New onset or exacerbation of psoriatic skin lesions in patients with definite rheumatoid arthritis receiving tumour necrosis factor   antagonists

Kary, Sonja

doi:10.1136/ard.2005.037424

Cited by 118 publications

(72 citation statements)

References 9 publications

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“…In contrast, cytokine-targeting approaches with neutralizing Abs might in fact enhance the activity of the cytokine in vivo (58). In line with this, induction of psoriasis during anti-TNF-␣ therapy of rheumatoid arthritis has been reported (59,60). Apart from other side effects associated with systemic administration of neutralizing anti-cytokine biologics, our present approach would circumvent such problems.…”

Section: Discussionmentioning

confidence: 67%

Targeting NF-κB with a Natural Triterpenoid Alleviates Skin Inflammation in a Mouse Model of Psoriasis

Wang

Syrovets

Keß

et al. 2009

The Journal of Immunology

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Psoriasis vulgaris is a common chronic inflammatory skin disease involving cytokines and an activated cellular immune system. At variance to skin from patients with atopic dermatitis or from healthy subjects, human psoriatic skin lesions exhibit strong activation of transcription factor NF-κB that is mainly confined to dermal macrophages, whereas only a few dendritic cells but no CD3+ lymphocytes show activated NF-κB. Since NF-κB signaling is required for the induction and/or function of many cytokines and aberrant cytokine expression has been proposed as an underlying cause of psoriasis, we investigated whether NF-κB targeting would affect the course of the disease in the CD18 hypomorphic (CD18hypo) mouse model of psoriasis. When mice with severe psoriasiform lesions were treated systemically or locally with the IκB kinase inhibitor acetyl-11-keto-β-boswellic acid (AKβBA), NF-κB signaling and the subsequent NF-κB-dependent cytokine production as shown by the TNF-α production of macrophages were profoundly suppressed. Additionally, application of the compound counteracted the intradermal MCP-1, IL-12, and IL-23 expression in previously lesional skin areas, led to resolution of the abundant immune cell infiltrates, and significantly reduced the increased proliferation of the keratinocytes. Overall, the AKβBA treatment was accompanied by a profound improvement of the psoriasis disease activity score in the CD18hypo mice with reconstitution of a nearly normal phenotype within the chosen observation period. Our data demonstrate that NF-κB signaling is pivotal for the pathogenesis in the CD18hypo mouse model of psoriasis. Therefore, targeting NF-κB might provide an effective strategy for the treatment of psoriasis.

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Section: Discussionmentioning

confidence: 67%

Targeting NF-κB with a Natural Triterpenoid Alleviates Skin Inflammation in a Mouse Model of Psoriasis

Wang

Syrovets

Keß

et al. 2009

The Journal of Immunology

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“…Grinblat and Scheinberg [23] reported a case of psoriasis with plaques induced by infliximab; a case of pustular psoriasis associated with infliximab was described by Thurber et al [18]; Flendrie et al [24] observed 3 cases of psoriasis triggered by adalimumab; 2 patients with psoriasis induced by biological drugs were reported by Dereure et al [20]; Beuthien et al [22] described a case of palmoplantar pustular psoriasis in a patient treated with adalimumab; 8 cases of psoriasis correlated with anti-TNF-αinhibitors were documented by Kary et al [25] and another 4 by Haibel et al [26]; Baeten et al [27] reported 3 observations of palmoplantar pustular psoriasis following the administration of infliximab; another case was described by Verea et al [28]; finally, 5 cases of psoriasis triggered by biological drugs were reported by Sfikakis et al [21], 2 by Michaëlsson et al [29], 1 by Peramiquel et al [30] and 3 by Pirard et al [17]. …”

Section: Disussion and Conclusionmentioning

confidence: 99%

Cutaneous Manifestations in Inflammatory Bowel Diseases: Eight Cases of Psoriasis Induced by Anti-Tumor-Necrosis-Factor Antibody Therapy

