Liver Congestion in Heart Failure Contributes to Inappropriately Increased Serum Hepcidin despite Anemia

• Material Type: 博士論文
• Title: Liver Congestion in Heart Failure Contributes to Inappropriately Increased Serum Hepcidin despite Anemia
• Author/Editor: Ohno, Yukako
• Publication, Distribution, etc.: 新潟大学
• Publication Date: 2015-03-23
• Publication Date (W3CDTF): 2015-03-23
• Alternative Title: Liver Congestion in Heart Failure Contributes to Inappropriately Increased Serum Hepcidin despite Anemia; 心不全に伴う肝うっ血は貧血に関わらずヘプシジンの不適切分泌の一因となる
• Degree grantor/type: 新潟大学
• Date Granted: 2015-03-23
• Date Granted (W3CDTF): 2015-03-23
• Dissertation Number: 甲第3987号
• Degree Type: 博士（医学）
• Conferring No. (Dissertation): 甲第3987号
• Text Language Code: eng
• Subject Heading: anemia; heart failure; hepcidin; iron deficiency; liver congestion
• Note (General): Hepcidin is a key regulator of mammalian iron metabolism and mainly produced by the liver. Hepcidin excess causes iron deficiency and anemia by inhibiting iron absorption from the intestine and iron release from macrophage stores. Anemia is frequently complicated with heart failure. In heart failure patients, the most frequent histologic appearance of liver is congestion. However, it remains unclear whether liver congestion associated with heart failure influences hepcidin production, thereby contributing to anemia and functional iron deficiency. In this study, we investigated this relationship in clinical and basic studies. In clinical studies of consecutive heart failure patients (n =\ 320), anemia was a common comorbidity (41%). In heart failure patients without active infection and ongoing cancer (n = 30), log-serum hepcidin concentration of patients with liver congestion was higher than those without liver congestion (p = 0.0316). Moreover, in heart failure patients with liver congestion (n = 19), the anemia was associated with the higher serum hepcidin concentrations, which is a type of anemia characterized by induction of hepcidin. Subsequently, we produced a rat model of heart failure with liver congestion by injecting monocrotaline that causes pulmonary hypertension. The monocrotaline-treated rats displayed liver congestion with increase of hepcidin expression at 4 weeks after monocrotaline injection, followed by anemia and functional iron deficiency observed at 5 weeks. We conclude that liver congestion induces hepcidin production, which may result in anemia and functional iron deficiency in some patients with heart failure.; 学位の種類: 博士（医学）. 報告番号: 甲第3987号. 学位記番号: 新大院博（医）甲第633号. 学位授与年月日: 平成27年3月23日; The Tohoku Journal of Experimental Medicine. 2015, 235(1), 69-79.; 新大院博（医）甲第633号; 元資料の権利情報 : Copyright (C) 2015 Tohoku University Medical Press; 開始ページ : 1; 終了ページ : 29
• DOI: info:doi/10.1620/tjem.235.69; https://doi.org/info:doi/10.1620/tjem.235.69
• Persistent ID (NDL): info:ndljp/pid/9425145; https://dl.ndl.go.jp/pid/9425145
• Collection: 障害者向け資料
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• Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• Acquisition Basis: 博士論文（自動収集）
• Date Accepted (W3CDTF): 2015-07-01T13:17:09+09:00
• Date Created (W3CDTF): 2019-08-05
• Format (IMT): application/pdf
• Access Restrictions: 国立国会図書館内限定公開
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• Periodical Title (URI): http://hdl.handle.net/10191/32271
• Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp