August 2012

The heartbreak of psoriasis: It’s more than merely skin deep

Cover of the August 2012 issue of the Journal of Lipid Research

Psoriasis is an autoimmune disease in which the rate of growth of skin cells increases as a result of the body’s mistaken immune response to skin cells as a pathogen. In the 1960s, the advertising campaign for Tegrin, a medicated shampoo containing coal tar, boasted that the product relieved eczema, seborrhea and “the heartbreak of psoriasis.” The cheeky phrase even reappeared in popular culture when it was referenced in the 1978 film “Grease.”

Some 50 years later, it might come as a surprise to the marketing team behind the oft-quoted advertisement that psoriasis has been linked in more recent years to systemic inflammation and systemic metabolic disorders, including cardiovascular ones that affect the heart. The increased risk of cardiovascular disease was first reported in the 1970s. Epidemiological studies that followed bolstered this notion, even when the studies controlled for usual CVD risk factors such as age, sex, diabetes, hypertension, hyperlipidemia, smoking and obesity, suggesting that psoriasis independently increases the risk for CVD. Additionally, studies indicate the more severe the manifestation of psoriasis, the greater the risk one has of developing CVD.

A person’s arm covered with plaque psoriasis. Photo courtesy of Wikipedia. 

While psoriasis is known to the lay community more as a problematic and disfiguring skin disease, the systemic inflammation inside the body that accompanies the disease should not be overlooked, emphasize Journal of Lipid Research Associate Editor Kenneth R. Feingold and editorial board member Carl Grunfeld, who wrote the commentary “Psoriasis: It’s more than just the skin” that appears in the August issue of the JLR. It is now well documented that an increased risk of atherosclerosis occurs in other chronic inflammatory disorders, such as HIV infection and rheumatoid arthritis; these disorders cause increases in serum triglyceride levels and HDL levels that also are observed in psoriasis, which Feingold and Grunfeld point out as reasons psoriasis should be considered a model relevant to the wide array of diseases that can cause systemic inflammation that can lead to CVD.

The commentary was written in response to “Psoriasis alters HDL composition and cholesterol efflux capacity,” a paper authored by Michael Holzer of the Medical University of Graz in Austria and colleagues; that article also appears in the August issue. In it, Holzer et al. explore the structure and function of HDL in patients with psoriasis. Using quantitative shotgun proteomic profiling, they determined that the composition of HDL of psoriasis patients is very different compared with healthy people.

A key observation in this paper is that even with modest inflammation attributed to psoriasis significant changes in HDL structure occur. Another notable finding is the discovery that HDL from psoriasis patients is less efficient at sending cholesterol out of macrophages, the critical first step in the reverse cholesterol transport pathway, noted for its potential importance in preventing atherosclerosis. The results of the study demonstrate that psoriasis, while widely viewed as a skin ailment whose physical manifestations often are challenging to treat, has real consequences on a molecular level, altering the structure of HDL and contributing to an increased risk for developing atherosclerosis and other CVD.


Mary L. Chang ( is managing editor of the Journal of Lipid Research and coordinating journal manager of the journal Molecular & Cellular Proteomics.


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