Passarini¹,

Infusino²,

Barbieri³

et al. 2007

Dermatology

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Background: Ulcerous rectocolitis and Crohn’s disease are the best known forms of inflammatory bowel disease (IBD). Skin manifestations are not uncommon in IBD and may be divided into specific cutaneous signs, aspecific cutaneous signs, and cutaneous signs caused by drugs used for IBD therapy. The specific signs (fistulas, rhagades and ulcers) are the result of the diffusion of the intestinal inflammatory process into the skin. Aspecific cutaneous signs (stomatic aphthosis, erythema nodosum, pyoderma gangrenosum, Sweet’s syndrome, vasculitis, bullous diseases) are quite frequently found in those suffering from IBD, but also in apparently healthy subjects, and may sometimes be the first sign of the intestinal disease. Cutaneous manifestations due to drugs vary in clinical aspect and are the direct consequence of the therapies adopted, which in IBD patients can be quite numerous: steroids, immunosuppressants, 5-aminosalicylic acid, biological agents, antibiotics. Objective and Methods:Due to the frequent finding of cutaneous manifestations in patients affected by IBD, a collaboration was set up between the Dermatological Clinic of the University of Bologna and the Center for the Study of IBD of the same university hospital. The aim was to diagnose the cutaneous signs appearing during IBD and to establish their etiopathogenesis in order to assess whether they were the result of epiphenomena of the IBD or side effects of the therapies adopted. Results: The cutaneous manifestations we observed can be divided into three distinct groups: signs that were specific to the basic disease, aspecific signs and finally signs attributable to the drugs used for therapy. Particular attention was given to the aspecific signs and those consequential to therapy. The aspecific cutaneous signs seen in our clinic generally reflect those reported in the literature. The cutaneous manifestations due to drugs were further divided into three groups: rosacea, acneiform dermatitis and psoriasis-like dermatitis. The most notable aspect of our series is the high number of patients presenting psoriasiform-type dermatitides with a generally widespread diffusion. Conclusion: We would like to draw attention to the fact that all patients with psoriasis had been undergoing treatment with drugs inhibiting tumor necrosis factor α (TNF-α) as part of IBD therapy. In all cases, the cutaneous reaction started after the third or fourth infusion of the biological drug. Anti-TNF-α agents have also been successfully used to treat psoriasis in the last few years. The reason for this apparently paradoxical effect of the therapy is still unclear.

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“…Paradoxically, the induction of psoriasiform lesions by these agents has been reported in recent years (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15). We report the case of a female patient suffering from CD who developed psoriatic lesions following treatment with infliximab.…”

mentioning

confidence: 95%

Psoriasis Induced by Infliximab in a Patient Suffering from Crohn's Disease

Manni

Barachini

2009

Int J Immunopathol Pharmacol

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We describe the case of a 30-year-old female with no family history of psoriasis and suffering from Crohn's disease successfully treated with infliximab at the dosage of 5 mg/kg. At the 15th week from the start of therapy, the patient developed a palmoplantar pustular psoriasis, which spread to the arms, trunk and scalp with erythematosquamous plaques. Deeming the dermatitis onset due to the anti-TNF-α, we decided to discontinue infliximab, while starting with a topical therapy with emollients and corticosteroids and a systemic therapy with cyclosporine. These treatments achieved a clear improvement of psoriasis after 2 months and a complete regression of skin lesions after 4 months. Several cases have been reported of psoriasis induced by anti-TNF-α, which have shown to exert an effective therapeutic action on this disease. The pathogenic mechanism of such a paradoxical effect has not yet been explained, though a number of hypotheses were proposed, among which one of the most intriguing is that the rapid and strong blockade of TNF-α could result in an enhancement of INF-α activity with consequent induction of psoriasis.

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New onset or exacerbation of psoriatic skin lesions in patients with definite rheumatoid arthritis receiving tumour necrosis factor antagonists

Cited by 118 publications

References 9 publications

Targeting NF-κB with a Natural Triterpenoid Alleviates Skin Inflammation in a Mouse Model of Psoriasis

Targeting NF-κB with a Natural Triterpenoid Alleviates Skin Inflammation in a Mouse Model of Psoriasis

Cutaneous Manifestations in Inflammatory Bowel Diseases: Eight Cases of Psoriasis Induced by Anti-Tumor-Necrosis-Factor Antibody Therapy

Psoriasis Induced by Infliximab in a Patient Suffering from Crohn's Disease

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