Exacerbation of psoriasis by interferon-alpha therapy for hepatitis C

Downs, A. M. R.; Dunnill, M.G.S.

doi:10.1046/j.1365-2230.2000.00655-4.x

Cited by 57 publications

(65 citation statements)

References 6 publications

(7 reference statements)

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“…IFN-α is a recommended treatment for patients with hepatitis C. The exacerbation or triggering of psoriasis by IFN-α has been previously reported [12,13,14,15,16,17]. However, in the present study, most hepatitis C patients were not taking IFN-α, and the association with psoriasis was strongly evident among patients not taking IFN-α.…”

Section: Discussioncontrasting

confidence: 62%

Psoriasis Associated with Hepatitis C but Not with Hepatitis B

Cohen

Weitzman²,

Birkenfeld³

et al. 2010

Dermatology

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Purpose: To investigate the association between psoriasis and viral hepatitis. Methods: Psoriasis patients were compared to controls regarding the prevalence of viral hepatitis in a case-control study using logistic multivariate models. The study was performed utilizing the medical database of Clalit Health Services. Results: The study included 12,502 psoriasis patients >20 years old and 24,287 age- and sex-matched controls. The prevalence of hepatitis C in patients with psoriasis was increased compared to the prevalence in controls (1.03 vs. 0.56%; p < 0.001). In a multivariate analysis, psoriasis was associated with hepatitis C. An interaction with smoking was noted (smokers: odds ratio, OR = 1.93, 95% confidence interval, CI = 1.30–2.67; nonsmokers: OR = 2.22, 95% CI = 1.63–3.04). The prevalence of hepatitis B in patients with psoriasis was higher than in the controls (0.74 vs. 0.56%; p = 0.043). However, in a multivariate analysis psoriasis was not associated with hepatitis B (OR = 1.22, 95% CI = 0.93–1.60, p = 0.15). Conclusion: Our observation supports previous reports of an association between psoriasis and hepatitis C but not with hepatitis B. Physicians who care for patients with psoriasis should be aware of this possible association and consider screening patients with psoriasis for hepatitis C.

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Section: Discussioncontrasting

confidence: 62%

Psoriasis Associated with Hepatitis C but Not with Hepatitis B

Cohen

Weitzman²,

Birkenfeld³

et al. 2010

Dermatology

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“…Psoriatic skin has a strong IFNI transcriptional fingerprint (e.g., activation of numerous IFNI-inducible genes (37,38)). Moreover, psoriasis patients receiving IFNI therapy for unrelated conditions can develop exacerbated psoriasis symptoms (39,40). Direct evidence for a pathogenic role for pDCs and IFNI in psoriasis is provided by a human/mouse skin xenograft model in which uninvolved skin of psoriasis donors is transplanted onto AGR129 mice that are deficient in recombination activating gene 2 and type I and II IFN receptors.…”

Section: Discussionmentioning

confidence: 99%

Secretory Leukocyte Proteinase Inhibitor-Competent DNA Deposits Are Potent Stimulators of Plasmacytoid Dendritic Cells: Implication for Psoriasis

Skrzeczyńska‐Moncznik

Włodarczyk

Zabieglo

et al. 2012

The Journal of Immunology

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Secretory leukocyte proteinase inhibitor (SLPI) is a well-established inhibitor of serine proteases such as human neutrophil elastase (HNE) and a NF-κB regulatory agent in immune cells. In this paper, we report that SLPI plays a previously uncharacterized role in regulating activation of plasmacytoid dendritic cells (pDCs). As the main source of IFN type I (IFNI), pDCs are crucial contributors to inflammatory and likely wound-healing responses associated with psoriasis. The mechanisms responsible for activation of pDCs in psoriatic skin are therefore of substantial interest. We demonstrate that in lesional skin of psoriasis patients, SLPI together with its enzymatic target HNE and DNA, is a component of neutrophil extracellular traps (NETs). Whereas SLPI+ neutrophils and NETs were found to colocalize with pDCs in psoriatic skin, a mixture of SLPI with neutrophil DNA and HNE induced a marked production of IFNI by pDCs. IFNI synthesis by stimulated pDCs was dependent on intracellular DNA receptor TLR9. Thus, SLPI may contribute to psoriasis by enabling pDCs to sense extracellular DNA and produce IFNI.

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“…Interferons modulate immune function through actions on natural killer cells, T-cell cytotoxicity and expression of human leukocyte antigens on cells [9,13,16,17] . Histopathologic studies have shown that development of T-cell-attracting compounds initiates the psoriatic process [9,13,18,19] .…”

Section: Discussionmentioning

confidence: 99%

“…Histopathologic studies have shown that development of T-cell-attracting compounds initiates the psoriatic process [9,13,18,19] . The mechanisms by which interferon may cause a fl are-up of psoriasis are unclear, but it has been speculated that it could involve an interaction between interferon and other cytokines [9,12] .…”

Section: Discussionmentioning

confidence: 99%

Exacerbation of Psoriasis due to Peginterferon alpha-2b plus Ribavirin Treatment of Chronic Active Hepatitis C

Kartal

Çolak²,

Özgüneş³

et al. 2005

Chemotherapy

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A 45-year-old woman with chronic hepatitis C was treated with peginterferon alpha-2b in combination with ribavirin, which activated psoriasis. In the patient, psoriasis reoccurred after being inactive for 10 years. One week after institution of therapy, she presented with plaques of psoriasis at her injection site having been administered a first dose of peginterferon alpha-2b. Psoriatic lesions of the patient worsened dramatically during therapy. Cutaneous lesions appeared at the injection sites, in the face, the scalp hair, at the back of the ears, under the breasts and armpits, and in the regions of the anus and elbows. In the second week of treatment, transaminase levels of the patient regressed to normal. Detectable hepatitis C virus RNA in the serum was eliminated at week 14 of treatment. Because of the severity of psoriatic disease activity, therapy was discontinued at the end of 14 weeks after treatment onset. This side effect of peginterferon alpha-2b plus ribavirin treatment should be kept in mind in the treatment of patients with a history of psoriasis combined with active hepatitis C.

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Exacerbation of psoriasis by interferon-alpha therapy for hepatitis C

Cited by 57 publications

References 6 publications

Psoriasis Associated with Hepatitis C but Not with Hepatitis B

Psoriasis Associated with Hepatitis C but Not with Hepatitis B

Secretory Leukocyte Proteinase Inhibitor-Competent DNA Deposits Are Potent Stimulators of Plasmacytoid Dendritic Cells: Implication for Psoriasis

Exacerbation of Psoriasis due to Peginterferon alpha-2b plus Ribavirin Treatment of Chronic Active Hepatitis C

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