| Item type |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2016-06-15 |
| タイトル |
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タイトル |
Lipoprotein(a) in Familial Hypercholesterolemia With Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) Gain-of-Function Mutations. |
| 言語 |
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言語 |
eng |
| 資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
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資源タイプ |
journal article |
| ID登録 |
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ID登録 |
10.24517/00014441 |
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ID登録タイプ |
JaLC |
| 著者 |
Tada, Hayato
Kawashiri, Masa-aki
Yoshida, Taiji
Teramoto, Ryota
Nohara, Atsushi
Konno, Tetsuo
Inazu, Akihiro
Mabuchi, Hiroshi
Yamagishi, Masakazu
Hayashi, Kenshi
|
| 著者別表示 |
多田, 隼人
川尻, 剛照
寺本, 了太
野原, 淳
稲津, 明広
馬渕, 宏
山岸, 正和
林, 研至
|
| 書誌情報 |
Circulation journal
巻 80,
号 2,
p. 512-518,
発行日 2016-01-25
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| ISSN |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
1346-9843 |
| NCID |
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収録物識別子タイプ |
NCID |
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収録物識別子 |
AA11591968 |
| DOI |
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関連タイプ |
isIdenticalTo |
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識別子タイプ |
DOI |
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関連識別子 |
10.1253/circj.CJ-15-0999 |
| 出版者 |
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出版者 |
Japanese Circulation Society = 日本循環器学会 |
| 抄録 |
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内容記述タイプ |
Abstract |
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内容記述 |
Background:It has been shown that serum lipoprotein(a) [Lp(a)] is elevated in familial hypercholesterolemia (FH) with mutation(s) of the LDL receptor (LDLR) gene. However, few data exist regarding Lp(a) levels in FH with gain-of-function mutations of the PCSK9 gene.Methods and Results:We evaluated 42 mutation-determined heterozygous FH patients with aPCSK9gain-of-function mutation (FH-PCSK9, mean age 52, mean LDL-C 235 mg/dl), 198 mutation-determined heterozygous FH patients with aLDLRmutation (FH-LDLR, mean age 44, mean LDL-C 217 mg/dl), and 4,015 controls (CONTROL, mean age 56, mean LDL-C 109 mg/dl). We assessed their Lp(a), total cholesterol, triglycerides, HDL-C, LDL-C, use of statins, presence of hypertension, diabetes, chronic kidney disease, smoking, body mass index (BMI) and coronary artery disease (CAD). Multiple regression analysis showed that HDL-C, use of statins, presence of hypertension, smoking, BMI, and Lp(a) were independently associated with the presence of CAD. Under these conditions, the serum levels of Lp(a) in patients with FH were significantly higher than those of the CONTROL group regardless of their causative genes, among the groups propensity score-matched (median Lp(a) 12.6 mg/dl [IQR:9.4–33.9], 21.1 mg/dl [IQR:11.7–34.9], and 5.0 mg/dl [IQR:2.7–8.1] in the FH-LDLR, FH-PCSK9, and CONTROL groups, respectively, P=0.002 for FH-LDLR vs. CONTROL, P=0.002 for FH-PCSK9 vs. CONTROL).Conclusions:These data demonstrate that serum Lp(a) is elevated in patients with FH caused by PCSK9 gain-of-function mutations to the same level as that in FH caused by LDLR mutations. (Circ J 2016; 80: 512–518) |
| 内容記述 |
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内容記述タイプ |
Other |
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内容記述 |
出版者照会後に全文公開 |
| 権利 |
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|
権利情報 |
Copyright © 2015 THE JAPANESE CIRCULATION SOCIETY |
| 著者版フラグ |
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出版タイプ |
VoR |
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出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| 関連URI |
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識別子タイプ |
URI |
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関連識別子 |
http://www.j-circ.or.jp/english/ |
| 関連URI |
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識別子タイプ |
URI |
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関連識別子 |
https://www.jstage.jst.go.jp/browse/circj |
ME-PR-YAMAGISHI-M-512.pdf (813.5 kB)
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