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Recent studies suggest suppressed hepcidin synthesis in the liver to be the molecular basis of hemochromatosis. However, a liver with acquired iron overload synthesizes an adequate amount of hepcidin. Thus, hepcidin could function as a biochemical marker for differential diagnosis of iron overload syndromes. Methods We measured serum iron parameters and hepcidin- 25 levels followed by sequencing HFE, HJV, HAMP, TFR2, and SLC40A1 genes in 13 Japanese patients with iron overload syndromes. In addition, we performed direct measurement of serum hepcidin-25 levels using liquid chromatography-tandem mass spectrometry in 3 Japanese patients with aceruloplasminemia and 4 Italians with HFE hemochromatosis. Results One patient with HJV hemochromatosis, 2 with TFR2 hemochromatosis, and 3 with ferroportin disease were found among the 13 Japanese patients. The remaining 7 Japanese patients showed no evidence for genetic basis of iron overload syndrome. As far as the serum hepcidin-25 was concerned, seven patients with hemochromatosis and 3 with aceruloplasminemia showed markedly decreased serum hepcidin-25 levels. In contrast, 3 patients with ferroportin disease and 7 with secondary iron overload syndromes showed serum hepcidin levels parallel to their hyperferritinemia. Patients with iron overload syndromes were divided into 2 phenotypes presenting as low and high hepcidinemia. These were then associated with their genotypes. Conclusion Determining serum hepcidin-25 levels may aid differential diagnosis of iron overload syndromes prior to genetic analysis. © Springer 2010.", "subitem_description_type": "Abstract"}]}, "item_4_description_5": {"attribute_name": "提供者所属", "attribute_value_mlt": [{"subitem_description": "石川県立中央病院", "subitem_description_type": "Other"}, {"subitem_description": "金沢大学医薬保健研究域医学系", "subitem_description_type": "Other"}]}, "item_4_publisher_17": {"attribute_name": "出版者", "attribute_value_mlt": [{"subitem_publisher": "Springer"}]}, "item_4_relation_12": {"attribute_name": "DOI", "attribute_value_mlt": [{"subitem_relation_type": "isVersionOf", "subitem_relation_type_id": {"subitem_relation_type_id_text": "10.1007/s00535-010-0259-8", "subitem_relation_type_select": "DOI"}}]}, "item_4_source_id_11": {"attribute_name": "NCID", "attribute_value_mlt": [{"subitem_source_identifier": "AA10988015", "subitem_source_identifier_type": "NCID"}]}, "item_4_source_id_9": {"attribute_name": "ISSN", 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Measurement of serum hepcidin-25 levels as a potential test for diagnosing hemochromatosis and related disorders
http://hdl.handle.net/2297/26279
http://hdl.handle.net/2297/26279719fcd2f-c711-44f3-8df9-a2c20ab361cc
名前 / ファイル | ライセンス | アクション |
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ME-PR-KANEKO-Y-1163.pdf (132.5 kB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2017-10-03 | |||||
タイトル | ||||||
タイトル | Measurement of serum hepcidin-25 levels as a potential test for diagnosing hemochromatosis and related disorders | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者 |
Kaneko, Yoshibumi
× Kaneko, Yoshibumi× Miyajima, Hiroaki× Piperno, Alberto× Tomosugi, Naohisa× Hayashi, Hisao× Morotomi, Natsuko× Tsuchida, Ken-ichi× Ikeda, Takaaki× Ishikawa, Akihisa× Ota, Yusuke× Wakusawa, Shinya× Yoshioka, Kentaro× Kono, Satoshi× Pelucchi, Sara× Hattori, Ai× Tatsumi, Yasuaki× Okada, Toshihide× Yamagishi, Masakazu |
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提供者所属 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 石川県立中央病院 | |||||
提供者所属 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 金沢大学医薬保健研究域医学系 | |||||
書誌情報 |
Journal of Gastroenterology 巻 45, 号 11, p. 1163-1171, 発行日 2010-11-01 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0944-1174 | |||||
NCID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA10988015 | |||||
DOI | ||||||
関連タイプ | isVersionOf | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1007/s00535-010-0259-8 | |||||
出版者 | ||||||
出版者 | Springer | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Iron overload syndromes include a wide spectrum of genetic and acquired conditions. Recent studies suggest suppressed hepcidin synthesis in the liver to be the molecular basis of hemochromatosis. However, a liver with acquired iron overload synthesizes an adequate amount of hepcidin. Thus, hepcidin could function as a biochemical marker for differential diagnosis of iron overload syndromes. Methods We measured serum iron parameters and hepcidin- 25 levels followed by sequencing HFE, HJV, HAMP, TFR2, and SLC40A1 genes in 13 Japanese patients with iron overload syndromes. In addition, we performed direct measurement of serum hepcidin-25 levels using liquid chromatography-tandem mass spectrometry in 3 Japanese patients with aceruloplasminemia and 4 Italians with HFE hemochromatosis. Results One patient with HJV hemochromatosis, 2 with TFR2 hemochromatosis, and 3 with ferroportin disease were found among the 13 Japanese patients. The remaining 7 Japanese patients showed no evidence for genetic basis of iron overload syndrome. As far as the serum hepcidin-25 was concerned, seven patients with hemochromatosis and 3 with aceruloplasminemia showed markedly decreased serum hepcidin-25 levels. In contrast, 3 patients with ferroportin disease and 7 with secondary iron overload syndromes showed serum hepcidin levels parallel to their hyperferritinemia. Patients with iron overload syndromes were divided into 2 phenotypes presenting as low and high hepcidinemia. These were then associated with their genotypes. Conclusion Determining serum hepcidin-25 levels may aid differential diagnosis of iron overload syndromes prior to genetic analysis. © Springer 2010. | |||||
著者版フラグ | ||||||
出版タイプ | AM | |||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa |