LAUSR

We recently reviewed the currently available data supporting the promising role of direct-acting antiviral (DAA) therapy for hepatitis C virus (HCV) in subset of psoriatic patients; HCV-positive. On the contrary, few recent reports of an exacerbated or triggered psoriasis has been published, that might be post-dated preparing of our original manuscript (Abdelmaksoud & Vestita, 2018). These reports drew our attention to review. As we reviewed these reports, we came to certain observations that might be of significance to both patients and treating physicians (Heppt & Sticherling, 2017; Oliveira et al., 2018; Wang & Liu, 2017). We observed the following: (a) total number of the reported cases in the three published reports were only six patients; (b) male: female ratio was 2:1; (c) all of the patients were above 40 years; (d) all had history of chronic plaque psoriasis, except one; (e) initial anti-psoriatic therapies before DAAs were: (i) traditional Chinese medicine, and ultraviolet irradiation, (ii) pegylated interferon (IFN)-α and ribavirin, (iii) topical remedies/ narrowband-ultraviolet B (NB-UVB); (f) the reactions developed within 23–90 days post-initiation of DAAs; (g) all showed exacerbation of chronic plaque psoriasis, except onewho developed erythrodermic psoriasis and erythema multiforme; (h) treat through, maintaining the treatment with DAAs (with greater improvement on discontinuation) in three cases and improvement in one patient within 7 weeks without withdrawal of the DAAs; (i) topical therapy and/or NB-UVB were the main treatment options; (j) only one case required cyclosporine (erythrodermic psoriasis); (k) three patients had history of hepatic cirrhosis, a known risk factor for hepatocellular carcinoma. Experts suggested that DAAs do not have direct carcinogenic effects. (l) DAA-induced or exacerbated psoriasis condition has no clear explanation, however it could be explained by direct immunological drug effects or by immune-infectious changes (“reconstitution” syndrome with DAAs) (Heppt & Sticherling, 2017; Najafi Fard et al., 2018). The reported cases of DAAs-induced/exacerbated psoriasis were summarized in Table 1. A higher prevalence of HCV in adults with psoriasis and a higher rate of hepatic decompensation in HCV+ individuals with moderate–severe psoriasis has been recently observed (Noe et al., 2017). HCV chronic infection causes overproduction of tumor necrosis factor-α (TNF-α), which might induce psoriasis in patients with a certain genetic and/or environmental predisposition. TNF-α represents a key cytokine for both hepatitis C progression and psoriasis. Chun et al. hypothesized that HCV infection may also increase expression of cathelicidin, IFN-γ, and TLR9, thus further contributing to the pathogenesis of psoriasis, regardless of IFN treatment (Chun et al., 2017). TNF-α inhibitors seem to be a safe and effective option in HCV positive psoriatic patients, but concerns