Hypophosphatemia 英 /haipəufɔsfə'ti:miə/
释 义 n. 血磷酸盐过少；低磷酸盐血
例 句 Objective To study the relation between postoperative total parenteral nutrition(TPN) and hypophosphatemia and relation between hypophosphatemia and infection following gastrointestinal damage. 目的探讨胃肠损伤术后全静脉营养和低磷血症的关系以及低磷血症和胃肠损伤术后并发感染的关系。
低磷血症是通过测量血液中磷酸盐的浓度来诊断的。磷酸盐浓度低于0.81 mmol/L（2.5 mg/dL）被认为可诊断为低磷血症，尽管可能还需要进行其他测试才能确定该疾病的根本原因。
作者： Signe Sparre Beck-Nielsen
期刊：Orphanet J Rare Dis
Downregulation of PHEX in XLH increases skeletal OPN deposition which contributes to local inhibition of mineralisation. Meanwhile, elevated levels of serum FGF23 increase urinary phosphate excretion by downregulating renal sodium-phosphate transporters, and limit intestinal phosphate absorption by restricting active vitamin D synthesis to levels that are abnormally low or normal despite hypophosphatemia. Since phosphate insufficiency and inappropriately low levels of calcitriol [also known as 1,25(OH)2D or active vitamin D] contribute to many symptoms of XLH, conventional therapy involves supplementation with oral phosphate and calcitriol or calcitriol analogues (commonly alfacalcidol). This can correct lower limb deformities, promote growth, and improve oral health, with earlier treatment leading to better results. However, conventional therapy insufficiently corrects the biochemistry and symptoms of XLH, and can further increase serum FGF23 levels. Conventional therapy has also been associated with adverse effects including secondary hyperparathyroidism, nephrocalcinosis, nephrolithiasis, and cardiovascular abnormalities. Although hypophosphatemia is the primary link between elevated FGF23 and the pathophysiology of XLH, FGF23 has recently been proposed to also contribute to XLH via other molecular mechanisms. This review describes the central role of FGF23 in XLH pathophysiology, outlining evidence that links upregulation of FGF23 to manifestations of XLH through various molecular pathways (outlined in Fig. 2). FGF23 is introduced along with its direct regulators and receptors, followed by a brief discussion of the dysregulation of serum FGF23 in various diseases of hypophosphatemia; animal models of these diseases are also described since they are essential for understanding molecular mechanisms involved in the pathology of XLH. Finally, the manifestations of XLH are grouped by molecular mechanism and discussed, with any potential involvement of FGF23 highlighted.