黄体機能不全
WordNet
- a lack of competence; "pointed out the insufficiencies in my report"; "juvenile offenses often reflect an inadequacy in the parents" (同)inadequacy
- (pathology) inability of a bodily part or organ to function normally
- lack of an adequate quantity or number; "the inadequacy of unemployment benefits" (同)inadequacy, deficiency
- a substance for packing a joint or coating a porous surface to make it impervious to gas or liquid (同)luting
- chordophone consisting of a plucked instrument having a pear-shaped body, a usually bent neck, and a fretted fingerboard
- a collection of writings; "he edited the Hemingway corpus"
- the main part of an organ or other bodily structure
PrepTutorEJDIC
- 不十分な[点],不足;不適当,不向き
- リュート(17世紀ごろまで用いられたギターに似た弦楽器)
- 封泥(ふうでい)(破れ目や穴をふさぐもの) / …‘を'封泥でふさぐ
- (特定の事に関する,または特殊の性質の)文書資料の集成 / (研究用に収集した)資料
UpToDate Contents
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English Journal
- Misregulated Progesterone Secretion and Impaired Pregnancy in Cyp11a1 Transgenic Mice.
- Chien Y, Cheng WC, Wu MR, Jiang ST, Shen CK, Chung BC.AbstractNormal pregnancy is supported by increased levels of progesterone (P4), which is secreted from ovarian luteal cells via enzymatic steps catalyzed by P450scc (CYP11A1) and HSD3B. The development and maintenance of the corpora lutea during pregnancy, however, are less well understood. Here we use Cyp11a1 transgenic mice to delineate the steps of luteal cell differentiation during pregnancy. Cyp11a1 in a bacterial artificial chromosome was injected into mouse embryos to generate transgenic mice with transgene expression that recapitulates the endogenous Cyp11a1 expression. Cyp11a1 transgenic females displayed reduced pregnancy rate, impaired implantation and placentation, and decreased litter size in utero, although they produced comparable numbers of blastocysts. The differentiation of transgenic luteal cells was delayed during early pregnancy as shown by the delayed activation of genes involved in steroidogenesis and cholesterol availability. Luteal cell mitochondria were elongated and their numbers were reduced similar to morphology and numbers observed in granulosa cells. Transgenic luteal cells accumulated lipid droplets and secreted less progesterone during early pregnancy. The progesterone level returned to normal on Gestation Day 9, but was not properly withdrawn at term, leading to delayed still birth. P4 supplement rescued the implantation rates but not the ovarian defects. Thus overexpression of Cyp11a1 disrupts normal development of the corpus luteum, leading to progesterone insufficiency during early pregnancy. The misregulation of the progesterone production in Cyp11a1 transgenic mice during pregnancy results in aberrant implantation, anomalous placentation, and delayed parturition.
- Biology of reproduction.Biol Reprod.2013 Aug 21. [Epub ahead of print]
- Normal pregnancy is supported by increased levels of progesterone (P4), which is secreted from ovarian luteal cells via enzymatic steps catalyzed by P450scc (CYP11A1) and HSD3B. The development and maintenance of the corpora lutea during pregnancy, however, are less well understood. Here we use Cyp1
- PMID 23966322
- Macrophages regulate corpus luteum development during embryo implantation in mice.
- Care AS, Diener KR, Jasper MJ, Brown HM, Ingman WV, Robertson SA.AbstractMacrophages are prominent in the uterus and ovary at conception. Here we utilize the Cd11b-Dtr mouse model of acute macrophage depletion to define the essential role of macrophages in early pregnancy. Macrophage depletion after conception caused embryo implantation arrest associated with diminished plasma progesterone and poor uterine receptivity. Implantation failure was alleviated by administration of bone marrow-derived CD11b+F4/80+ monocytes/macrophages. In the ovaries of macrophage-depleted mice, corpora lutea were profoundly abnormal, with elevated Ptgs2, Hif1a, and other inflammation and apoptosis genes and with diminished expression of steroidogenesis genes Star, Cyp11a1, and Hsd3b1. Infertility was rescued by exogenous progesterone, which confirmed that uterine refractoriness was fully attributable to the underlying luteal defect. In normally developing corpora lutea, macrophages were intimately juxtaposed with endothelial cells and expressed the proangiogenic marker TIE2. After macrophage depletion, substantial disruption of the luteal microvascular network occurred and was associated with altered ovarian expression of genes that encode vascular endothelial growth factors. These data indicate a critical role for macrophages in supporting the extensive vascular network required for corpus luteum integrity and production of progesterone essential for establishing pregnancy. Our findings raise the prospect that disruption of macrophage-endothelial cell interactions underpinning corpus luteum development contributes to infertility in women in whom luteal insufficiency is implicated.
