hypophosphataemia

低リン血症、低リン酸血症

関

hypophosphataemic、hypophosphatemia、hypophosphatemic

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2015/10/30 22:59:06」(JST)

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Hypophosphatemia
Phosphate group chemical structure
Classification and external resources
Specialty	endocrinology
ICD-10	E83.3
ICD-9-CM	275.3
DiseasesDB	6503
MedlinePlus	000307
eMedicine	med/1135
Patient UK	Hypophosphatemia
MeSH	D017674

Hypophosphatemia is an electrolyte disturbance in which there is an abnormally low level of phosphate in the blood. The condition has many causes, but is most commonly seen when malnourished patients (especially chronic alcoholics) are given large amounts of carbohydrates, which creates a high phosphorus demand by cells, removing phosphate from the blood (refeeding syndrome).

Because a decrease in phosphate in the blood is sometimes associated with an increase in phosphate in the urine, the terms hypophosphatemia and "phosphaturia" are occasionally used interchangeably; however, this is improper since there exist many causes of hypophosphatemia besides overexcretion and phosphaturia, and in fact the most common causes of hypophosphatemia are not associated with phosphaturia.

Common causes of hypophosphatemia

• Refeeding syndrome This causes a demand for phosphate in cells due to the action of Hexokinase, an enzyme that attaches phosphate to glucose to begin metabolism of glucose. Also, production of ATP when cells are fed and recharge their energy supplies, requires phosphate.
• Respiratory alkalosis Any alkalemic condition moves phosphate out of the blood into cells. This includes most common respiratory alkalemia (a higher than normal blood pH from low carbon dioxide levels in the blood), which in turn is caused by any hyperventilation (such as may result from sepsis, fever, pain, anxiety, drug withdrawal, and many other causes). This phenomenon is seen because in respiratory alkalosis carbon dioxide (CO2) decreases in the extracellular space, causing intracellular CO2 to freely diffuse out of the cell. This drop in intracellular CO2 causes a rise in cellular pH which has a stimulating effect on glycolysis. Since the process of glycolysis requires phosphate (the end product is adenosine triphosphate), the result is a massive uptake of phosphate into metabolically active tissue (such as muscle) from the serum. It is interesting to note, however, that this effect is not seen in metabolic alkalosis, for in such cases the cause of the alkalosis is increased bicarbonate rather than decreased CO2. Bicarbonate, unlike CO2, has poor diffusion across the cellular membrane and therefore there is little change in intracellular pH.
• Alcohol abuse Alcohol impairs phosphate absorption. Alcoholics are usually also malnourished with regard to minerals. In addition, alcohol treatment is associated with refeeding, and the stress of alcohol withdrawal may create respiratory alkalosis, which exacerbates hypophosphatemia (see above).
• Malabsorption This includes GI damage, and also failure to absorb phosphate due to lack of vitamin D, or chronic use of phosphate binders such as sucralfate, aluminum-containing antacids, and (more rarely) calcium-containing antacids.

Primary hypophosphatemia is the most common cause of nonnutritional rickets. Laboratory findings include low-normal serum calcium, moderately low serum phosphate, elevated serum alkaline phosphatase, and low serum 1,25 dihydroxy-vitamin D levels, hyperphosphaturia, and no evidence of hyperparathyroidism.

Other rarer causes include

• Certain blood cancers such as lymphoma or leukemia
• Hereditary causes
• Liver failure
• Tumor-induced osteomalacia

Pathophysiology

Hypophosphatemia is caused by the following three mechanisms:

• Inadequate intake (often unmasked in refeeding after long-term low phosphate intake)
• Increased excretion (e.g. in hyperparathyroidism, hypophosphatemic rickets)
• Shift from extracellular to intracellular space (seen in treatment of diabetic ketoacidosis, refeeding, short-term increases in cellular demand (e.g., hungry bones syndrome) and acute respiratory alkalosis)

Major signs and symptoms

• Muscle dysfunction and weakness. This occurs in major muscles, but also may manifest as: diplopia, low cardiac output, dysphagia, and respiratory depression due to respiratory muscle weakness.
• Mental status changes. This may range from irritability to gross confusion, delirium, and coma.
• White cell dysfunction, causing worsening of infections.
• Instability of cell membranes due to low ATP levels: this may cause rhabdomyolysis with increased CPK, and also hemolytic anemia.
• Increased affinity for oxygen in the blood caused by decreased production of 2,3BPG.
• Large pulp chambers in the teeth.

Treatment

Standard intravenous preparations of potassium phosphate are available and are routinely used in malnourished patients and alcoholics. Oral supplementation also is useful where no intravenous treatment is available. Historically one of the first demonstrations of this was in concentration camp victims who died soon after being re-fed: it was observed that those given milk (high in phosphate) had a higher survival rate than those who did not get milk.

monitoring parameters during correction with IV phosphate

Phosphorus levels should be monitored after 2 to 4 hours after each dose, also monitor serum potassium, calcium and magnesium. Cardiac monitoring is also advised.

