Profile of patients with psoriasis associated with hepatitis C virus infection
Shinichi Imafuku1, Juichiro Nakayama
1Department of Dermatology, Faculty of Medicine, Fukuoka University, Fukuoka, Japan. dermatologist@mac.com
Abstract:
Psoriasis is a chronic inflammatory skin disease associated with various complications such as arthritis, diabetes mellitus and hypertension. Hepatitis C is caused by chronic infection of hepatitis C virus (HCV), and eventually leads to liver cirrhosis and hepatocellular carcinoma. Although an association between psoriasis and HCV has been reported, there have been no large case series to date. The aim of the present study was to outline the profiles of HCV-positive psoriatic patients. Patients with a diagnosis of psoriasis who visited Fukuoka University from 1991-2011 were sought in the database, and their medical records were manually checked for detailed information about serum liver enzymes, anti-HCV antibodies, medical history, and treatments and outcomes of both psoriasis and hepatitis. There were 54 (7.5%) anti-HCV antibody-positive patients among the 717 psoriatic patients detected. Male predominance (male/female ratio, 44:10) and late onset (median age, 55 years) were the characteristics of the 54 patients. HCV infection preceded the onset of psoriasis definitely in 80% and probably in 11%. Interferon therapy exacerbated 70% of pre-existing psoriasis cases, and induced de novo psoriasis in eight patients. Complication with diabetes mellitus was found in 35% of the patients. Our observations suggest that HCV infection can be an inducing factor for psoriasis. In hepatitis C patients, elevated tumor necrosis factor-α is known to cause progression of hepatic disease and possibly induces psoriasis in patients with a certain predisposition.
More Related Videos
Related Concept Videos
Hepatitis
Viral Hepatitis I: Introduction
Cirrhosis II: Pathophysiology
Cirrhosis I: Introduction
Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test
Chronic Pancreatitis II: Pathophysiology

