Fulminant bilateral cerebral infarction caused by paradoxical embolism in a patient with protein S Ala525Val substitution

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  • Yoji Yoshikawa
    Cerebrovascular and Neurology Center National Hospital Organization Fukuoka Higashi Medical Center Kyushu University Fukuoka Japan
  • Jiro Kitayama
    Cerebrovascular and Neurology Center National Hospital Organization Fukuoka Higashi Medical Center Kyushu University Fukuoka Japan
  • Hiromi Ishikawa
    Cerebrovascular and Neurology Center National Hospital Organization Fukuoka Higashi Medical Center Kyushu University Fukuoka Japan
  • Asako Nakamura
    Cerebrovascular and Neurology Center National Hospital Organization Fukuoka Higashi Medical Center Kyushu University Fukuoka Japan
  • Fumina Taniguchi
    Department of Clinical Laboratory Science Kanazawa University Graduate School of Medical Science Kanazawa University Hospital Kanazawa Japan
  • Eriko Morishita
    Department of Clinical Laboratory Science Kanazawa University Graduate School of Medical Science Kanazawa University Hospital Kanazawa Japan
  • Tetsuro Ago
    Department of Medicine and Clinical Science Graduate School of Medical Sciences Kyushu University Fukuoka Japan
  • Hiroshi Nakane
    Cerebrovascular and Neurology Center National Hospital Organization Fukuoka Higashi Medical Center Kyushu University Fukuoka Japan
  • Takanari Kitazono
    Department of Medicine and Clinical Science Graduate School of Medical Sciences Kyushu University Fukuoka Japan

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<jats:title>Abstract</jats:title><jats:p>We report a 42‐year‐old woman who developed sudden fulminant cerebral infarction in the bilateral middle cerebral artery territories, causing status epilepticus and a decreased level of consciousness. Investigation showed thrombus in the right soleus vein and a patent foramen ovale, but no obvious embolic source, such as atrial fibrillation or a carotid or cerebral artery atherosclerotic lesion. Blood coagulation tests showed decreased levels of free protein S (25%) and total protein S (52%), and decreased protein S activity (15%). The patient was diagnosed with cerebral infarction as a result of paradoxical embolism, and type I protein S deficiency. <jats:styled-content style="fixed-case">DNA</jats:styled-content> sequencing identified a novel point mutation in the <jats:italic><jats:styled-content style="fixed-case">PROS</jats:styled-content>1</jats:italic> gene, leading to the amino acid substitution, Ala525Val. It should be noted that this protein S mutation can cause thrombophilia and cerebral infarction.</jats:p>

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