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homozygous for factor V Leiden variant&#46; Personal history&#58; high blood pressure&#44; gout and a previous episode of VAT&#58; left humerocephalic fistula&#44; which was functional for twelve months&#46; No family history of thrombosis&#46; The patient was admitted after another thrombosis of a right humerus median fistula&#44; which lasted for four months&#46; A temporary right femoral catheter was introduced without any immediate complications and haemodialysis was performed&#59; five days later the catheter was removed due to dysfunction and the left femoral vein was cannulated&#46; The patient complained of pain in his right thigh&#44; which had increased in diameter&#46; The echo-Doppler of right femoral vessels showed thrombosis of the right common femoral vein and the proximal segment of the deep femoral vein&#44; without images suggestive of fistula or aneurysm&#59; the CT angiogram of the thorax ruled out pulmonary thromboembolism&#46; The patient was treated with enoxaparin and subsequently with acenocoumarol&#46; A left humerobasilic arteriovenous fistula was performed and it continues to be functional after two years&#46;</p><p class="elsevierStylePara">The study of thrombophilia prior to the start of anticoagulation therapy showed a pathological value of activated protein C resistance of 1&#46;29 &#40;normal&#58;&#62;2&#46;1&#41;&#44; the genetic study revealed that the patient was homozygous for factor V Leiden variant&#59; anti-cardiolipin antibodies&#44; anti&#946;2 glycoprotein I antibodies&#44; antithrombin III&#44; protein C&#44; free protein S&#44; homocysteine&#44; lupus anticoagulant and prothrombin gene &#40;G20210A mutation&#41; normal&#47;negative&#59; no thrombocytopenia was observed&#46;</p><p class="elsevierStylePara">Resistance to activated protein C is the most common cause of inherited thrombophilia in the general population and a major risk factor for venous thrombosis&#46; Activated protein C resistance of genetic origin is usually due to a missense factor V &#40;factor V Leiden&#41; mutation&#44; which causes the adenine nucleotide to be replaced by guanine at gene position 1691&#59; in the peptide chain&#44; this modification results in the replacement of the amino acid arginine 506 by glutamine&#46; This mutation&#44; which is transmitted in an autosomal dominant way with incomplete penetrance&#44; makes factor V resistant to inhibition by activated protein C&#44; which makes more factor available and increases coagulability&#46;<span class="elsevierStyleSup">3</span></p><p class="elsevierStylePara">The role of factor V Leiden as a cause of VAT in haemodialysis is a subject of debate&#46; F&#246;dinger et al&#46;<span class="elsevierStyleSup">4</span> studied 152 haemodialysis patients&#44; of which 7 were heterozygous for the factor V Leiden&#59; they did not find a higher incidence of unexplained thrombosis in these cases&#44; although they did not rule out the possibility of homozygosity being a risk factor for VAT&#46; Knoll et al&#46;<span class="elsevierStyleSup">5</span> in a case-control study did find an increased risk of VAT in heterozygous individuals for the factor V</p><p class="elsevierStylePara">This patient also developed femoral thrombosis after the placement of a catheter&#46; It was considered that the femoral catheterisation had a higher incidence of thrombosis than the jugular&#44; but a recent study shows that the incidence is similar&#46;<span class="elsevierStyleSup">6</span></p><p class="elsevierStylePara">In this case&#44; the thromboses appeared after starting dialysis&#46; Therefore&#44; it seems that the factor V Leiden acted as a risk factor in combination with other thrombogenic causes&#58; hypercoagulability secondary to renal failure&#44; vascular damage&#44; stasis&#46;<span class="elsevierStyleSup">7</span> In conclusion&#44; in dialysis patients with repeated VAT&#44; the presence of inherited thrombophilia should be ruled out&#44; in order to prevent subsequent thrombotic vascular access events&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The authors declare that they have no conflicts of interest related to the contents of this article&#46;</p>"
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Recurrent haemodialysis vascular access thrombosis in a patient with factor V Leiden
Trombosis recurrente de acceso vascular para hemodiálisis en paciente con factor V Leiden
Ana Llamas-Álvareza, Ricardo Enríquezb, Ana E. Sirventb, M.ª Dolores Redondo-Pachónb, Isabel Millánb, Alicia Araquec, Francisco Amorósb
a Servicio de Medicina Intensiva, Hospital General de Elche, Alicante,
b Sección de Nefrología, Hospital General de Elche, Alicante,
c Centro de Hemodiálisis, ASHDO, Orihuela, Alicante,
