data were acquired from 129 individuals with a mean age of 13.6 years (SD: 4.0); 45.0% were male. The scalp was the most commonly affected area (47.5%), followed by the ears (30.8%). Most (63.3%) patients were continued on TNFα inhibitor therapy. Among those who switched TNFα inhibitors, only 32.0% had complete clearance of their skin lesions. Among patients who were switched to a non-TNFα inhibitor, 81% had complete clearance of their paradoxical psoriasis.Limitations: Data were acquired from retrospective studies including case reports and case series. Conclusion:TNFα inhibitor-induced psoriasis is a common adverse effect; however, most patients can continue their original therapy and be managed with skin-directed topical or systemic medications. If a patient requires medication discontinuation, switching to a new TNFα inhibitor is unlikely to lead to resolution of their skin lesions.

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Paradoxical Psoriasis Induced by Anti-TNFα Treatment: Evaluation of Disease-Specific Clinical and Genetic Markers

Cited by 23 publications

References 54 publications

Harnessing Tumor Necrosis Factor Alpha to Achieve Effective Cancer Immunotherapy

Harnessing Tumor Necrosis Factor Alpha to Achieve Effective Cancer Immunotherapy

Approach to the Management of Recently Diagnosed Inflammatory Bowel Disease Patients: A User’s Guide for Adult and Pediatric Gastroenterologists

Paradoxical psoriasis in pediatric patients: A systematic review

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