The distinction between lesional and non-lesional skin in psoriasis vulgaris through expression of adhesion molecules ICAM-1 and VCAM-1

Čabrijan, Leo; Batinac, Tanja; Lenković, Maja; Gruber, Franjo

doi:10.1016/j.mehy.2008.06.049

Cited by 23 publications

(26 citation statements)

References 17 publications

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“…There is accumulating evidence from prospective studies for a predictive role of elevated circulating levels of sICAM-1 in initially healthy people, and of sVCAM-1 in patients at high risk or with overt cardiovascular disease. Likewise, it has been implied that several adhesion molecules including ICAM-1 and VCAM-1 are upregulated in psoriasis 26, 27, implicating their involvement in the pathogenesis of psoriasis.…”

Section: Resultsmentioning

confidence: 99%

Pathogenic Mechanisms Shared between Psoriasis and Cardiovascular Disease

Ghazizadeh¹,

Shimizu²,

Tosa³

et al. 2010

Int. J. Med. Sci.

100

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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 from several 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 blood vessel 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 or atherosclerotic 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.

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Section: Resultsmentioning

confidence: 99%

Pathogenic Mechanisms Shared between Psoriasis and Cardiovascular Disease

Ghazizadeh¹,

Shimizu²,

Tosa³

et al. 2010

Int. J. Med. Sci.

100

View full text Add to dashboard Cite

show abstract

“…[3132] Adhesion molecules including Intercellular adhesion molecule-1 ICAM-1 and vascular cell adhesion molecule VCAM-1 are upregulated in psoriasis promoting adhesion of inflammatory cells to vascular endothelium, which in turn promote the formation of atherosclerotic plaques and obesity-related insulin resistance by oxidation of low-density lipoprotein in vessel wall. [33] Proinflammatory glycoproteins like osteopontin, peptide hormones like leptin and adiponectin and other markers like homocysteine and CRP have also been implicated in bringing the two conditions together. [34] Dysregulation of T-cell interactions and overexpression of proinflammatory cytokines lead to the hyperproliferaton of keratinocytes and activation of neutrophils in the epidermis.…”

Section: Diseases Of the Skin Associated With Met Smentioning

confidence: 99%

Metabolic syndrome and skin: Psoriasis and beyond

Padhi

Garima

2013

Indian J Dermatol

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Metabolic syndrome (Met S) is a clustering of risk factors comprising of abdominal obesity, dyslipidemia, elevated blood pressure, and abnormal glucose tolerance. The prevalence of Met S has been increasing in the last few years throughout the world. Psoriasis has consistently been associated with Met S as well as its various components. However, the association is no longer limited to psoriasis alone. Various dermatological conditions such as lichen planus, androgenetic alopecia, systemic lupus erythematosus, skin tags, acanthosis nigricans, and even cutaneous malignancies have also been found to be associated with this syndrome. Though chronic inflammation is thought to be the bridging link, the role of oxidative stress and endocrine abnormalities has recently been proposed in bringing them together.

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“…De Boer et al [18] stated that there is a weak ICAM-1 expression in the dermis as 5-25% of T cells in normal skin express ICAM-1. In 2009, Cabrijan et al [19] assumed that even non-lesional skin in psoriatic patients has non-visible immunological changes, such as high expression of adhesion molecules ICAM-1 and VCAM-1, which are similar to those in lesional skin. They referred to the Köbner phenomena, which is a provocation of lesional skin in psoriatic patients by repeated trauma or pressure to the skin as a possible explanation of their hypothesis.…”

Section: Discussionmentioning

confidence: 99%