Diabetes and Psoriasis: Different Sides of the Same Prism
Rachel Abramczyk,1 Jenna N Queller,2 Amy W Rachfal,3 Stanley S Schwartz4,5 1Main Line Health System, Wynnewood, PA, USA; 2Private Practice, Boca Raton, FL, USA; 3Stage Gate Partners, LLC, Ardmore, PA, USA; 4Stanley Schwartz, LLC, Main Line Health System, Ardmore, PA, USA; 5University of Pennsylvania...
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Formato: | article |
Lenguaje: | EN |
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Dove Medical Press
2020
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Acceso en línea: | https://doaj.org/article/026465d784344851a9b22459c786bef3 |
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Sumario: | Rachel Abramczyk,1 Jenna N Queller,2 Amy W Rachfal,3 Stanley S Schwartz4,5 1Main Line Health System, Wynnewood, PA, USA; 2Private Practice, Boca Raton, FL, USA; 3Stage Gate Partners, LLC, Ardmore, PA, USA; 4Stanley Schwartz, LLC, Main Line Health System, Ardmore, PA, USA; 5University of Pennsylvania, Philadelphia, PA, USACorrespondence: Stanley S SchwartzStanley Schwartz, MD, LLC, 233 E Lancaster Ave, Suite 305, Ardmore, PA 19003, USATel/Fax +1 610 642 6850Email stschwar@gmail.comAbstract: Diabetes and psoriasis are prevalent conditions with a spectrum of serious adverse outcomes. Both diseases are common comorbidities for each other, and diabetes is considered as a risk factor for psoriasis and vice versa. However, it is our contention that these diseases are not merely comorbidities of each other but rather share common underlying pathophysiologies (ie, genes and epigenetic changes, inflammation, abnormal environment, and insulin resistance) that drive disease. As such, they can be viewed as facets of the same prism. Genes can cause or permit susceptibility to damage from abnormal external and internal environmental factors, inflammation, and insulin resistance which can also drive epigenetic changes. These co-existing mechanisms act in a vicious cycle over time to potentiate cell and tissue damage to ultimately drive disease. Viewing diabetes and psoriasis through the same prism suggests potential for therapies that could be used to treat both conditions. Although additional controlled trials and research are warranted, we believe that our understanding of the overlapping pathophysiologies continues to grow, so too will our therapeutic options.Keywords: genes, epigenetics, inflammation, abnormal environment, insulin resistance |
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