好酸球増多による多発性脳梗塞が疑われたT 細胞性リンパ腫の1 剖検例
要旨：症例は69 歳男性．胸腹水貯留，好酸球増多の原因精査中に多発性脳梗塞を発症した．基礎疾患はT 細胞性リンパ腫と診断でき，リンパ腫に付随した好酸球増多であった．頭部MRI では大脳皮質・皮質下の境界領域，小脳半球などに多発する微小梗塞を認めた．好酸球増多症候群の1 症状としての脳梗塞と考え，ステロイドパルス療法を施行し，反応性に好酸球数が低下した．T 細胞性リンパ腫に対し化学療法を施行するも奏功せず，DIC を発症し多臓器不全となり死亡に至った．剖検では脳の血管内・実質には好酸球の浸潤を認めなかった．好酸球増多による脳梗塞の病理学的症例報告は少なく，貴重な症例と考え報告する．...
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| Published in | 脳卒中 Vol. 36; no. 5; pp. 361 - 365 |
|---|---|
| Main Authors | , , , , |
| Format | Journal Article |
| Language | Japanese |
| Published |
一般社団法人 日本脳卒中学会
2014
日本脳卒中学会 |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0912-0726 1883-1923 |
| DOI | 10.3995/jstroke.36.361 |
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| Abstract | 要旨：症例は69 歳男性．胸腹水貯留，好酸球増多の原因精査中に多発性脳梗塞を発症した．基礎疾患はT 細胞性リンパ腫と診断でき，リンパ腫に付随した好酸球増多であった．頭部MRI では大脳皮質・皮質下の境界領域，小脳半球などに多発する微小梗塞を認めた．好酸球増多症候群の1 症状としての脳梗塞と考え，ステロイドパルス療法を施行し，反応性に好酸球数が低下した．T 細胞性リンパ腫に対し化学療法を施行するも奏功せず，DIC を発症し多臓器不全となり死亡に至った．剖検では脳の血管内・実質には好酸球の浸潤を認めなかった．好酸球増多による脳梗塞の病理学的症例報告は少なく，貴重な症例と考え報告する． |
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| AbstractList | 要旨：症例は69 歳男性．胸腹水貯留，好酸球増多の原因精査中に多発性脳梗塞を発症した．基礎疾患はT 細胞性リンパ腫と診断でき，リンパ腫に付随した好酸球増多であった．頭部MRI では大脳皮質・皮質下の境界領域，小脳半球などに多発する微小梗塞を認めた．好酸球増多症候群の1 症状としての脳梗塞と考え，ステロイドパルス療法を施行し，反応性に好酸球数が低下した．T 細胞性リンパ腫に対し化学療法を施行するも奏功せず，DIC を発症し多臓器不全となり死亡に至った．剖検では脳の血管内・実質には好酸球の浸潤を認めなかった．好酸球増多による脳梗塞の病理学的症例報告は少なく，貴重な症例と考え報告する． 「要旨」 : 症例は69歳男性. 胸腹水貯留, 好酸球増多の原因精査中に多発性脳梗塞を発症した. 基礎疾患はT細胞性リンパ腫と診断でき, リンパ腫に付随した好酸球増多であった. 頭部MRIでは大脳皮質・皮質下の境界領域, 小脳半球などに多発する微小梗塞を認めた. 好酸球増多症候群の1症状としての脳梗塞と考え, ステロイドパルス療法を施行し, 反応性に好酸球数が低下した. T細胞性リンパ腫に対し化学療法を施行するも奏功せず, DICを発症し多臓器不全となり死亡に至った. 剖検では脳の血管内・実質には好酸球の浸潤を認めなかった. 好酸球増多による脳梗塞の病理学的症例報告は少なく, 貴重な症例と考え報告する. 「はじめに」好酸球増多症候群 (hypereosinophilic syndrome ; HES) とは, 1975年にChusidが末梢血好酸球数1500/μl以上が6ヵ月以上持続し, アレルギー性, 寄生虫, 悪性腫瘍, 血管炎, その他の好酸球増多を来す疾患が除外され, 好酸球浸潤による臓器障害がみられる特発性の疾患を定義した. |
| Author | 萩原, 麻衣 松井, 大 中奥, 由里子 奥野, 知子 水本, 智咲 |
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| DOI | 10.3995/jstroke.36.361 |
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| References | 7) Weller PF, Bubley GJ: The idiopathic hypereosinophilic syndrome. Blood 83: 2759–2779, 1994 18) Grigoryan M, Geisler SD, St Louis EK, et al: Cerebral arteriolar thromboembolism in idiopathic hypereosinophilic syndrome. Arch Neurol 66: 528–531, 2009 15) Fletcher S, Bain B: Diagnosis and treatment of hypereosinophilic syndromes. Curr Opin Hematol 14: 37–42, 2007 2) Roufosse FE, Goldman M, Cogan E: Hypereosinophilic syndromes. Orphanet J Rare Dis 2: 37, 2007 8) McMillan HJ, Johnston DL, Doja A: Watershed infarction due to acute hypereosinophilia. Neurology 70: 80–82, 2008 11) Caplan LR, Hennerici M: Impaired clearance of emboli (washout) is an important link between hypoperfusion, embolism, and ischemic stroke. Arch Neurol 55: 1475–1482, 1998 1) Chusid MJ, Dale DC, West BC, et al: The hypereosinophilic syndrome: analysis