Abstract Number ‐ 225: COVID‐19 As A Potential Inducer Of Antiphospholipid Syndrome In A Patient With Acute Ischemic Stroke
Introduction COVID‐19 has been linked to hypercoagulability and acute ischemic stroke, though the precise mechanism is not well understood [1]. Various mechanisms have been suggested, including the potential release of autoantibodies‐ either via self‐production or exacerbation of the release of alre...
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
2023-03-01
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| Series: | Stroke: Vascular and Interventional Neurology |
| Online Access: | https://www.ahajournals.org/doi/10.1161/SVIN.03.suppl_1.225 |
| _version_ | 1797803522878603264 |
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| author | Sheetal Hegde Siegfried Hirczy Mehari Gebreyohanns |
| author_facet | Sheetal Hegde Siegfried Hirczy Mehari Gebreyohanns |
| author_sort | Sheetal Hegde |
| collection | DOAJ |
| description | Introduction COVID‐19 has been linked to hypercoagulability and acute ischemic stroke, though the precise mechanism is not well understood [1]. Various mechanisms have been suggested, including the potential release of autoantibodies‐ either via self‐production or exacerbation of the release of already produced autoantibodies [2‐3]. Antiphospholipid antibodies have been identified in severe disease [3‐4] and implicated in thrombosis [1‐2], though the significance is unclear. In this report, we describe a young woman with asymptomatic COVID‐19 presenting with acute ischemic stroke and postulate it was a manifestation of activated autoimmunity from COVID‐19. Methods Case Report Results A 22 year‐old previously healthy woman presented with acute onset dysarthria and right upper extremity weakness and numbness. On presentation, blood pressure was 158/101. NIHSS was 2 for right upper extremity drift and decreased sensation. Neurologic exam was otherwise unremarkable. Thrombolytic therapy was not administered given presentation outside the time window. CT head showed scattered left centrum semiovale hypodensities without hemorrhage. MRI brain demonstrated multifocal areas of diffusion restriction in the left centrum semiovale, anterior frontal lobe, and parietal lobe. CT angiogram demonstrated a possible thrombus at the left carotid bifurcation which was redemonstrated on MR angiography of the neck. No atherosclerotic plaque, hemodynamically significant stenosis, nor other vascular abnormality were appreciated. Heparin drip was started. Hemoglobin was 6.9 for which 1 unit of packed red blood cells was transfused. White blood cell count was 9.02. Platelet count was 761. PT/INR and PTT were 13.4/1.2 and 30.1. HIV was negative, RPR was positive at 1:128 titer, and COVID PCR was positive. She did not experience respiratory symptoms. Urine drug screen was positive for cannabinoids. LDL was 66. Transthoracic echo demonstrated minimal right to left shunting, suggesting patent foramen ovale. Ejection fraction was 60–65% and chamber sizes were normal. Bilateral lower extremity ultrasound was negative for deep vein thrombosis as a potential embolic source given cardiac shunt. Given history of miscarriage and extensive family history of sickle cell trait, possible lupus anticoagulant, and thrombosis at young ages, hypercoagulable workup was sent. Sickle cell preparation and ANA were negative. ESR was 12. High sensitivity CRP was 2.71. Anticardiolipin IgM antibody was elevated significantly at 125.9 MPL and IgG antibody was indeterminately elevated at 19.2 GPL. Beta‐2 glycoprotein IgM antibodies were also elevated at 42 SMUnits. Atypical neurosyphilis was considered given positive titer, middle cerebral artery distribution, and young age, but deemed unlikely given embolic rather than inflammatory stroke pattern [5]. Ultimately, with a possible diagnosis of antiphospholipid syndrome, anticoagulation was transitioned to warfarin via enoxaparin bridge with plan for repeat hypercoagulable workup as outpatient. Conclusions COVID‐19 has been observed in association with hypercoagulable states such as deep venous thrombosis and stroke. Here we present a case of COVID‐19 associated ischemic stroke with concomitant antiphospholipid antibodies. This case highlights the potential for even asymptomatic/mild COVID‐19 to induce autoimmunity through modulation of host antibody activity. This may be more profound in those with a predisposition to thrombosis. Autoimmunity should be considered in cases of concurrent COVID‐19 and acute ischemic stroke without clear etiology. |
| first_indexed | 2024-03-13T05:22:09Z |
| format | Article |
| id | doaj.art-4a08d5267a564f71bfcbd61b2537d301 |
| institution | Directory Open Access Journal |
| issn | 2694-5746 |
| language | English |
| last_indexed | 2024-03-13T05:22:09Z |
| publishDate | 2023-03-01 |
| publisher | Wiley |
| record_format | Article |
| series | Stroke: Vascular and Interventional Neurology |
