Bambi

Psoriasis is associated with an increased risk of cardiovascular disease, a hallmark of which is atherosclerosis. The objective of this study was to review the pertinent literature and highlight pathogenic mechanisms shared between psoriasis and atherosclerosis in an effort to advocate early therapeutic or preventive measures. We conducted a review of the current literature available fromseveral biomedical search databases focusing on the developmental processes common between psoriasis and atherosclerosis. Our results revealed that the pathogenic mechanisms shared between the two diseases converged onto “inflammation” phenomenon. Within the lymph nodes, antigen-presenting cells activate naive T-cells to increase expression of LFA-1 following which activated T-cells migrate to bloodvessel and adhere to endothelium. Extravasation occurs mediated by LFA-1 and ICAM-1 (or CD2 and LFA-3) and activated T-cells interact with dendritic cells (and macrophages and keratinocytes in psoriasis or smooth muscle cells in atherosclerosis). These cells further secrete chemokines and cytokines that contribute to the inflammatory environment, resulting in the formation of psoriatic plaque oratherosclerotic plaque. Additionally, some studies indicated clinical improvement in psoriasis condition with treatment of associated hyperlipidemia. In conclusion, therapeutic or preventive strategies that both reduce hyperlipidemia and suppress inflammation provide potentially useful approaches in the management of both diseases.
Keywords: psoriasis, cardiovascular disease, atherosclerosis,shared pathogenic mechanism
*  Other Sections▼
* Abstract
* Introduction
* Review of the Literature
* Results and Discussion
* Conclusion
* References
Introduction
Psoriasis is a hereditary, chronic immune-mediated inflammatory skin disorder of unknown etiology. The disease is estimated to affect 2-3% of the general population worldwide 1. Indeed,psoriasis has a complex genetic predisposition, but its development and/or exacerbation appear to involve an interaction between multiple genetic and environmental risk factors. Hereditary or genetic factors play a part in the development of the disease. In some patients, family members may also be affected by psoriasis. However, the exact pattern of inheritance remains to be clarified. With theadvent of recent developments in understanding the role of inflammation in the pathogenesis of psoriasis, it is now widely believed that psoriasis is not just a skin disease but a systemic inflammatory process 2, 3. On the other hand, cardiovascular disease frequently develops in individuals with persistent hyperlipidemia. Other risk factors such as hypertension, vascular endothelial celldysfunction, oxidative stress, hyperhomocysteinemia, diabetes, smoking, high alcohol consumption, obesity, metabolic syndrome and intra-abdominal adipose visceral tissue and their adipokines, can also be involved 4-6. These factors contribute to the formation of atherosclerosis which is a hallmark of cardiovascular disease and in which inflammation plays a major role 7, 8. In addition, the same factorsare also implicated in psoriasis patients 9, 10.Cardiovascular disease is an important cause of morbidity and mortality in patients with psoriasis. The risk factors for cardiovascular disease as well as myocardial infarction occur with higher incidence in patients with psoriasis and appear to be highest for those with more severe disease 11. Moreover, psoriasis was suggested as an independentrisk factor for cardiovascular disease 12, however some recent studies have not supported this notion 13-15, therefore this issue remains to be controversial. Here, we review the pertinent literature to highlight pathogenic mechanisms shared between psoriasis and atherosclerosis in an effort to advocate early therapeutic or preventive measures.
*  Other Sections▼
* Abstract
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