May-Thurner Syndrome and Protein SDeficiency: A Case of Extensive IliofemoralDeep Vein Thrombosis in a Young Adult

Abstract

Venous thromboembolism is a common cardiovascular disorder that can lead to pulmonary embolism, recurrent
thrombosis, and post-thrombotic syndrome (PTS), with iliofemoral deep vein thrombosis (DVT) carrying a high
thrombus burden, severe symptoms, and risk of persistent venous obstruction. May-Thurner syndrome (MTS)
is an anatomic cause of left-sided iliofemoral DVT due to right common iliac artery compression of the left
common iliac vein, and protein S deficiency can further increase the thrombotic propensity, creating a dual-hit
mechanism. This report describes the diagnostic evaluation and management of extensive iliofemoral DVT in
a young adult with concomitant MTS and protein S deficiency and highlights the implications for etiological
workup and combined therapy. A 27-year-old previously healthy man presented with 4 days of left lower limb
pain and swelling (circumference 39 cm vs. 34 cm on the right). Doppler ultrasonography confirmed extensive
thrombosis involving the common femoral, great saphenous, femoral, and popliteal veins. Laboratory testing
showed leukocytosis and elevated inflammatory markers (erythrocyte sedimentation rate of 60 mm/h, C-reactive
protein of 153.57 mg/L) with normal baseline coagulation indices. Hypercoagulability workup revealed factor V
Leiden negativity, normal antithrombin III activity, weakly positive antinuclear antibody, and severely reduced
protein S (<8%). Contrast-enhanced computed tomography venography revealed an occlusive thrombus from the
left common iliac vein-inferior vena cava junction through multiple iliac and femoropopliteal segments, with iliac
vein compression consistent with MTS and additional right internal iliac vein occlusion. He received heparin,
streptokinase thrombolysis, thrombectomy/angioplasty, improved clinically, and was discharged on apixaban with
planned venoplasty.