The association between psoriasis, a chronic autoimmune skin disease that causes dry, red, scaly patches ("lesions") to appear on the skin, and cardiovascular disease was first observed more than 30 years ago in case-control studies; and in recent years, there have been increased efforts to understand the biology of psoriasis and cardiovascular disease. It is known that T cells, macrophages, and inflammatory cytokines are involved in the development of both atherosclerosis, a condition in which plaque collects along the walls of arteries, commonly referred to as hardening of the arteries, and psoriasis. However, the contribution of psoriasis to cardiovascular disease remains unclear.
Patients with psoriasis have an increased risk for diabetes, hypertension, hyperlipidemia, obesity, and smoking, which are known cardiovascular risk factors. Mechanisms for the higher prevalence of cardiovascular disease in patients with psoriasis include sharing of common risk factors for cardiovascular disease, treatments for psoriasis that may increase cardiovascular disease through hypertension (e.g., cyclosporine) or dyslipidemia (e.g., acitretin), inflammation, undertreatment of cardiovascular disease risk factors due to attention to psoriasis, and shared genetics between psoriasis and cardiovascular disease.
The question remains: Does psoriasis cause cardiovascular disease? Evidence suggests that this is a possibility. The sequence is well established, there is biologic credibility, and a dose-response exists--at least, for a few studies. Most studies have found an effect; and although the strength of association is modest, it is clinically important.
Another question has arisen: Could sleep disorders explain some of the increased risk that psoriatic arthritis sufferers have for cardiovascular disease? Data from the Utah Psoriasis Initiative showed that psoriasis patients have higher rates of obesity, smoking, diabetes, and depression; and they don't sleep well. Sleep disorders originally were thought to be due to severe itching, depression, and other problems; but a small study showed that 9 of 25 patients had sleep apnea. Sleep has significant links to inflammation. In addition, sleep apnea and sleep deprivation increase insulin resistance cytokine levels.
It is well established that inflammation drives atherothrombotic events. One study showed that individuals with high-sensitivity C-reactive protein without lipidemia (low levels of low-density lipoprotein cholesterol) benefit from statin therapy. In this particular study, individuals taking rosuvastatin had reduced rates of nonfatal myocardial infarction, nonfatal stroke, hospitalization for unstable angina, revascularization, and confirmed death from cardiovascular causes. Diagnostic tests, biomarkers, and noninvasive imaging are needed to predict atherosclerotic growth and disease and to improve risk prediction. In addition, vitamin D deficiency may be an important link to cardiovascular disease; more information is needed to understand this potential relationship.
To increase understanding of the relationship between psoriasis and cardiovascular disease, it is important that answers to key clinical questions be answered. Immunomodulatory therapeutics and animal models will be important tools for making clear the common and disparate mechanisms between psoriasis and atherosclerosis. There is much work to be done.
--Source: Excerpted from "Psoriasis and Atherosclerosis," Elizabeth J. Horn, Ph.D., MBI, from MedscapeCME Dermatology, November 20, 2009