of fourteen cases with review of the literature. Medicine (Baltimore) 54: 1–27, 1975 16) Roufosse F, Cogan E, Goldman M: Recent advances in pathogenesis and management of hypereosinophilic syndromes. Allergy 59: 673–689, 2004 5) Sethi HS, Schmidley JW: Cerebral infarcts in the setting of eosinophilia: three cases and a discussion. Arch Neurol 67: 1275–1277, 2010 10) Aida L, Parkhutik V, Tembl JI, et al: Embolism and impaired washout: a possible explanation of border zone strokes in hypereosinophilic syndrome. J Neurol Sci 325: 162–164, 2013 12) Kaplan PW, Waterbury L, Kawas C, et al: Reversible dementia with idiopathic hypereosinophilic syndrome. Neurology 39: 1388–1391, 1989 13) Roche-Lestienne C, Lepers S, Soenen-Cornu V, et al: Molecular characterization of the idiopathic hypereosinophilic syndrome (HES) in 35 French patients with normal conventional cytogenetics. Leukemia 19: 792–798, 2005 9) Sarazin M, Caumes E, Cohen A, et al: Multiple microembolic borderzone brain infarctions and endomyocardial fibrosis in idiopathic hypereosinophilic syndrome and in Schistosoma mansoni infestation. J Neurol Neurosurg Psychiatr 75: 305–307, 2004 4) Tefferi A, Patnaik MM, Pardanani A: Eosinophilia: secondary, clonal and idiopathic. Br J Haematol 133: 468–492, 2006 17) Ishii T, Koide O, Hosoda Y, et al: Hypereosinophilic multiple thrombosis. A proposal of a new designation of disseminated eosinophilic “collagen disease”. Angiology 28: 361–375, 1977 3) Moore PM, Harley JB, Fauci AS: Neurologic dysfunction in the idiopathic hypereosinophilic syndrome. Ann Intern Med 102: 109–114, 1985 19) Ogbogu PU, Rosing DR, Horne MK: Cardiovascular manifestations of hypereosinophilic syndromes. Immunol Allergy Clin North Am 27: 457–475, 2007 14) Cools J, DeAngelo DJ, Gotlib J, et al: A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome. N Engl J Med 348: 1201–1214, 2003 6) Kwon SU, Kim JC, Kim JS: Sequential magnetic resonance imaging findings in hypereosinophilia-induced encephalopathy. J Neurol 248: 279–284, 2001 |
| References_xml | – reference: 17) Ishii T, Koide O, Hosoda Y, et al: Hypereosinophilic multiple thrombosis. A proposal of a new designation of disseminated eosinophilic “collagen disease”. Angiology 28: 361–375, 1977 – reference: 19) Ogbogu PU, Rosing DR, Horne MK: Cardiovascular manifestations of hypereosinophilic syndromes. Immunol Allergy Clin North Am 27: 457–475, 2007 – reference: 6) Kwon SU, Kim JC, Kim JS: Sequential magnetic resonance imaging findings in hypereosinophilia-induced encephalopathy. J Neurol 248: 279–284, 2001 – reference: 12) Kaplan PW, Waterbury L, Kawas C, et al: Reversible dementia with idiopathic hypereosinophilic syndrome. Neurology 39: 1388–1391, 1989 – reference: 2) Roufosse FE, Goldman M, Cogan E: Hypereosinophilic syndromes. Orphanet J Rare Dis 2: 37, 2007 – reference: 5) Sethi HS, Schmidley JW: Cerebral infarcts in the setting of eosinophilia: