• #4-1. Etiology and Incidence of Varicose Veins


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    Cause of varicose veins


    Many factors are involved in the etiology of varicose veins. Among these, heredity accounts for 80-90% of cases. Various factors are related to the onset and progression of varicose veins.


    Hereditary factors


    Primary varicose veins tends to have a familial aspect and is more prevalent in women than men. It is suspected to be hereditary and many explanations exist regarding its presentation. Considering its common onset immediately after adolescence, it may arise from a congenital defect. It is unclear whether the congenital defect is in the venous valve, venous wall or both.


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    In humans, only constitutional factors (collagen properties) are inherited and not the varicose veins itself. Primary varicose veins is most likely to arise from venous valvular incompetence due to either congenital defect in external iliac venous valve or primary valvular incompetence. Short spikes in venous pressure due to daily activities such as coughing or physical exertion, compress the saphenofemoral junction (SFJ) which triggers venous valvular incompetence in this area. This leads to subsequent valvular incompetence of descending superficial veins through the great saphenous vein (GSV), which causes varicose veins.

    Varicose veins of the small saphenous vein (SSV) are not as common as in GSV but can occur in the same pathophysiological mechanism. Valvular incompetence in the saphenopopliteal junction (SPJ) or pressure from already existing varicose veins in GSV damages the valves of subcutaneous penetrating veins and triggers varicose veins in SSV through the mechanism of secondary valvular incompetence. Varicose veins occur in the branches of the medial iliac venous system in the same mechanism, with tortuous protrusions appearing in posterior thigh or external genitalia.

    In short, hereditary or congenital anatomical defect affect the lateral iliac veins and the resulting secondary valvular incompetence in the superficial veins of saphenous venous system is suspected to cause varicose veins.


    Endocrine hormones


    Varicose veins in women are often associated with pregnancy and child birth, events entailing drastic hormonal changes. Female varicose veins are caused by mechanistic and hormonal factors. Mostly, endocrine hormones are involved in its pathophysiology.

    As venography shows, in the supine position, the pregnant uterus compresses the lower limb veins. The femoral venous pressure also rises 2-3 times during pregnancy. These factors serve as mechanistic causes of varicose veins. In other words, during pregnancy, circulation volume increases in the uterus and placenta and the enlarged uterus directly compresses femoral or iliac veins within the abdominal cavity, mechanistically causing venous stasis or higher venous pressure. However, varicose veins are much more prevalent in pre-pregnancy women and often manifest in the early phase of the pregnancy when the uterus is not enlarged. Moreover, varicose veins worsen immediately before menstruation, degenerate with the death of the fetus, or do not occur in the presence of a large fibroma in the uterus. Considering these factors, varicose veins are more likely caused by female hormones such as estrogen in pregnant women rather than mechanistic factors.

    The theory of hormonal causes explains varicose veins with the impact of pregnancy and sex hormones on the blood vessels. Estrogen and progesterone levels gradually rise until delivery and plunge after delivery. Estrogen causes bleeding and vasodilation whereas progesterone dilates veins during pregnancy, thereby causing venous hypotention and muscle relaxation.

    Women who have long-term exposure to sex hormone drugs such as oral contraceptives are particularly susceptible to varicose veins. They complain of fatigue, heaviness and erythema of lower limbs and develop varicose veins in a couple of years. Sex hormone therapy had harmful impact on vascular coagulation and metabolism. The most harmful effect of estrogen therapy on blood vessels is seen in patients with prostate cancer who were on long-term estrogen therapy. Use of estrogen increased the incidence of thrombophlebitis in pulmonary thromboembolism and myocardial infarction.

    A histological study showed increased intima-media thickness, collagen degeneration and presence of estrogen receptors in endothelial cells. Progesterone had vasorelaxing effect on the veins. During the process of coagulation, estrogen increases coagulation factors – especially, factor VII (proconvertine) – as well as thrombin and fibronogen, a progenitor of fibrin. It also reduces coagulation inhibitor (reduction of antithrombin III) and fibrinolysis. In many epidemiologic studies, oral estrogenic therapy has been shown to affect metabolism by overaccumulation of ethinyloestradiol in hepatocytes. Therefore, female patients with varicose veins should consult their OB/GYN about discontinuing hormonal contraceptives depending on the severity of varicose veins.


    -To be continued-


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