Severe Cerebral Venous Sinus Thrombosis and Deep Vein Thrombosis Induced by Non-Criteria aPI and aPS/PT Positive Antiphospholipid Antibodies: A Case Report and Mini Review

Background Antiphospholipid syndrome (APS) is a systemic autoimmune disorder that causes thrombotic events. APS rarely leads to cerebral venous sinus thrombosis (CVST), and it is even more uncommon for non-criteria antiphospholipid antibodies (aPI, aPS/PT-IgM) to contribute to CVST. Case presentation: A 32-year-old male patient was admitted to the hospital with a chief complaint of "headache for five days and limb convulsions for one hour." CT revealed a subarachnoid hemorrhage and a high-density shadow in the right transverse sinus area. CTV and DSA demonstrated a filling defect in the right internal jugular vein, right sigmoid sinus, right transverse sinus, straight sinus, and superior sagittal sinus. Following repeated thrombectomy, venous sinus imaging showed improvement after the removal of a large thrombus. The patient received sequential anticoagulant therapy with low-molecular-weight heparin and warfarin, dehydration therapy with mannitol, nimodipine for cerebral vasospasm prevention, levetiracetam for seizure management, and antibiotics. During treatment, the patient experienced swelling in the left upper limb at the site of an indwelling needle infusion. B-mode ultrasound revealed venous thrombosis in the left axillary and basilic veins. Laboratory tests showed an antinuclear antibody (ANA) titer of 1:100, and positivity for anti-SS-A antibodies. However, a labial gland biopsy revealed only a small number of lymphocytes, ruling out Sjögren’s syndrome. Genetic testing for folate metabolism showed mild abnormalities. The antiphospholipid antibody panel indicated positivity for anti-phosphatidylinositol antibody-IgM (aPI-IgM) and an elevated level of anti-phosphatidylserine/prothrombin complex antibody-IgM (aPS/PT-IgM) at 93.44 ng/mL (normal range: 0–75 ng/mL). Bone marrow cytology was normal. The diagnosis was confirmed as cerebral venous sinus thrombosis due to APS. Four months later, follow-up CTV showed complete resolution of the thrombosis, but the antiphospholipid antibody panel remained positive for aPS/PT-IgM and anti-phosphatidylethanolamine antibody (aPE). Conclusions Non-criteria antiphospholipid antibodies, particularly aPI-IgM and aPS/PT-IgM, can contribute to CVST. Vitamin K antagonists (VKAs) are the preferred anticoagulants, and mechanical thrombectomy should be considered in severe cases. The presence of aPS/PT-IgM may be closely associated with CVST and could serve as a potential molecular marker for APS.