67-year-old patient with a history of arterial hypertension, transient ischaemic accident, osteoporosis, deep vein thrombosis of the left lower limb with oral anticoagulation with antivitamin K, and atrial fibrillation. He was admitted to the Internal Medicine Department for acute abdominal pain, of three days' evolution, with normal stool rhythm and no fever. The patient is being treated with alendronate, atenolol, torasemide, olmesartan, bisoprolol. Physical examination was normal, except for arrhythmic heart sounds and epigastric abdominal pain on palpation. Abdominal ultrasound showed mesenteric and portal venous thrombosis. The study was completed with an abdominal CT scan, confirming portal, splenic and superior mesenteric venous thrombosis. INR was checked and correct anticoagulation levels were observed (INR 2-3) from the beginning to the present. Laboratory tests showed moderate thrombocytosis with 400,000 platelets, 12,000 leukocytes and normal haemoglobin levels. Biochemistry with proteinogram and immunofixation in serum and urine, thrombophilic study determining lupus anticoagulant, Ac anticardiolipin and beta 2 glycoprotein I, Factor V Leiden mutation, prothrombin 20,210 G-A with normal result and JAK2 mutation being positive. The diagnosis of portal axis thrombosis was confirmed, probably related to a positive JAK2 myeloproliferative syndrome.
Treatment was started with unfractionated heparin in relation to the possible need for surgery due to mesenteric ischaemia, which was replaced on the 4th day by enoxaparin at a dose of 1mg/kg /12h. On the seventh day after starting unfractionated heparin and the third day with LMWH, platelet levels began to decrease from one million to 500,000 with a progressive decrease to 123,000/ml on day 12, associated with dyspnoea, hypoxaemia and bilateral pleural effusion. Thoracic CT angiography confirmed bilateral pulmonary thromboembolism. With suspicion of HIT, the technique (ID-PaGIA Heparine/PF4/heparin antibody test/ID-Car) was performed with a positive result and in combination with a high probability, score 7-8, in the "4Ts test "2 , treatment was started with lepirudin, which was modified after 36 h. to dabigatran with the consent of the patient. the patient progressed satisfactorily with disappearance of pleural effusion and an increase in the number of platelets to values close to 300,000 in 48 h. and with disappearance of pulmonary emboli in angioCT two weeks after the start of treatment, remaining until the present time with this treatment in relation to AF, and failure of treatment with associated VKA.