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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">To the Editor&#58;</span></p><p class="elsevierStylePara">Thrombosis of internal arteriovenous fistulas in haemodialysis patients is usually caused by peri-anastomotic stenosis or factors such as external compression or low blood pressure&#46; The femoral vein allows rapid access in patients without vascular access who require haemodialysis&#46; The main complications of femoral catheterisation are infection and catheter dysfunction&#44; but it may also result in severe haemorrhage<span class="elsevierStyleSup">1</span> or femoral vein thrombosis&#46;<span class="elsevierStyleSup">2</span></p><p class="elsevierStylePara">The role played by inherited thrombophilia in haemodialysis vascular access thrombosis &#40;VAT&#41; is a debatable issue&#46;</p><p class="elsevierStylePara">We report the case of a 51-year-old male on haemodialysis due to chronic renal failure secondary to obstructive lithiasic nephropathy with recurrent thrombosis of arteriovenous fistula and femoral vein&#44; homozygous for factor V Leiden variant&#46; Personal history&#58; high blood pressure&#44; gout and a previous episode of VAT&#58; left humerocephalic fistula&#44; which was functional for twelve months&#46; No family history of thrombosis&#46; The patient was admitted after another thrombosis of a right humerus median fistula&#44; which lasted for four months&#46; A temporary right femoral catheter was introduced without any immediate complications and haemodialysis was performed&#59; five days later the catheter was removed due to dysfunction and the left femoral vein was cannulated&#46; The patient complained of pain in his right thigh&#44; which had increased in diameter&#46; The echo-Doppler of right femoral vessels showed thrombosis of the right common femoral vein and the proximal segment of the deep femoral vein&#44; without images suggestive of fistula or aneurysm&#59; the CT angiogram of the thorax ruled out pulmonary thromboembolism&#46; The patient was treated with enoxaparin and subsequently with acenocoumarol&#46; A left humerobasilic arteriovenous fistula was performed and it continues to be functional after two years&#46;</p><p class="elsevierStylePara">The study of thrombophilia prior to the start of anticoagulation therapy showed a pathological value of activated protein C resistance of 1&#46;29 &#40;normal&#58;&#62;2&#46;1&#41;&#44; the genetic study revealed that the patient was homozygous for factor V Leiden variant&#59; anti-cardiolipin antibodies&#44; anti&#946;2 glycoprotein I antibodies&#44; antithrombin III&#44; protein C&#44; free protein S&#44; homocysteine&#44; lupus anticoagulant and prothrombin gene &#40;G20210A mutation&#41; normal&#47;negative&#59; no thrombocytopenia was observed&#46;</p><p class="elsevierStylePara">Resistance to activated protein C is the most common cause of inherited thrombophilia in the general population and a major risk factor for venous thrombosis&#46; Activated protein C resistance of genetic origin is usually due to a missense factor V &#40;factor V Leiden&#41; mutation&#44; which causes the adenine nucleotide to be replaced by guanine at gene position 1691&#59; in the peptide chain&#44; this modification results in the replacement of the amino acid arginine 506 by glutamine&#46; This mutation&#44; which is transmitted in an autosomal dominant way with incomplete penetrance&#44; makes factor V resistant to inhibition by activated protein C&#44; which makes more factor available and increases coagulability&#46;<span class="elsevierStyleSup">3</span></p><p class="elsevierStylePara">The role of factor V Leiden as a cause of VAT in haemodialysis is a subject of debate&#46; F&#246;dinger et al&#46;<span class="elsevierStyleSup">4</span> studied 152 haemodialysis patients&#44; of which 7 were heterozygous for the factor V Leiden&#59; they did not find a higher incidence of unexplained thrombosis in these cases&#44; although they did not rule out the possibility of homozygosity being a risk factor for VAT&#46; Knoll et al&#46;<span class="elsevierStyleSup">5</span> in a case-control study did find an increased risk of VAT in heterozygous individuals for the factor V</p><p class="elsevierStylePara">This patient also developed femoral thrombosis after the placement of a catheter&#46; It was considered that the femoral catheterisation had a higher incidence of thrombosis than the jugular&#44; but a recent study shows that the incidence is similar&#46;<span class="elsevierStyleSup">6</span></p><p class="elsevierStylePara">In this case&#44; the thromboses appeared after starting dialysis&#46; Therefore&#44; it seems that the factor V Leiden acted as a risk factor in combination with other thrombogenic causes&#58; hypercoagulability secondary to renal failure&#44; vascular damage&#44; stasis&#46;<span class="elsevierStyleSup">7</span> In conclusion&#44; in dialysis patients with repeated VAT&#44; the presence of inherited thrombophilia should be ruled out&#44; in order to prevent subsequent thrombotic vascular access events&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The authors declare that they have no conflicts of interest related to the contents of this article&#46;</p>"
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