SKIN CHANGES AND PECULIARITIES IN PATIENTS WITH METABOLIC SYNDROME
Approximately 20-25 % of the World’s adult population aged 40 - 75 years have metabolic syndrome (MS). MS is one of the most widespread risk factors for: diabetes mellitus, cardiovascular disorders and skin disorders MS, due to the oxidative stress, supports a chronic inflammatory reaction in the skin and in the other parts of the body. During oxidative stress the net amount of reactive oxygen species (ROS) exceeds the antioxidant capacity of the body causing lipid peroxidation, protein oxidation and oxidative DNA damage. The role of oxidative stress in pathogenesis of early skin changes in patients with MS is not clearly defined. The aim of our study was to compare visual skin changes between patients with MS and without it, and to reveal early histological manifestations of MS in the skin. The study was conducted at the Clinic of Aesthetic Dermatology, Riga, Latvia. 50 patients aged 45-55 were enrolled. The research consisted of a clinical examination, biochemical testing and Punch biopsies. Tissue samples were stained with haematoxylin-eosin, Masson’s Trichrome and also immunohistochemically stainining with antibodies to CD34, CD117, CD20, CD8 and bcl-2. CD1a positive Langerhans cells were evaluated in 3 fields of vision. Data was analyzed with Microsoft Excel 2010 software. Gender ratio was women: men= 1.6:1. Histological changes in the skin of patients with MS were: hyperkeratosis, acanthosis, dermal fibrosis, elastosis and mild thickening of the stratum spinosum. Infiltrates around blood vessels were composed of T lymphocytes (CD3+). More significant expression and accumulation of apoptotic protein Bcl2 in skin of patients with MS in comparison to patients without MS was noted. Initial skin histological changes in MS are dermal elastosis, thickening of stratum spinosum and acanthosis. Mild T lymphocytic infiltration around capillaries possibly reflects the inflammatory component of MS. Increased accumulation of bcl2 anti-apoptotic protein in epidermis was more significantly expressed in patients with MS.
Adams, J. M. & Cory, S. (2007). Bcl-2-regulated apoptosis: mechanism and therapeutic potential. Curr Opin Immunol., 19 (5), 488-496. http://dx.doi.org/10.1016/j.coi.2007.05.004 PMid:17629468 PMCid:PMC2754308
Akase, T., Nagase, T., Huang, L., Ibuki, A. & Minematsu, T. (2012). Aging-like skin changes induced by ultraviolet irradiation in animal model of metabolic syndrome. Biol Res Nurs., 14 (2), 180-187. http://dx.doi.org/10.1177/1099800411401013, PMid:21444332
Alberti, K. G., Zimmet, P. & Shaw, J. (2006). Metabolic syndrome--a new world-wide definition. A Consensus Statement from the International Diabetes Federation. Diabet Med.,23 (5), 469-480. http://dx.doi.org/10.1111/j.1464-5491.2006.01858.x, PMid:16681555
Bershad, S., Rubinstein, A. & Paterniti, J. R. (1985). Changes in plasma lipids and lipoproteins during isotretinoin therapy for acne. N Engl J Med, 313, 981- 985. doi: 10.1056/NEJM198510173131604
Bickers, D. R., & Athar, M. (2006). Oxidative Stress in the Pathogenesis of Skin Disease. Journal of Investigative Dermatology, 126(12), 2565–2575. doi:10.1038/sj.jid.5700340
Cao, C. & Wan, Y. (2009). Parameters of protection against ultraviolet radiation- induced skin cell damage. J Cell Physiol., 220 (2), 277-284. http://dx.doi.org/10.1002/jcp.21780, PMid:19360745
Filip, M., Maciag, J., Nosalski, R., Korbut, R. & Guzik, T. (2012). Endothelial dysfunction related to oxidative stress and inflammation in perivascular adipose tissue. Postepy Biochem., 58 (2), 186-194. PMid:23214142
Gauglitz, G., Herndon, D. N., Kulp, G. A., Meyer, W. J. 3rd & Jeschke, M. G. (2009). Abnormal insulin sensitivity persists up to three years in pediatric patients post-burn. J Clin Endocrinol Metab, 94, 1656–1664. http://dx.doi.org/10.1210/jc.2008-1947, PMid:19240154 PMCid:PMC2684478
Gosenca, M. & Gashperlin, M. (2011). Main approaches for delivering antioxidant vitamins through the ski to prevent skin ageing. Expert Opin Drug Deliv., 8 (7), 905-919. PMid:21599565 http://dx.doi.org/10.1517/17425247.2011.581657
Grattagliano, I., Palmieri, V.O., Portincasa, P. & Moschetta, A. (2008). Oxidative stress- induced risk factors associated with the metabolic syndrome: a unifying hypothesis. J Nutr Biochem, 19, 491-504. http://dx.doi.org/10.1016/j.jnutbio.2007.06.011, PMid:17855068
Hanefeld, M., Schönauer, M. & Forst, T. (2010). Glycemic control and cardiovascular benefit: What do we know today? Dtsch Med Wochenschr., 135 (7), 301-307. doi:10.1055/s-0029-1244853
Heather, B. (2008). Fitzpatrick Classification Scale. About.com Guide, retrieved from http://dermatology.about.com/od/ cosmeticprocedure/a/fitzpatrick.htm
Higgins, S. P., Freemark, M. & Prose, N. S. (2008). Acanthosis nigricans: a practical approach to evaluation and management. Dermatol Online J, 14, 2.
