Induction and exacerbation of psoriasis with Interferon‐alpha therapy for hepatitis C: A review and analysis of 36 cases

Abstract

Background Interferon-alpha (IFN-α) therapy is used to treat hepatitis C infection. The exacerbation and occurrence of psoriasis in hepatitis C patients treated with IFN-α is increasingly recognized, but the distinct associated features, etiology, and management have not been reviewed. Objective To review all published cases of hepatitis C patients who developed psoriasis while receiving IFN-α therapy. Methods The review was conducted by searching the PubMed database using the keywords “hepatitis C” AND “psoriasis.” In addition, references to additional publications not indexed for PubMed were followed to obtain a complete record of published data. Results We identified 32 publications describing 36 subjects who developed a psoriatic eruption while receiving IFN-α therapy for hepatitis C. Topical therapies were a commonly employed treatment modality but led to resolution in only 30% of cases in which they were employed solely. Cessation of IFN-α therapy led to resolution in 93% of cases. 100% of those who developed psoriasis while on IFN-α therapy responded to systemic therapy and were able to continue the drug. Conclusion Further studies and analysis of IFN-α-induced lesions are necessary to clarify the role of IFN-α and the hepatitis C virus in the development of psoriatic lesions.

Study of T helper 1 and T helper 2 responses in pemphigus vulgaris patients receiving interferon alpha 2a injections in addition to a standard protocol therapy: a randomized controlled trial

“…Furthermore, for this whereas, in the current study only four weekly doses were given for a total period of 1 month. Moreover, IFN is mainly involved in causing Th1 autoimmune diseases such as psoriasis and lichen planus rather than Th2 autoimmune disorders [1,18]. Furthermore, the concomitantly given immunosuppressive therapy would offer a safety belt against the occurrence of such a remote complication.…”

Therapeutic Elimination of the Type 1 Interferon Receptor for Treating Psoriatic Skin Inflammation

“…Although correlative evidence from human studies (Afshar et al, 2013, Tas and Atsu, 2015, Kolb-Maurer et al, 2015, Baechler et al, 2006) and results obtained in human psoriatic skin grafted onto immunocompromised mice (Nestle et al, 2005) suggested the role of IFN in psoriatic inflammation, the mechanistic importance of IFN signaling remained controversial based on variable strength of attenuation of the imiquimod-induced inflammation in Ifnar1 -null mice (Grine et al, 2015, Wohn et al, 2013). The latter phenotype might have been underestimated because it was compared with wild type mice where wild type IFNAR1 can undergo accelerated inflammation-induced ubiquitination and downregulation.…”

“…Several lines of evidence suggest the importance of IFN in the pathogenesis of psoriasis. First, iatrogenic development or exacerbation of psoriasis associated with the use of pharmacologic IFN was reported in patients who received IFN to treat hepatitis C, multiple sclerosis, or malignant melanoma (Afshar et al, 2013, Tas and Atsu, 2015, Kolb-Maurer et al, 2015). Second, induction of the IFN-stimulated gene expression signature has been described in samples from psoriasis patients (Baechler et al, 2006, Kim and Krueger, 2015).…”

Dual Inhibition of TNFR1 and IFNAR1 in Imiquimod-Induced Psoriasiform Skin Inflammation in Mice

“…This is an upregulation of type I IFN-inducible genes or genes containing IFN-sensitive response elements (ISREs) found in tissues such as skin lesions in psoriasis and the inflamed joints of rheumatoid arthritis patients (16)(17)(18)(19). Similarly, treatment of patients affected by hepatitis C or multiple sclerosis with IFN-a or IFN-b, respectively, is associated with induction or exacerbation of psoriasis, indicating that type I IFNs can be involved in the pathogenesis of psoriasis (20)(21)(22). Paradoxically, TNF-blocking agents can also induce cutaneous psoriasis-like lesions in patients treated for other autoimmune disorders.…”