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CVD: a condition of underestimated severity.

ABSTRACT Chronic venous disease affects approximately a quarter of the adult population and causes a considerable burden on the health of these patients. The true extent of the severity of the disease is hampered because of reduced public awareness, operational difficulties in diagnosis, and the perception that varicose veins are mainly a cosmetic inconvenience. Consequently the disease receives little attention in public health care systems which focus on life threatening conditions and those which cause obvious morbidity like cancer, cardiac disease and stroke. This review aims to correct these misconceptions by addressing the full scope of CVD, including the postthrombotic syndrome and venous ulceration. The severity of conditions like telangectasiae and edema and the symptoms they cause are frequently underestimated, especially if varicose veins are not present to alert the patient or doctor. The definition, diagnosis, scope, epidemiology, progression and cost of CVD are discussed with evidence to explain how these underestimate the severity of the disease. It is anticipated that once CVD achieves greater recognition this will open up greater opportunities for treatment. These include surgery, endovenous ablation, stenting, compression, venoactive drugs like micronized purified flavonoid fraction and other drugs such as sulodexide and pentoxifylline.

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    ABSTRACT: Chronic venous disease encompasses a spectrum of disorders caused by an abnormal venous system. They include chronic venous insufficiency, varicose veins, lipodermatosclerosis, post-thrombotic syndrome, and venous ulceration. Some evidence suggests a genetic predisposition to chronic venous disease due to gene polymorphisms associated mainly with vein wall remodelling. The literature exploring these polymorphisms has not been reviewed and compiled thus far. In this narrative and systematic review, we present the current evidence available on the role of polymorphisms in genes involved in vein wall remodelling and other pathways as contributors to chronic venous disease. We searched the EMBASE, Medline, and PubMed databases from inception to 2013 for basic science or clinical studies relating to genetic associations in chronic venous disease, and obtained 38 relevant studies for this review. Important candidate genes/proteins include the matrix metalloproteinases (extracellular matrix degradation), vascular endothelial growth factors (angiogenesis and vessel wall integrity), FOXC2 (vascular development), HFE (venous ulceration and iron absorption) and various types of collagen (contributors to vein wall strength). The data on associations between these genes/proteins and the post-thrombotic syndrome is limited and additional studies are required. These associations might have future prognostic and therapeutic implications.
    Blood 07/2014; · 9.78 Impact Factor