Porokeratosis in patients with hepatitis C virus infection: does hepatitis C virus infection provide a link between porokeratosis and immunosuppression?

Identification of a genetic locus for autosomal dominant disseminated superficial actinic porokeratosis on chromosome 1p31.3–p31.1

“…These results provided a framework for the ultimate identiWcation of a new gene for DSAP. Except for sun exposure, several risk factors, including radioactivity, virus infection (Mizukawa and Shiohara 1999), renal transplantation (Anzai et al 1999), and bone marrow transplantation (Rio et al 1997), had been associated with the development of DSAP. However, none of the above risk factors was reported in the Chinese family under this study.…”

Human Papillomavirus Isolated from Transplant-Associated Porokeratoses of Mibelli Responsive to Topical 5% Imiquimod Cream

“…15 Owing to the high incidence of porokeratoses and hepatitis C in transplant recipients, some have suggested hepatitis C as the transmissible agent. 11,12,15 Our patients were hepatitis C negative, but their lesions did demonstrate another transmissible agent, HPV.…”

“…There are increasing numbers of reports of porokeratoses associated with organ transplant, bone marrow transplant, hepatitis C, and HIV. [8][9][10][11][12][13] Porokeratoses have been reported in up to 10% of renal transplant patients. 8 In addition, irradiation with UV light has induced the formation of porokeratoses in susceptible patients.…”

Disseminated Superficial Actinic Porokeratosis in a Patient With Sjögren Syndrome

“…Many genetic alterations have been identified and sometimes the expression of p53 gene was altered 3–6 . The onset of PK probably depends on a variable interaction of genetic factors and exogenous trigger factors that are not sufficient for the expression of clinical lesions 7 . It has been suggested that some clones of epidermal cells are inherited as mutants whose phenotypic expression is the result of activation by exogenous trigger factors such as trauma, infections, irradiation, and immunologic disorders 2,8 .…”

“…It has been suggested that some clones of epidermal cells are inherited as mutants whose phenotypic expression is the result of activation by exogenous trigger factors such as trauma, infections, irradiation, and immunologic disorders 2,8 . Some reports show development of DSAP and other variants of PK during autoimmune disease (e.g., systemic lupus erythematosus, pemphigus foliaceus and vulgaris, vitiligo); kidney, heart, and liver transplantation; liver disease (chronic hepatitis C, biliary cirrhosis); HIV infection; and immunosuppressive therapy (e.g., steroids, cyclosporin A, azathioprine) 2,7,9 . So the different conditions of immunosuppression (primary or secondary) reported above looks to be the important exogenous factor able to incite the expression of PK in genetically predisposed patients.…”