A case of erythrodermia from exacerbated psoriasis vulgaris due to treatment of acute hepatitis C
© The Author(s). 2016
Received: 19 November 2015
Accepted: 17 May 2016
Published: 26 May 2016
Skin side effects during interferon-alpha and ribavirin treatment are common, but autoimmune dermatosis triggered by interferon-alpha is rare. We describe a case of erythrodermia from exacerbated psoriasis during the treatment of acute hepatitis C with pegylated-interferon-alpha and ribavirin. The incidence of psoriasis in this circumstance is unknown and only 36 cases are described in the literature, of which only one describes an erythrodermic psoriasis flare.
A 50-years old healthy white man presented with the complaints of headache, muscle pain, appetite loss, yellow skin complexion and fatigue. The laboratory results showed elevated liver enzymes above 50 times the upper limit of normal and a positive antibody test and RNA for hepatitis C. A screening test 6 months earlier was negative and therefore the diagnosis of an acute hepatitis C infection was most likely. In the absence of spontaneous clearance of the virus a therapy with pegylated- interferon-α and ribavirin was initiated. After 3 weeks the patient developed red scaly papular skin lesions that evolved despite treatment with prednisone to a severe erythrodermia. A skin biopsy showed typical signs for psoriasis vulgaris. Treatment with steroids was intensified and the hepatitis C therapy stopped. The patient achieved sustained virological response for hepatitis C, but psoriatic lesions were still present 6 months after treatment.
Although autoimmune skin reactions under pegylated-interferon-α and ribavirin treatment are rare it is important to recognise them early to start an adequate treatment to guarantee hepatitis C treatment continuation.
KeywordsErythrodermia Psoriasis Acute hepatitis C Pegylated-interferon-α
Therapy of chronic hepatitis C (HCV) has changed from treatment with pegylated interferon-α (peg-INF-α) and ribavirin to combinations of direct acting agents (DAA’s) that enable interferon- or even ribavirin-free regimens. Interferon-free treatment regimens show cure rates >90 %, shorter treatment durations and less side effects. But access to DAA’s is limited to patients with chronic HCV infection and because of financial constraints even to patients with advanced liver damage (severe fibrosis or cirrhosis) in most countries [1, 2]. The effect of DAA therapies in acute HCV is not clear and data are lacking. Therefore treatment with peg-INF-α +/- ribavirin for 12–24 weeks is still the standard of care for acute HCV.
Treatment related skin reactions under interferon therapy are common (13 %), but usually they are mild and discontinuation of the drugs is not necessary [3, 4]. Injection site reactions are the most frequently encountered lesions. But also alopecia, eczematous drug reactions, fixed drug or lichenoid eruptions, pigmentation changes and sarcoidosis can be seen . Seldom may an autoimmune skin disease such as psoriasis or lupus erythematodes be triggered by interferon treatment. We describe a case of erythrodermia from exacerbated psoriasis during the treatment of acute HCV with peg-INF-α and ribavirin.
Over the next weeks after HCV treatment cessation prednisone could be tapered and replaced by 50 mg acitretin per day. 6 months after treatment termination the patient still had some psoriatic lesions and acitretin was maintained.
Even though new interferon-free DAA therapies are available for the treatment of chronic HCV, standard therapy for acute HCV remains peg-INF-α for 12–24 weeks (plus ribavirin under certain conditions e.g. HIV/HCV-co-infection) . Data of treatment for acute HCV with DAA’s is lacking. Only one study in HIV/HCV co-infected men who have sex with men showed an increased sustained virological response at week 12 in patients treated with combination therapy of telaprevir/peg-INF-α/ribavirin compared to peg-INF-α/ribavirin alone . Additionally since access to interferon-free treatment is limited to patients with advanced liver damage because of high costs even treatment of chronic HCV with peg-INF-α has still to be considered in rare cases.
Erythrodermic psoriasis is a rare but a severe and disabling variant of psoriasis vulgaris . The incidence of psoriasis exacerbation by peg-INF-α therapy is unknown, but several case reports were published [8–11]. One small uncontrolled explorative study with 28 patients reported an occurrence of psoriasis in 2 % (3/28) . A case compilation by Afshar et al. found 36 cases of INF-α associated psoriasis flares ; most cases were classic plaque-type psoriasis vulgaris and only one patient showed erythrodermic psoriasis. Most psoriasis flares happened with an average delay of 1.6 months after interferon treatment initiation but with a high inter-individual variation (1 week -7 months) . Our patient’s psoriatic flare was early in the treatment course starting at week three and showing the full picture of erythrodermic psoriasis at week 10. In our case treatment had to be stopped. This is usually not necessary since mostly psoriatic skin side effects are not severe and diminish after stopping therapy . Retrospectively our patient had mild psoriatic lesions already at the initial diagnosis of HCV infection. Since they seemed well controlled without specific treatment at the time HCV treatment with peg-INF-α was not contraindicated .
The report highlights the importance of a throughout patient history and clinical examination at hepatitis C treatment initiation and – most importantly – in regular intervals thereafter. It is of utmost importance to recognise autoimmune processes like psoriasis early to be able to initiate an adequate therapy early and avoid hepatitis C treatment interruptions. It should be noted that a well-controlled psoriasis is not a contraindication to a treatment with peg-INF-α and ribavirin since combination therapies with immunosuppressive treatment seem safe .
CMV, Cytomegalovirus; DAA, direct acting agent; EBV, Ebstein-Barr virus; HCV, hepatitis C; HIV, Human immunodeficiency virus; Peg-INF-α, pegylated interferon-α; RNA, Ribonucleic acid.
The authors thank Dr. med. Ch. Öhlschlegel from the Department of Pathology, Kantonsspital St.Gallen for providing the histology picture.
The authors state that there was no funding.
Availability of data and materials
All authors took care of the patient and participated in the diagnosis and treatment of the disease. They all prepared the manuscript, read and approved the final version.
The authors declare that they have no competing interests.
Written informed consent was obtained from the patient for publication of this case report and the images.
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