hepatitis c virus ( hcv ) is a leading cause of chronic liver diseases , and an important cause of morbidity and mortality worldwide . hcv - related chronic hepatitis c might lead to both cellular and humoral abnormalities . in several studies , the prevalence of hcv - ab was higher in patients with psoriasis than in the normal population . these results have suggested that infection and/or hcv treatment may act as a triggering factor for development or exacerbation of psoriasis . there are several reports of vesicular erythematous eruptions , vitiligo and subcutaneous sarcoidosis in patients treated with interferon and ribavirin . we present the case of a 50 year old male patient diagnosed with psoriasis who referred to our clinic at tehran university of medical sciences . 
 
 on his first admission in april 2007 , he had a positive anti - hcv antibody ( anti - hcv ab ) test . except for the history of psoriasis , which was under control with anti - psoriatic medications , his past medical history was unremarkable . physical examination revealed healing silvery scale psoriatic plaques distributed over both forearms and lower legs without pustules and pitting of nails caused by the disease ( picture 1,2 ) . psoriatic scaly skin lesions over right elbow ( upper arrow ) and right buttock ( lower arrow ) scaly lesions of psoriasis over anterior aspect of both knees ( right and left arrows ) 
 the patient was infected with genotype 3a and the viral count was 223,000 iu / ml . levels of thyroid stimulating hormone , albumin , bilirubin , prothrombin time , blood urea , alkaline phosphatase and creatinine were within normal limits . a liver biopsy was performed which showed an inflammation grade of 11/18 and fibrosis stage of 3/6 according to the ishak classification . ( pegaferon@ , pooyesh daru , iran ) and ribavirin for 24 weeks . 
 
 at the first week of treatment , the patient suffered from arthro - myalgias , which were not severe enough to warrant treatment . during the second week , he developed generalized itching , particularly at night . this was managed by night - time oral hydroxyzine and topical calamine - d lotion . psoriatic lesions were observed from week three of treatment and new lesions appeared on his legs , elbows , back and knees . his skin lesions became more severe and his dermatologist , in consultation with the hepatologist , recommended cyclosporine 100 mg , twice daily . on week eight of therapy , the patient became neutropenic ( absolute neutrophil count : < 1000 cell / ml ) , thus granulocyte colony stimulating factor ( g- csf ) at a dose of 300 g per week was started . 
 
 on the third month of therapy , as the healing of psoriatic lesions was not satisfactory , the patient also received 100 sessions of puva therapy ( psoralen plus ultra violet a treatment 3 times a week , each session ranging from 2 to 250 sec ) . although the patient s psoriatic lesions worsened in severity , there were no lesions or any evidence of psoriatic nail or joint complications . he tolerated hcv therapy well until the end of the 24 week of treatment . within one month after treatment cessation , the psoriatic lesions receded without the need for additional therapy . hcv rna was undetectable 6 months after discontinuation of treatment , which indicated sustained viral response . one and a half years after treatment , hcv rna is still undetectable and the patient has had no exacerbation of his psoriatic lesions . this case highlights several key issues in initiating and managing hcv therapy in a patient with co - existing psoriasis . the patient presented with a relatively high hcv viral level and compensated liver disease ( stage 2 fibrosis ) , which indicated that he was likely to benefit from anti - hcv treatment . other hematologic and biochemical laboratory findings were acceptable and did not present any contraindication to treatment . however , his history of co - existing psoriasis , although controlled , increased the risk of exacerbation . cyclosporine had dual therapeutic actions both for the psoriatic lesions and inhibition of hcv replication . despite the flare up of psoriatic lesions , the subsequent management led to both successful eradication of hcv and control of psoriasis . 
 
 in conclusion , we suggest that concomitant psoriasis could not be seen as a contraindication for hcv treatment and exacerbations can be successfully managed by cyclosporine and puva .
chronic hepatitis c might lead to several immunological dysfunctions . 
 studies have shown a positive association between hepatitis c virus ( hcv ) infection and psoriasis . 
 these results suggest that the infection may be one of the triggering factors for the development or exacerbation of psoriasis.here , we present a case of chronic hcv infection with psoriasis who developed exacerbation of skin lesions during therapy with peginterferon alpha2a plus ribavirin . 
 we discuss the management , course and results of hcv treatment in this patient .