常染色体優性低リン血症性くる病 autosomal dominant hypophosphatemic rickets
WordNet
- in the Christian era; used before dates after the supposed year Christ was born; "in AD 200" (同)A.D., anno_Domini
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- 1. 遺伝性低リン血症性くる病と腫瘍誘発性骨軟化症 hereditary hypophosphatemic rickets and tumor induced osteomalacia
- 2. 低リン血症の原因 causes of hypophosphatemia
- 3. 骨軟化症の疫学および病因 epidemiology and etiology of osteomalacia
- 4. 高リン血症の原因および治療の概要 overview of the causes and treatment of hyperphosphatemia
English Journal
- Iron Supplementation Associated With Loss of Phenotype in Autosomal Dominant Hypophosphatemic Rickets.
- Kapelari K1, Köhle J1, Kotzot D1, Högler W1.
- The Journal of clinical endocrinology and metabolism.J Clin Endocrinol Metab.2015 Sep;100(9):3388-92. doi: 10.1210/jc.2015-2391. Epub 2015 Jul 17.
- CONTEXT: Autosomal dominant hypophosphatemic rickets (ADHR) is the only hereditary disorder of renal phosphate wasting in which patients may regain the ability to conserve phosphate. Low iron status plays a role in the pathophysiology of ADHR.OBJECTIVE: This study reports of a girl with ADHR, iron d
- PMID 26186302
- Phosphate homeostasis and genetic mutations of familial hypophosphatemic rickets.
- Razali NN, Hwu TT, Thilakavathy K.
- Journal of pediatric endocrinology & metabolism : JPEM.J Pediatr Endocrinol Metab.2015 Sep;28(9-10):1009-17. doi: 10.1515/jpem-2014-0366.
- Hypophosphatemic rickets (HR) is a syndrome of hypophosphatemia and rickets that resembles vitamin D deficiency, which is caused by malfunction of renal tubules in phosphate reabsorption. Phosphate is an essential mineral, which is important for bone and tooth structure. It is regulated by parathyro
- PMID 25894638
- [Bone and Nutrition. The relationship between iron and phosphate metabolism].
- Takashi Y1, Fukumoto S.
- Clinical calcium.Clin Calcium.2015 Jul;25(7):1037-42. doi: CliCa150710371042.
- Fibroblast growth factor 23 (FGF23) is an essential hormone for phosphate metabolism. It has been shown that intravenous administration of some iron formulations including saccharated ferric oxide induces hypophosphatemic osteomalacia with high FGF23 levels. On the other hand, iron deficiency promot
- PMID 26119317
Japanese Journal
- Molecular Bases of Diseases Characterized by Hypophosphatemia and Phosphaturia : New Understanding
- Ozono Keiichi,Michigami Toshimi,Namba Noriyuki,Nakajima Shigeo,Yamamoto Takehisa
- Clinical pediatric endocrinology 15(4), 129-135, 2006-10
- NAID 110006794331
- 目で見るBone Biology(第6回)FGF23と血清リンの調節機構
- 山下 武美,高橋 直之
- 骨粗鬆症治療 5(2), 98-101, 2006-04
- NAID 40007239053
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★リンクテーブル★
| リンク元 | 「FGF23」「常染色体優性低リン血症性くる病」 |
| 関連記事 | 「ADH」「AD」 |
「FGF23」
- 2000年、常染色体優性低リン血症性くる病(ADHR)の原因遺伝子として同定され、2001年に腫瘍性くる病/骨軟化症(tumor-induced rickets/osteomalacia TIO)の原因として報告された。
- リン利尿因子として作用している；腎臓近位尿細管上皮細胞のFGF受容体1cとKlothoの複合体に作用し、刷子縁膜上に存在するNa-P共輸送体の発現を抑制してリン利尿をもたらす。
- FGF23は慢性腎臓病の進行と共に血中濃度が上昇し、透析患者では100-1000倍に達する。
- FGF23はビタミンDの活性化に関与する1α水酸化酵素に対して抑制的に作用し、腎性骨異栄養症に関与していると言われている。
「常染色体優性低リン血症性くる病」
「ADH」
「AD」