| spelling | doaj.art-4a08d5267a564f71bfcbd61b2537d3012023-06-15T10:40:49ZengWileyStroke: Vascular and Interventional Neurology2694-57462023-03-013S110.1161/SVIN.03.suppl_1.225Abstract Number ‐ 225: COVID‐19 As A Potential Inducer Of Antiphospholipid Syndrome In A Patient With Acute Ischemic StrokeSheetal Hegde0Siegfried Hirczy1Mehari Gebreyohanns2UT Southwestern Medical Center Dallas Texas United States of AmericaUT Southwestern Medical Center Dallas Texas United States of AmericaUT Southwestern Medical Center Dallas Texas United States of AmericaIntroduction COVID‐19 has been linked to hypercoagulability and acute ischemic stroke, though the precise mechanism is not well understood [1]. Various mechanisms have been suggested, including the potential release of autoantibodies‐ either via self‐production or exacerbation of the release of already produced autoantibodies [2‐3]. Antiphospholipid antibodies have been identified in severe disease [3‐4] and implicated in thrombosis [1‐2], though the significance is unclear. In this report, we describe a young woman with asymptomatic COVID‐19 presenting with acute ischemic stroke and postulate it was a manifestation of activated autoimmunity from COVID‐19. Methods Case Report Results A 22 year‐old previously healthy woman presented with acute onset dysarthria and right upper extremity weakness and numbness. On presentation, blood pressure was 158/101. NIHSS was 2 for right upper extremity drift and decreased sensation. Neurologic exam was otherwise unremarkable. Thrombolytic therapy was not administered given presentation outside the time window. CT head showed scattered left centrum semiovale hypodensities without hemorrhage. MRI brain demonstrated multifocal areas of diffusion restriction in the left centrum semiovale, anterior frontal lobe, and parietal lobe. CT angiogram demonstrated a possible thrombus at the left carotid bifurcation which was redemonstrated on MR angiography of the neck. No atherosclerotic plaque, hemodynamically significant stenosis, nor other vascular abnormality were appreciated. Heparin drip was started. Hemoglobin was 6.9 for which 1 unit of packed red blood cells was transfused. White blood cell count was 9.02. Platelet count was 761. PT/INR and PTT were 13.4/1.2 and 30.1. HIV was negative, RPR was positive at 1:128 titer, and COVID PCR was positive. She did not experience respiratory symptoms. Urine drug screen was positive for cannabinoids. LDL was 66. Transthoracic echo demonstrated minimal right to left shunting, suggesting patent foramen ovale. Ejection fraction was 60–65% and chamber sizes were normal. Bilateral lower extremity ultrasound was negative for deep vein thrombosis as a potential embolic source given cardiac shunt. Given history of miscarriage and extensive family history of sickle cell trait, possible lupus anticoagulant, and thrombosis at young ages, hypercoagulable workup was sent. Sickle cell preparation and ANA were negative. ESR was 12. High sensitivity CRP was 2.71. Anticardiolipin IgM antibody was elevated significantly at 125.9 MPL and IgG antibody was indeterminately elevated at 19.2 GPL. Beta‐2 glycoprotein IgM antibodies were also elevated at 42 SMUnits. Atypical neurosyphilis was considered given positive titer, middle cerebral artery distribution, and young age, but deemed unlikely given embolic rather than inflammatory stroke pattern [5]. Ultimately, with a possible diagnosis of antiphospholipid syndrome, anticoagulation was transitioned to warfarin via enoxaparin bridge with plan for repeat hypercoagulable workup as outpatient. Conclusions COVID‐19 has been observed in association with hypercoagulable states such as deep venous thrombosis and stroke. Here we present a case of COVID‐19 associated ischemic stroke with concomitant antiphospholipid antibodies. This case highlights the potential for even asymptomatic/mild COVID‐19 to induce autoimmunity through modulation of host antibody activity. This may be more profound in those with a predisposition to thrombosis. Autoimmunity should be considered in cases of concurrent COVID‐19 and acute ischemic stroke without clear etiology.https://www.ahajournals.org/doi/10.1161/SVIN.03.suppl_1.225 |
| spellingShingle | Sheetal Hegde Siegfried Hirczy Mehari Gebreyohanns Abstract Number ‐ 225: COVID‐19 As A Potential Inducer Of Antiphospholipid Syndrome In A Patient With Acute Ischemic Stroke Stroke: Vascular and Interventional Neurology |
| title | Abstract Number ‐ 225: COVID‐19 As A Potential Inducer Of Antiphospholipid Syndrome In A Patient With Acute Ischemic Stroke |
| title_full | Abstract Number ‐ 225: COVID‐19 As A Potential Inducer Of Antiphospholipid Syndrome In A Patient With Acute Ischemic Stroke |
| title_fullStr | Abstract Number ‐ 225: COVID‐19 As A Potential Inducer Of Antiphospholipid Syndrome In A Patient With Acute Ischemic Stroke |
| title_full_unstemmed | Abstract Number ‐ 225: COVID‐19 As A Potential Inducer Of Antiphospholipid Syndrome In A Patient With Acute Ischemic Stroke |
| title_short | Abstract Number ‐ 225: COVID‐19 As A Potential Inducer Of Antiphospholipid Syndrome In A Patient With Acute Ischemic Stroke |
| title_sort | abstract number 225 covid 19 as a potential inducer of antiphospholipid syndrome in a patient with acute ischemic stroke |
| url | https://www.ahajournals.org/doi/10.1161/SVIN.03.suppl_1.225 |
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