The concept of the "psoriatic march," proposed more than a decade ago by Boehncke et al, provided a valuable framework to explain how chronic cutaneous inflammation could lead to systemic metabolic dysfunction, endothelial injury, and ultimately, cardiovascular disease.1 This model, which focuses on downstream vascular biology driven by persistent Th1/Th17 activation, has been deeply influential and continues to shape clinical reasoning.
Rubén Queiro (Sun,) studied this question.