PROGRESSIVE VENOUS THROMBOEMBOLISM AND WARFARIN-INDUCED SKIN NECROSIS ON BACKGROUND DIABETUS MELLITUS TYPE 2 IN COMBINATION WITH ACCOMPANIED DISEASE: A CLINICAL CASE
Authors: Malchevska Т.Y. , Lukianchuk V.A. 
Published: December 2024

Background. Oral anticoagulants used in clinical practice in atrial fibrillation, deep vein thrombosis, pulmonary embolism (PE), as well as in heart valves protesis, heart thrombosis. Warfarin is the medicine with the largest evidence base and a long history of use more than 70 years. The optimal anticoagulant effect of warfarin is INR from 2,0-3,0 with 70% of measurements (TTR 70%). In one case there is a risk of ischemic stroke in non-compliance, in another - bleeding. Although cutaneous manifestations are rare, however, warfarin-induced skin necrosis is extremely dangerous.
Present`s clinical case of progressive venous thromboembolism on the background of anticoagulant therapy in a 64-year-old woman with comorbid pathology. The described clinical, laboratory and instrumental data, that confirmed thrombotic and thromboembolic complications, which were ineffective in relation to the traditional anticoagulant strategy.
Aim: to describe a clinical case and analyze the challenges in diagnosing and treatment of progressive venous thromboembolism in a patient with concomitant diabetus mellitus type 2, obese,cirrhosis of liver , ineffective anticoagulants and developing warfarin skin necrosis.
Materials and methods. The article presents the clinical case of pulmonary embolism, progressive venous thromboembolism in a 64- year -old woman with concomitant diabetus mellitus type 2, obese,cirrhosis of liver that was observed in IUC in the Hospital” Medbud’.
Results. A 64-year-old woman, was hospitalized in the therapeutic department of «Medbud» with a previous diagnosis of cirrhosis of the liver unknown etiology, Child-Pugh class A, hepatolienal syndrome, articular and hemorrhagic syndrome, de novo diabetus mellitus of type 2, paroxysmal atrial fibrillation tachisystolic variant. Preliminarily prescribed dabigatran without “bridge therapy”at a dose of 150 mg twice a day every other day on the recommendation of a gastroenterologist. Suspected pulmonary embolism made adjustments to treatment and anticoagulant therapy was switched from NOAC to UFH, then to LMWH with the addition of warfarin. There was progression of venous thromboembolism in the upper and lower limbs with the appearance of warfarin skin necrosis.
Conclusion. Thus, cumulative influence of start therapy dabigatran without bridge heparin therapy, disturbance dabigatran regimes and drug interaction with glucocorticoids, postinjection phlebitis, liver disease, thrombocytopenia and hypothetical insufficiency antithrombin-III, protein C had influenced on progressive venous thromboembolism on background diabetus mellitus type 2, obese. Warfarin-induced skin necrosis is rare complication, but is often dangerous. In the absence of protein C, antithrombin – III, if possible, consider an alternative anticoagulant. The failures of anticoagulant therapy are not only associated with delays in its appointment, switching of anticoagulants, but also taking into account the drug interaction, concomitant pathology, the choice of the optimal drug and the prediction of its adverse effects.