Inflammation in atherosclerosis and psoriasis: common pathogenic mechanisms and the potential for an integrated treatment approach
- PMID: 18700910
- DOI: 10.1111/j.1365-2133.2008.08780.x
Inflammation in atherosclerosis and psoriasis: common pathogenic mechanisms and the potential for an integrated treatment approach
Abstract
Inflammation plays a key role in the pathogenesis of a number of chronic inflammatory systemic diseases (CISDs), including psoriasis, rheumatoid arthritis, systemic lupus erythematosus and Crohn's disease, and also in the pathogenesis of atherosclerosis. CISDs and cardiovascular diseases, such as atherosclerosis, share common pathogenic features, and cardiovascular disease is an important cause of morbidity and mortality in patients with CISDs. Activated inflammatory cells and pro-inflammatory cytokines contribute to the development of psoriatic lesions and play an important role in the breakdown of atherosclerotic plaques. Psoriasis and atherosclerosis also have similar histological characteristics involving T cells, macrophages and monocytes. In particular, the extravasation of T cells through the epithelium is characteristic of both psoriatic and atherosclerotic plaques. Cardiovascular disease is an important cause of morbidity and mortality in patients with psoriasis, which is associated with an increased cardiovascular risk profile compared with the general population. Patients with psoriasis are at increased risk of arterial hypertension, coronary heart disease, hyperlipidaemia, obesity and type II diabetes, which are more prevalent than in control patients. This increased risk could be due to the effects of chronic inflammatory changes, particularly the infiltration of T cells and subsequent secretion of pro-inflammatory cytokines. Some drugs used in the treatment of cardiovascular disease, such as 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) and angiotensin-converting enzyme inhibitors have anti-inflammatory activity. In addition, systemic treatments for psoriasis may, by decreasing inflammation, reduce the risk of cardiovascular disease. It is suggested, therefore, that an integrated approach to the treatment of the inflammatory processes underlying both psoriasis and atherosclerosis may be beneficial in reducing cardiovascular risk in patients with psoriasis. The newer targeted biological therapies, such as efalizumab and infliximab, which offer the potential for long-term disease control in psoriasis, may be of particular use in this setting.
Similar articles
-
[Atherosclerosis and arteriitis: implications for therapy of cardiovascular disease].Herz. 2004 Feb;29(1):4-11. doi: 10.1007/s00059-004-2520-5. Herz. 2004. PMID: 14968336 Review. German.
-
[Rheumatoid arthritis, inflammation, and atherosclerosis].Herz. 2004 Dec;29(8):760-8. doi: 10.1007/s00059-004-2636-7. Herz. 2004. PMID: 15599672 Review. German.
-
More than skin deep: atherosclerosis as a systemic manifestation of psoriasis.Br J Dermatol. 2009 Jul;161(1):1-7. doi: 10.1111/j.1365-2133.2009.09281.x. Epub 2009 Jun 4. Br J Dermatol. 2009. PMID: 19500102 Review.
-
Long-term prognosis in patients with psoriasis.Br J Dermatol. 2008 Aug;159 Suppl 2:2-9. doi: 10.1111/j.1365-2133.2008.08779.x. Br J Dermatol. 2008. PMID: 18700909 Review.
-
Psoriasis: can statins play a dual role?Dermatol Online J. 2010 Feb 15;16(2):2. Dermatol Online J. 2010. PMID: 20178698 Review.
Cited by
-
The Association Between Psoriasis and Cardiovascular Diseases.Eur Cardiol. 2021 May 13;16:e19. doi: 10.15420/ecr.2020.15.R2. eCollection 2021 Feb. Eur Cardiol. 2021. PMID: 34040653 Free PMC article. Review.
-
Carotid intima-media thickness in patients with psoriasis with and without metabolic syndrome.Arch Cardiol Mex. 2022 Jul 1;92(3):305-311. doi: 10.24875/ACM.21000106. Arch Cardiol Mex. 2022. PMID: 34499634 Free PMC article.
-
Looking beyond the Skin: Pathophysiology of Cardiovascular Comorbidity in Psoriasis and the Protective Role of Biologics.Pharmaceuticals (Basel). 2022 Sep 3;15(9):1101. doi: 10.3390/ph15091101. Pharmaceuticals (Basel). 2022. PMID: 36145322 Free PMC article. Review.
-
Cyanidin-3-O-beta-glucoside inhibits LPS-induced expression of inflammatory mediators through decreasing IkappaBalpha phosphorylation in THP-1 cells.Inflamm Res. 2010 Sep;59(9):723-30. doi: 10.1007/s00011-010-0183-7. Epub 2010 Mar 23. Inflamm Res. 2010. PMID: 20309718
-
Inflammation, atherosclerosis, and psoriasis.Clin Rev Allergy Immunol. 2013 Apr;44(2):194-204. doi: 10.1007/s12016-012-8308-0. Clin Rev Allergy Immunol. 2013. PMID: 22359071 Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical