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6 results

  • Chapter 5.3 - Chapter

  • from 5 - Hereditary and Genetic Causes of Stroke
  • Edited by Derya Uluduz, Istanbul Üniversitesi
  • Anita Arsovska
  • Book:
    Rare Causes of Stroke
    Published online:
    06 October 2022
    Print publication:
    01 September 2022, pp 253-261

  • Summary

    SLE is an autoimmune chronic progressive disease which affects the central and peripheral nervous system and causes different neuropsychiatric symptoms. Stroke is the most severe complication of SLE and the incidence rate is approximately 3-20% especially in the first five years of the disease. Many factors such as high level of aPL, hyperhomocysteinemia, lupus disease activity, cerebral vasculitis, emboli from Libman-Sacks endocarditis, accelerated atherosclerosis cause stroke in SLE. Immune complex deposition in vascular endothelium, intrathecal immune complexes and other inflammatory mediators are involved in the pathogenesis of vasculopathy and vasculitis. Here, we present a 41-year-old Syrian woman with diagnosis of SLE and antiphospholipid antibody syndrome

  • Chapter 3.1 - Antiphospholipid Antibody Syndrome

  • from 3 - Hypercoagulable Causes of Stroke
  • Edited by Derya Uluduz, Istanbul Üniversitesi
  • Anita Arsovska
  • Book:
    Rare Causes of Stroke
    Published online:
    06 October 2022
    Print publication:
    01 September 2022, pp 151-156

  • Summary

    Antiphospholipid antibody syndrome (APS) is a multisystem autoimmune disease characterized by venous or arterial thrombosis and/or pregnancy morbidity in the presence of persistent antiphosholipid antibodies (aPLs). Central nervous system is often affected and thrombotic or embolic ischaemic stroke (IS) is the most frequent complication. Intracranial stenosis or occlusion accounts for about 50% of APS patients, especially in the Middle cerebral artery territory (MCA). We report a case of a young woman with recurrent cerebral ischemic lesions and history of miscarriages. In 2015 a 43 years old woman was admitted to Emergency Department (ED) due to a left brachial weakness at wake-up from an ischemic fronto-parietal lesions and steno-occlusion of the proximal M1 segment of the right Middle Cerebral Artery (MCA). She had a history of arterial hypertension, migraine, previous transient ischemic attack (TIA) and was a tobacco smoker. Diagnostic workup showed high levels of aPLs. She was discharged with improved clinical conditions on antiplatelet and steroid therapy, but she had recurrent IS a month later and three years later. In the same period, she reported two miscarriages. Follow up lab tests confirmed high-titre of aPLs. Therefore, diagnosis of APS was validated. A direct oral anticoagulant was started. No recurrent events occurred over the next 2-year follow-up. Stroke is a common manifestation in APS. Diagnosis of APS is not easy. Prospective data on the therapeutic approach to APS patients with IS are scarce and recurrence rate of thrombotic events among APS patients are high, despite anticoagulation

  • When the Problem Became the Solution

  • Ari Shemesh, Laila Al-Shafai, Timo Krings, Edward Margolin
  • Journal:
    Canadian Journal of Neurological Sciences / Volume 46 / Issue 6 / November 2019
    Published online by Cambridge University Press:
    04 July 2019, pp. 767-769
    • Article
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  • We present a unique case where a young man developed subtle cavernous sinus thrombosis (CST) due to underlying hypercoagulable state. He also had coexisting frontal lobe brain dural arteriovenous fistula (bdAVF). After CST developed, venous drainage from the optic nerve was redirected into the frontal lobe which was already under high venous pressure because of preexisting bdAVF. This caused backflow of venous blood into the optic nerve causing massive persistent optic nerve head swelling. Presumed acute venous hypertension event within bdAVF caused frontal mass effect presenting as seizure leading to thrombosis of bdAVF.

  • Libman–Sacks endocarditis as the first manifestation of systemic lupus erythematosus in an adolescent, with a review of the literature

  • Jayendra Sharma, Zoran Lasic, Abraham Bornstein, Rubin Cooper, Jonathan Chen
  • Journal:
    Cardiology in the Young / Volume 23 / Issue 1 / February 2013
    Published online by Cambridge University Press:
    18 July 2012, pp. 1-6

  • Libman–Sacks endocarditis is rare in children and adolescents, more so as a first manifestation of systemic lupus erythematosus. Currently, sterile verrucous lesions of Libman–Sacks endocarditis are recognised as a cardiac manifestation of both systemic lupus erythematosus and antiphospholipid syndrome. They are clinically silent in a majority of the cases. The presence of antiphospholipid antibodies in systemic lupus erythematosus is associated with three times higher prevalence of mitral valve nodules and significant mitral regurgitation. We present the case of isolated mitral regurgitation with abnormal looking mitral valve, detected in early childhood, which deteriorated to a severe degree in the next decade and was diagnosed as Libman–Sacks endocarditis after surgical repair from histopathology. The full-blown clinical spectrum of systemic lupus erythematosus with antiphospholipid antibodies was observed several weeks after cardiac surgery. We discuss the atypical course of Libman–Sacks endocarditis with follow-up for 10 years, along with a review of the literature.

  • 45 - Thrombophilia and Implanation Failure

  • from PART III - ASSISTED REPRODUCTION
  • Edited by Botros R. M. B. Rizk, University of South Alabama, Juan A. Garcia-Velasco, Hassan N. Sallam, Antonis Makrigiannakis, University of Crete
  • Book:
    Infertility and Assisted Reproduction
    Published online:
    04 August 2010
    Print publication:
    15 September 2008, pp 407-415

  • Summary

    This chapter focuses on the association between acquired and inherited thrombophilia and implantation failure (IF). The pathogenesis of recurrent IF in patients with thrombophilic gene mutation may involve the effect of hypofibrinolysis on trophoblast migration. Trophoblastic migration and invasion during implantation involve extracellular matrix degradation, which is facilitated by matrix metalloproteinases (MMP). Recently, a variety of pathogenetic mechanisms have been suggested to explain the prothrombotic effect of antiphospholipid antibody (APA), the main cause of acquired thrombophilia. Recently, it has been suggested that APA may negatively impact the transformation of the endometrium into decidua, creating a hostile environment for blastocyst implantation. The chapter investigates the main therapeutic modalities such as heparin, aspirin (ASA), corticosteroids, and intravenous immunoglobulin alone or in combinations for treatment of IF. It is premature to recommend anticoagulation for patients with thrombophilia and IF.