Ice, C., Murphy, E., Minor, V., & Neal, W. (2009). Metabolic syndrome in fifth grade children with acanthosis nigricans: results from the CARDIAC project. World Journal of Pediatrics, 5(1), 23–30. doi:10.1007/s12519-009-0004-7
Janiczek-Dolphin, N., Cook, J., Thiboutot, D., Harness, J. & Clucas, A.(2010). Can sebum reduction predict acne outcome? Br J Dermatol, 163, 683–688. doi: 10.1111/j.1365-2133.2010.09878.x
Keller, U., Kümin, A., Braun, S. & Werner, S. (2006). Reactive oxygen species and their detoxification in healing skin wounds. J Investig Dermatol Symp Proc., 11 (1), 106-111. http://dx.doi.org/10.1038/sj.jidsymp.5650001
Kraemer- Aguiar L. G. (2012). Obesity, metabolic syndrome, impaired fasting glucose, and microvascular dysfunction a principal component analysis approach. BMC Cardiovasc Disord., 13 (12), 102.
Ma, X. & Zhu, S. (2013). Metabolic syndrome in the prevention of cardiovascular diseases and diabetes-still a matter of debate? Eur J Clin Nutr., 67 (5), 518-21 13.
Petersen, A. B. & Gniadecki, R. (2000). Hydrogen peroxide is responsible for UVA-induced DNA damage measured by alkaline comet assay in HaCaT keratinocytes. Journal of Photochemistry and Photobiology. B, Biology 59 (1-3), 123-31. http://dx.doi.org/10.1016/S1011-1344(00)00149-4
Pusztaszeri, M. P., Seelentag, W. & Bosman, F. T. (2006). Immunohistochemical expression of endothelial markers CD31, CD34, von Willebrand factor, and Fli-1 in normal human tissues. J Histochem Cytochem., 54 (4), 385-95. http://dx.doi.org/10.1369/jhc.4A6514.2005
Roberts, C. K. & Sindhu, K. K. (2009). Oxidative stress and metabolic syndrome. Life Sci, 84, 705- 712. http://dx.doi.org/10.1016/j.lfs.2009.02.026
Rodondi, N., Darioli, R., Ramelet, A. A, Hohl, D., Lenain, V., Perdrix, J., Wietlisbach, V., Riesen, W.F., Walther, T., Medinger, L., Nicod, P., Desvergne, B., Mooser, V. (2002). High risk for hyperlipidemia and the metabolic syndrome after an episode of hypertriglyceridemia during 13-cis retinoic acid therapy for acne: a pharmacogenetic study. Ann Intern Med, 136, 582–589. http://dx.doi.org/10.7326/0003-4819-136-8-200204160-00007, PMid:11955026
Sellheyer, K. (2003). Pathogenesis of solar elastosis: synthesis or degradation? J Cutan Pathol.,30 (2), 123-7. http://dx.doi.org/10.1034/j.1600-0560.2003.00018.x, PMid:12641791
Trouba, K. J, Hamadeh, H. K. & Amin, R. P. (2002). Oxidative stress and its role in skin disorders. Antioxid Redox Signal., 4 (4), 665-73. http://dx.doi.org/10.1089/15230860260220175
Zech, L. A., Gross, E. G., Peck, G. L. & Brewer, H. B. (1983). Changes in plasma cholesterol and triglyceride levels after treatment with oral isotretinoin. Arch Dermatol, 119, 987- 993. http://dx.doi.org/10.1001/archderm.1983.01650360033009, PMid:6228196
Zhang, C.L., Song, F., Zhang, J. & Song, Q. H. (2010). Hypoxia-induced Bcl-2 expression in endothelial cells via p38 MAPK pathway. Biochem Biophys Res Commun., 394 (4), 976-80. http://dx.doi.org/10.1016/j.bbrc.2010.03.102, PMid:20307495
Zhou, S. S., Li, D., Zhou, Y. M. & Cao, J. M. (2012). The skin function: a factor of anti-metabolic syndrome. Diabetol Metab Syndr., 4 (1), 15. http://dx.doi.org/10.1186/1758-5996-4-15
- Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License (Creative Commons Attribution License 3.0 - CC BY 3.0) that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.
- Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.
- Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access).
firstname.lastname@example.org, www.iseic.cz, ojs.journals.cz