Psoriasis Associated with HCV and Exacerbated by Interferon Alpha: Complete Clearance with Acitretin during Interferon Alpha Treatment for Chronic Active Hepatitis

Erkek, Emel; Karaduman, Ayşen; Akcan, Yusuf; Sökmensüer, Cenk; Bükülmez, Gül

doi:10.1159/000018447

Cited by 27 publications

(40 citation statements)

References 12 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: 63%

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: 63%

Psoriasis Associated with Hepatitis C but Not with Hepatitis B

Cohen

Weitzman²,

Birkenfeld³

et al. 2010

Dermatology

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“…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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“…Nevertheless, several observations suggest that IFN-a might be involved. The use of IFN-a as a therapeutic agent in some susceptible individuals has led to the development or aggravation of psoriasis (Conlon et al, 1990;Funk et al, 1991;Pauluzzi et al, 1993;Brenard, 1997;Calvino et al, 1999;Erkek et al, 2000), and the association between psoriasis and chronic viral infections has been reported (Yamamoto et al, 1995;Erkek et al, 2000). Furthermore, the immunoregulatory actions of IFN-a include upregulation of type 1 immune responses through the direct or indirect enhancement of differentiation and activation of both CD4 þ Th1 cells and CD8 þ Tc1 cells, and NK cell activation (Ortaldo et al, 1980;Brinkmann et al, 1993;Tough et al, 1996;Brassard et al, 2002).…”

mentioning

confidence: 99%

Increased Sensitivity to Interferon-α in Psoriatic T Cells

Eriksen

Lovato

Skov

et al. 2005

Journal of Investigative Dermatology

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Psoriasis is a chronic inflammatory skin disease characterized by abnormal epidermal proliferation. Several studies have shown that skin-infiltrating activated T cells and cytokines play a pivotal role during the initiation and maintenance of the disease. Interferon (IFN)-alpha plays an important role in host defense against infections, but recent data have also implicated IFN-alpha in psoriasis. Thus, IFN-alpha induces or aggravates psoriasis in some patients, and mice lacking a transcriptional attenuator of IFN-alpha/beta signaling spontaneously develop a psoriasis-like inflammatory skin disease characterized by CD8(+)-infiltrating T cells. In this study, we therefore investigate IFN-alpha signaling in T cells isolated from involved skin of psoriatic patients. We show that psoriatic T cells have increased and prolonged responses to IFN-alpha, on the level of signal transducers and activators of transcription (STAT) activation, compared with infiltrating T cells from skin of non-psoriatic donors. Functionally, the increased IFN-alpha signaling leads to an increased binding of STAT4 to the IFN-gamma promotor, IFN-gamma production, and inhibition of T cell growth. In contrast, to STAT responses to other cytokines were not changed in psoriasis. In conclusion, we provide evidence that psoriatic T cells have an increased sensitivity to IFN-alpha. Thus, our data suggest that increased IFN-alpha signaling is involved in the pathogenesis of psoriasis.

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Psoriasis Associated with HCV and Exacerbated by Interferon Alpha: Complete Clearance with Acitretin during Interferon Alpha Treatment for Chronic Active Hepatitis

Cited by 27 publications

References 12 publications

Psoriasis Associated with Hepatitis C but Not with Hepatitis B

Psoriasis Associated with Hepatitis C but Not with Hepatitis B

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

Increased Sensitivity to Interferon-α in Psoriatic T Cells

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