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High Complement Levels: Is It an Unknown Risk Factor for Recurrent Ischemic Stroke? FREE TO VIEW

Meera Yogarajah, MD; Bhradeev Sivasambu, MD
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Interfaith Medical Center, Brooklyn, NY

Chest. 2015;148(4_MeetingAbstracts):278A. doi:10.1378/chest.2260536
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SESSION TITLE: Critical Care Student/Resident Case Report Posters II

SESSION TYPE: Student/Resident Case Report Poster

PRESENTED ON: Tuesday, October 27, 2015 at 01:30 PM - 02:30 PM

INTRODUCTION: Ischemic stroke is caused by several pathophysiologic processes involving the blood vessels of the brain. The possibility of high complement levels predisposing to recurrent ischemic stroke has not been reported. However there are few studies which demonstrate the increase risk of thromobosis associated with hypercomplementemia.

CASE PRESENTATION: A 52 year old female presented with acute distrubances in her vison on both eyes. She denied any limb weakness or slurring of speech. She had no other medical problems. She was a smoker for many years. Physical examination revealed superior visual field defect of both eyes. Other systems examination was unrevealing. Initial complete blood count and chemistry was normal. Magnetic resonance imaging of brain showed bilateral occipital infarcts. Her electrocardiogram did not show any rhythm abnormalities. Carotid doppler, echocardiogram and magnetic resonance angiogram of brain were normal. Antinuclear antibody, antiphospholipid antibodies, vasculitic workup, rapid plasma reagin and human immunodeficiency virus serology were negative. Her complement components C3 and C4 were significantly elevated respectively to 230 mg/dl (normal range 79-152) and 67 mg/dl (normal range 16-38). Her Erythrocyte sedimentation rate(ESR) and C-reactive protein(CRP) were normal. She presented again within a month with weakness of her left side of her body and dizziness and Magnetic resonance imaging revealed new right cerebellar and right temporal lobe infarct. The C3 and C4 levels during this new stroke were also found to be elevated with normal ESR and CRP. Magnetic resonance angiogram of brain, echocardiogram, carotid doppler and vasculitic workup were repeated and normal. The only possible risk factor for recurrent stroke in this patient was high complement levels.

DISCUSSION: The pathophysiology of ischemic stroke is multifactorial. Intrinsic disease of the cerebral vessels, embolus from the heart or extracranial circulation and inadequate cerebral perfusion are the mechanisms of ischemic stroke. However the role of high complement levels as a risk factor for recurrent stroke has not been reported. High complement levels can occur with inflammation and infection. There have been studies showing that high complement levels increases the risk of thrombosis. In a study of patients with antiphospholipid syndrome patients with high complement levels had increased risk of thrombosis. There was a reported case of Inferior vena cava thrombosis and hypercomplimentemia which described the thrombogenicity of complement proteins.

CONCLUSIONS: Further studies are necessary to confirm the potential of high complement levels as a risk factor for thrombotic events. High complement level is the possible explanation for this patient’s recurrent stroke.

Reference #1: Chandelia S1, Inferior vena cava thrombosis in a case of amoebic liver abscess: is hypercomplementemia responsible for this rare entity? Indian J Pathol Microbiol. 2014 Apr-Jun;57(2):329-31

DISCLOSURE: The following authors have nothing to disclose: Meera Yogarajah, Bhradeev Sivasambu

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