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R.C. Sam

Researcher at University of Birmingham

Publications -  13
Citations -  670

R.C. Sam is an academic researcher from University of Birmingham. The author has contributed to research in topics: Varicose veins & Chronic venous insufficiency. The author has an hindex of 10, co-authored 13 publications receiving 617 citations.

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Obesity and Thrombosis

TL;DR: Obesity appears to be associated with thrombosis via several mechanisms that are all improved by weight loss, including the actions of so-called adipocytokines from adipose tissue.
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Nerve injuries and varicose vein surgery.

TL;DR: The true incidence and, most importantly, natural history of such injuries are poorly described, meaning that surgeons have limited information to pass on to their patients and that the questions most frequently posed to ‘expert witnesses’ in medico-legal cases are difficult to answer with authority.
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Higher prevalence of thrombophilia in patients with varicose veins and venous ulcers than controls

TL;DR: Patients with VV, and particularly CVU, have significantly higher prevalences of single and multiple thrombophilias than age- and sex-matched controls without clinical or duplex evidence of lower limb venous disease, and this data support the hypothesis that thROMbophilia predisposes to the development of superficial and deep lower limb Venous reflux.
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Changes in health-related quality of life after ultrasound-guided foam sclerotherapy for great and small saphenous varicose veins

TL;DR: Ulasound-guided foam sclerotherapy for great and small saphenous varicose veins leads to significant improvements in generic and disease-specific HRQOL for at least 12 months after treatment.
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The prevalence of hyperhomocysteinemia, methylene tetrahydrofolate reductase C677T mutation, and vitamin B12 and folate deficiency in patients with chronic venous insufficiency.

TL;DR: Hyperhomocysteinemia is common in patients with chronic venous insufficiency, especially those with ulceration, however, inasmuch as fewer than a third of patients with HHcy were C677T MTHFR homozygous or had vitamin B(12) or folate deficiency, other mechanisms must be responsible in the majority.