Genetic biases related to chronic venous ulceration
Chronic wounds represent a major socioeconomic problem. Chronic venous ulceration is one of the least well-understood types of chronic wounds. A chronic venous ulcer arises as a result of chronic venous insufficiency (CVI), which affects approximately 10–35% of people in the developed world, yet not all people with CVI develop ulceration. The question of why some patients with CVI develop chronic ulceration and others do not, still remains unanswered. Risk factors for the development of chronic ulceration are poorly understood and include age, residual iliofemoral vein obstruction, residual deep incompetence, persistent venous hypertension, obesity and genetics. The genetic aspects of CVI have only been vaguely evaluated. This paper reports on a literature review of the variation in genetic polymorphisms and gene expression associated with the development of a chronic venous ulceration.
Genetic studies, together with insights into biochemical, physiological and pathophysiological processes related to wound healing on the molecular level, have broadened our understanding of chronic venous ulcer aetiology.1–3 History has taught us that new pathophysiological findings may lead to new and improved treatment methods. For example, findings in the treatment of chronic venous ulceration (CVU) have shown that a combination of compression therapies with modern wound dressings leads to a significant reduction in the necessary treatment period, and therefore overall treatment costs.4,5 Nevertheless, to further increase the healing rate of such wounds without additional cost to the patient, hospitals or insurance companies, a profound understanding of the chronic wound pathophysiology and extensive knowledge of available state-of-the-art wound dressing materials are required. An increasingly important factor in the management of such wounds is the genetic aspect, which is the focus of this review.
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