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Psoriasis and serum lipid abnormalities

Psoriasis affects approximately 120–180 million people worldwide. Interestingly, its incidence increased significantly from 50.8 in the period 1970–1974 to 100.5 per 100,000 in the period 1995– 1999 (1). In recent years, pathophysiological phenomena in psoriasis and disease-related psychosocial aspects have been approached quite differently. The multiaspect nature of psoriasis as a systemic disease associated with numerous multiorgan abnormalities and complications has been recognized. The available studies indicate that the etiology of psoriasis may be extremely diverse in individual patients. It is known that its prevalence in the population is affected by genetic, environmental, immunological, viral, infectious, biochemical, endocrine, and psychological (trauma, stress) factors as well as alcohol and drug abuse (2,3). Psoriasis is associated with cardiovascular abnormalities; moreover, it increases the risk of the numerous diseases, including atherosclerosis, metabolic syndrome, dyslipidemia, hypertension, diabetes type 2, obesity, cancer, depression, osteoporosis, chronic obstructive pulmonary disease, and even cerebral stroke (4,5,6). The knowledge concerning new parameters involved in the psoriatic process increases continuously. The recent findings presented by Chen and coworkers (2009) (3) demonstrate elevated levels of osteopontins (OPNs) in peripheral blood of psoriatic patients. According to them, high levels of OPNs in plasma are unfavorable risk factors of cardiovascular diseases in psoriatic patients. It should be stressed that the regulation of cellular cholesterol metabolism is fully shaped already in the fetal life. The maintenance of its steady cellular levels is an important element of cellular and systemic homeostasis (7). Alterations in the organization of lipids may lead to serious consequences affecting such cellular functions as signal transduction and membrane trafficking (8). The main features of the corneous layer observed under scanning electron microscope include widened intracellular spaces, lack of resistant intercellular junctions, and impaired intracellular adhesion, which may result in markedly abnormal cholesterol homeostasis (8,9). This phenomenon may be reflected by other lipid metabolism disturbances in psoriasis. Cholesterol is one of the essential regulators of lipid organization, and mammals have developed sophisticated mechanisms to maintain low cellular cholesterol levels in membranes. As soon as these homeostatic mechanisms are overwhelmed, as in late stages of atherosclerosis, the results can be very dangerous (8). The objective of the present study is to review the available literature data on lipid metabolism abnormalities in psoriasis, relations of such abnormalities with systemic changes, and effects of lipid diet on psoriasis together with drugs’ influence on lipid parameters. In 1924 Ishimaru, one of the pioneers of lipid metabolism research in psoriasis, quantitavely analyzed serum cholesterol in psoriatic patients. However, his findings were not conclusive. In subsequent years, numerous researchers addressed this issue. Lortat–Jacob and coworkers (1926) were the first to pay attention to hypercholesterolemia in psoriatic patients and possible alleviation of disease clinical symptoms by decreasing cholesterol levels (10,11). In the same year, Lacroix demonstrated significant amount of cholesterol in scaly plagues. He detected elevated cholesterol levels in serum – in 40% of patients, this index was higher than 200 mg % – and suggested that psoriasis might be the form of cholesterol elimination through the skin (10). In the 30s, Grutz and Burger considered psoriasis as “lipoidosis” and put forward the hypothesis that the intestinal epithelial cells, like psoriatic keratinocytes, contained excessive lipids, which is likely to hinder the absorption of lipids through the intestinal wall. They considered the development