Déficit de proteína C y S de la coagulación como causa de trombosis recurrente

Abstract

Thrombosis is defined as a local obstruction of blood flow in an arterial or venous blood vessel, causing the tissues and cells supplied by the vessel to become ischemic. Its most frequent clinical manifestations are stroke and myocardial infarction as representatives of arterial thromboembolism, and deep vein thrombosis (DVT) and pulmonary embolism as the main venous thromboembolism. In Ecuador, it is reported that 5 to 10% of hospital deaths are due to thromboembolic diseases. The prothrombotic state is defined as thrombophilia which can be acquired or hereditary, so this study is mainly focused on hereditary thrombophilias due to protein C and S deficiency, resulting in the loss of these anticoagulant properties, which leads to a Uncontrolled thrombin generation leading to thromboembolism.. We present the case of a 49-year-old patient with a history of episodes of superficial venous thrombosis in the right leg at the age of 42 and arterial thrombosis in the right arm at the age of 45, the latter complication resulting in a thrombectomy. The patient began with a treatment based on dabigatran 110 mg after arterial thrombosis, but discontinued the medication a year after starting it, due to its high cost. The reason for consultation for which he attended the following care was pain in the lower limbs, on inspection venous dilations were observed in both lower limbs and an increase in the diameter of the right lower limb, symptoms that have been present after the last thrombotic event. After this evaluation, interconsultation was requested from Vascular Surgery to Internal Medicine, to start the investigation of the cause of the thrombosis. Laboratory tests were taken, including biometry, coagulation times, liver function, tumor markers, D-dimer, and measurement of anticoagulant factors. In the first test, the levels of antithrombin III, factor V Leiden, protein C and S were low, which was attributed to xii

the use of dabigatran as anticoagulant therapy, but to rule out a new measurement was requested where an antithrombin III 89% was detected ( Normal), protein C 52% (Low), protein S 51% (Low) confirming the diagnosis of thrombophilia secondary to protein C and S deficiency. Treatment with warfarin and enoxaparin was started, then treatment was adjusted to warfarin 5mg 3 times a week and the rest of the days 2.5 mg.