three cases and a discussion. Arch Neurol 67: 1275–1277, 2010 – reference: 8) McMillan HJ, Johnston DL, Doja A: Watershed infarction due to acute hypereosinophilia. Neurology 70: 80–82, 2008 – reference: 9) Sarazin M, Caumes E, Cohen A, et al: Multiple microembolic borderzone brain infarctions and endomyocardial fibrosis in idiopathic hypereosinophilic syndrome and in Schistosoma mansoni infestation. J Neurol Neurosurg Psychiatr 75: 305–307, 2004 – reference: 11) Caplan LR, Hennerici M: Impaired clearance of emboli (washout) is an important link between hypoperfusion, embolism, and ischemic stroke. Arch Neurol 55: 1475–1482, 1998 – reference: 16) Roufosse F, Cogan E, Goldman M: Recent advances in pathogenesis and management of hypereosinophilic syndromes. Allergy 59: 673–689, 2004 – reference: 4) Tefferi A, Patnaik MM, Pardanani A: Eosinophilia: secondary, clonal and idiopathic. Br J Haematol 133: 468–492, 2006 – reference: 7) Weller PF, Bubley GJ: The idiopathic hypereosinophilic syndrome. Blood 83: 2759–2779, 1994 – reference: 10) Aida L, Parkhutik V, Tembl JI, et al: Embolism and impaired washout: a possible explanation of border zone strokes in hypereosinophilic syndrome. J Neurol Sci 325: 162–164, 2013 – reference: 14) Cools J, DeAngelo DJ, Gotlib J, et al: A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome. N Engl J Med 348: 1201–1214, 2003 – reference: 13) Roche-Lestienne C, Lepers S, Soenen-Cornu V, et al: Molecular characterization of the idiopathic hypereosinophilic syndrome (HES) in 35 French patients with normal conventional cytogenetics. Leukemia 19: 792–798, 2005 – reference: 3) Moore PM, Harley JB, Fauci AS: Neurologic dysfunction in the idiopathic hypereosinophilic syndrome. Ann Intern Med 102: 109–114, 1985 – reference: 1) Chusid MJ, Dale DC, West BC, et al: The hypereosinophilic syndrome: analysis of fourteen cases with review of the literature. Medicine (Baltimore) 54: 1–27, 1975 – reference: 18) Grigoryan M, Geisler SD, St Louis EK, et al: Cerebral arteriolar thromboembolism in idiopathic hypereosinophilic syndrome. Arch Neurol 66: 528–531, 2009 – reference: 15) Fletcher S, Bain B: Diagnosis and treatment of hypereosinophilic syndromes. Curr Opin Hematol 14: 37–42, 2007 |
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| Snippet | 要旨：症例は69 歳男性．胸腹水貯留，好酸球増多の原因精査中に多発性脳梗塞を発症した．基礎疾患はT 細胞性リンパ腫と診断でき，リンパ腫に付随した好酸球増多であった．頭部MRI では大脳皮質・皮質下の境界領域，小脳半球などに多発する微小梗塞を認めた．好酸球増多症候群の1... 「要旨」 : 症例は69歳男性. 胸腹水貯留, 好酸球増多の原因精査中に多発性脳梗塞を発症した. 基礎疾患はT細胞性リンパ腫と診断でき, リンパ腫に付随した好酸球増多であった. 頭部MRIでは大脳皮質・皮質下の境界領域, 小脳半球などに多発する微小梗塞を認めた. 好酸球増多症候群の1症状としての脳梗塞と考え,... |
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| SubjectTerms | borderzone infarcts hypereosinophilia-induced encephalopathy hypereosinophilic syndrome (HES) microembolism multiple cerebral infarcts |
| Title | 好酸球増多による多発性脳梗塞が疑われたT 細胞性リンパ腫の1 剖検例 |
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