- The Journal of clinical investigation.J Clin Invest.2013 Aug 1;123(8):3472-87. doi: 10.1172/JCI60561. Epub 2013 Jul 8.
- Macrophages are prominent in the uterus and ovary at conception. Here we utilize the Cd11b-Dtr mouse model of acute macrophage depletion to define the essential role of macrophages in early pregnancy. Macrophage depletion after conception caused embryo implantation arrest associated with diminished
- PMID 23867505
- Liver receptor homolog-1 is essential for pregnancy.
- Zhang C, Large MJ, Duggavathi R, Demayo FJ, Lydon JP, Schoonjans K, Kovanci E, Murphy BD.Source1] Centre de recherche en reproduction animale, Université de Montréal, Saint-Hyacinthe, Québec, Canada. [2] Key Laboratory of Animal Resistance Research, College of Life Science, Shandong Normal University, Ji'nan, Shandong, China.
- Nature medicine.Nat Med.2013 Aug;19(8):1061-6. doi: 10.1038/nm.3192. Epub 2013 Jun 30.
- Successful pregnancy requires coordination of an array of signals and factors from multiple tissues. One such element, liver receptor homolog-1 (Lrh-1), is an orphan nuclear receptor that regulates metabolism and hormone synthesis. It is strongly expressed in granulosa cells of ovarian follicles and
- PMID 23817023
Japanese Journal
- 安藤 紀子,五来 逸雄,平吹 知雄,小野瀬 亮,平原 史樹,水口 弘司
- 日本産科婦人科學會雜誌 44(6), 650-656, 1992-06-01
- 当科不育症外来を受診した106組の不育症患者に対し内分泌学的ならびに免疫学的検索を行い不育症におけるプロラクチン分泌異常の意義について検討した. 1) 不育症患者の中には高プロラクチン血症8人および潜在性高プロラクチン血症31人と, プロラクチン分泌異常を示す患者が高率(36.8%)に認められた. 2) これらプロラクチン分泌異常患者のうち臨床的に黄体機能不全が認められたのは高プロラクチン血症8例 …
- NAID 110002106503
- 282. The Effects of, Bromocriptine on Normoprolactinemic Women with Corpus Luteum Insufficiency Judging from the Luteal Index
- ASUKAI K.,UEMURA T,MINAGUCHI H.
- 日本産科婦人科學會雜誌 38(8), 1404, 1986-08-01
- NAID 110002232100
Related Links
- 17 Feb 2013 ... Corpus luteum deficiency, also known as corpus luteum defect, means that the corpus luteum does not produce enough progesterone to allow a pregnancy to develop. Without sufficient progesterone levels, the lining of the ...
- The corpus luteum is controlled by luteinizing hormone (LH) and intraovarian morphofunctional specialization and autocrine/paracrine mechanisms. Corpus luteal insufficiency produces luteal phase defects (LPD). The poor precision and ...
★リンクテーブル★
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- 英
- luteal insufficiency, corpus luteum insufficiency, luteal phase deficiency, luteal dysfunction
- 関
- 黄体、プロゲスチン
[show details]
概念
- 黄体ホルモン(プロゲステロン)分泌不全により、子宮内膜が分泌期に至らない、体温の上昇、高温相の持続の異常をきたす。
治療はプロゲステロン投与で黄体ホルモンを補うか、あるいはヒト絨毛ゴナドトロピン hCGで黄体を刺激する。
定義
参考1
- 「黄体からのエストロゲンとプロゲステロンとの分泌不全により、子宮内膜の分泌性変化が起こらないものをいう。妊卵の着床障害による不妊原因として重要である。」(日本産科婦人科学会)
G9M
- 1. 黄体期中期の血中プロゲステロン＜10ng/ml (通常は5-28ng/mlくらい)
- 2. 基礎体温
- 2-1. 低温相から高温相の移行に3日要する
- 2-2. 高温相は10日以内
- 2-3. 高温相と低温相の差が0.3℃以内 (正常は0.3-0.6℃の上昇)
治療
- 1-1. ゲスターゲンの周期的投与
- 1-2. 黄体機能刺激療法
- 2-1. クロミフェン療法
- 2-2. ゴナドトロピン療法(hMG-hCG療法)
参考
- 1. クリニカル・カンファレンス 4．不育症の病態解明と治療の展望 3）黄体機能の視点から - 日産婦誌５5巻９号
- http://www.jsog.or.jp/PDF/55/5509-249.pdf
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- 関
- dearth、deficient、deficit、dysfunction、failing、failure、hypofunction、imperfecta、in short、inadequate、incompetence、insufficient、insufficiently、lack、low、malfunction、paucity、poorly、regurgitation、scanty、scarce、scarcity、short、shortage、shortness、stun
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- 関
- corpuscle