BACKGROUND: Systemic lupus erythematosus (SLE) is an autoimmune disease associated with increased risk of stroke. Antiphospholipid syndrome is another autoimmune disease that frequently overlaps with SLE. We report the case of a patient presenting with subarachnoid hemorrhage after ischemic stroke associated with SLE and antiphospholipid syndrome. CASE DESCRIPTION: A 22-year-old man presented with cerebral infarction of the right corona radiata. He had no contributory past or family histories. On imaging at this time, a 4-mm fusiform aneurysm of the right anterior cerebral artery was incidentally detected. Several examinations were performed, but no abnormalities or abnormal lesions were seen on echography or whole-body computed tomography. Blood tests yielded positive results for antinuclear antibody, lupus anticoagulant, and anti-beta-2 glycoprotein І antibody. He presented 70 days later with subarachnoid hemorrhage. Cerebral angiography showed the same fusiform aneurysm without any change in shape and no new aneurysms. The balloon occlusion test was performed without any neurologic symptoms, so the right anterior cerebral artery was trapped using coils. After 6 months, he presented with new optic hyperesthesia and facial butterfly-shaped erythema and fulfilled the criteria for SLE. At 2 years after initial presentation, he showed no recurrence of either aneurysm or ischemic stroke. CONCLUSIONS: The patient's first ischemic stroke was induced by antiphospholipid syndrome and underlying SLE. Fusiform aneurysm may have resulted from focal vasculitis, with activation of SLE leading to aneurysm rupture.
BACKGROUND:Systemic lupus erythematosus (SLE) is an autoimmune disease associated with increased risk of stroke. Antiphospholipid syndrome is another autoimmune disease that frequently overlaps with SLE. We report the case of a patient presenting with subarachnoid hemorrhage after ischemic stroke associated with SLE and antiphospholipid syndrome. CASE DESCRIPTION: A 22-year-old man presented with cerebral infarction of the right corona radiata. He had no contributory past or family histories. On imaging at this time, a 4-mm fusiform aneurysm of the right anterior cerebral artery was incidentally detected. Several examinations were performed, but no abnormalities or abnormal lesions were seen on echography or whole-body computed tomography. Blood tests yielded positive results for antinuclear antibody, lupus anticoagulant, and anti-beta-2 glycoprotein І antibody. He presented 70 days later with subarachnoid hemorrhage. Cerebral angiography showed the same fusiform aneurysm without any change in shape and no new aneurysms. The balloon occlusion test was performed without any neurologic symptoms, so the right anterior cerebral artery was trapped using coils. After 6 months, he presented with new optic hyperesthesia and facial butterfly-shaped erythema and fulfilled the criteria for SLE. At 2 years after initial presentation, he showed no recurrence of either aneurysm or ischemic stroke. CONCLUSIONS: The patient's first ischemic stroke was induced by antiphospholipid syndrome and underlying SLE. Fusiform aneurysm may have resulted from focal vasculitis, with activation of SLE leading to aneurysm rupture.