See also

• Hyperphosphatemia
• Hypophosphatasia
• X-linked hypophosphatemia

External links

• eMedicine review
• Tutorial - complications
• Refeeding Syndrome

References

UpToDate Contents

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• 1. 低リン血症の評価および治療 evaluation and treatment of hypophosphatemia
• 2. 低リン血症の徴候および症状 signs and symptoms of hypophosphatemia
• 3. 低リン血症の原因 causes of hypophosphatemia
• 4. アルコール中毒患者における低リン血症 hypophosphatemia in the alcoholic patient
• 5. 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

English Journal

• Evaluation of a New Fully Automated Assay for Plasma Intact FGF23.

• Souberbielle JC1, Prié D1, Piketty ML1, Rothenbuhler A2, Delanaye P3, Chanson P4,5, Cavalier E6.
• Calcified tissue international.Calcif Tissue Int.2017 Nov;101(5):510-518. doi: 10.1007/s00223-017-0307-y. Epub 2017 Jul 31.
• PMID 28761972

• Pseudohypophosphatemia associated with high-dose liposomal amphotericin B therapy.

• Mays JA1, Greene DN1, Poon A2, Merrill AE3.
• Clinical biochemistry.Clin Biochem.2017 Nov;50(16-17):967-971. doi: 10.1016/j.clinbiochem.2017.05.016. Epub 2017 May 31.
• PMID 28578095

• Outcomes of orthopedic surgery in a cohort of 49 patients with X-linked hypophosphatemic rickets (XLHR).

• Gizard A1, Rothenbuhler A2,3,4, Pejin Z5, Finidori G5, Glorion C5, de Billy B1, Linglart A6,3,4,7, Wicart P8,5.
• Endocrine connections.Endocr Connect.2017 Nov;6(8):566-573. doi: 10.1530/EC-17-0154.
• PMID 28954742

Japanese Journal

• リフィーディング症候群 (特集 メンタルヘルスと栄養)

• 中屋 豊,阪上 浩,原田 永勝
• 四国医学雑誌 68(1・2), 23-28, 2012-04-25
• … Refeeding syndrome can manifest as either metabolic changes（hypokalaemia, hypophosphataemia, vitamin B１deficiency, and altered glucose metabolism）orphysiological changes（cardiac arrhythmias, unconsciousness, seizures, cardiac or respiratory depression）and potentially death. …
• NAID 40019338763

• 意識障害・呼吸不全の増悪に refeeding syndrome が関与した1例

• 宮崎 裕也,岩本 謙荘,谷川 隆久,相原 啓二,蒲地 正幸,佐多 竹良
• 日本集中治療医学会雑誌 = Journal of the Japanese Society of Intensive Care Medicine 16(1), 51-56, 2009-01-01
• NAID 10024841633

Related Links

• Hypophosphataemia - Ganfyd

consider other electrolytes such as potassium and magnesium that are sometimes also depleted by some of the causes of hypophosphataemia.. External Links emedicine article (emergency medicine slant) emedicine ...

• Hypophosphataemia | Doctor | Patient.co.uk

A low level of blood phosphate is defined as a level below 0.8 mmol/L (the normal range should be given by the assaying laboratory but is about 0.8 to... A low level of blood phosphate is defined as a level below 0.8 mmol/L (the normal ...

Related Pictures

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★リンクテーブル★

リンク元	「低リン血症」「hypophosphatemic」「hypophosphataemic」

「低リン血症」

　　[★]

英

hypophosphatemia、hypophosphataemia

同

(国試)低リン血症、低P血症

関

リン。低リン血症性。低リン血症性。hypophosphatemic、hypophosphataemic

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低リン酸血症 hypophosphatemia : 約 52 件
低リン血症 hypophosphatemia : 約 83 件

低リン酸血症 : 約 86 件
低リン血症 : 約 313,000 件

概念

• 循環血液中のリン酸塩濃度値が低い状態。

原因

uptodate

改変

生体内での再分布

• インスリン分泌の増加：特にrefeeding syndrome：飢餓状態から急に末梢血にブドウ糖が供給されると、インスリン、ブドウ糖と共にリン酸が細胞内に移動し細胞内で盛んにATP産生が行われるが、この結果末梢血のリン酸濃度が低下する。
• 糖尿病性ケトアシドーシス
• 急性呼吸性アルカローシス：血液のpHが上昇するとホスホフルクトキナーゼの活性が亢進するため、血液中のリン酸が細胞内に取り込まれる結果、低リン血症を来す
• 飢餓骨症候群(hungry bone syndrome)：副甲状腺機能亢進状態から正常に復帰後、骨から放出されていたリン酸とカルシウムを再吸収し骨形成が進む結果、末梢血のリン酸濃度が低下する。
• 急性アルコール中毒
• 高カロリー輸液

腸管からの吸収低下

• 摂取量低下
• リン酸の吸収を阻害する薬剤の摂取(制酸剤(アルミニウム制酸剤)、リン酸結合物質(炭酸カルシウム)、ナイアシンなど)
• 嘔吐
• 脂肪便、下痢
• 吸収不良症候群
• ビタミンD欠乏、ビタミンD抵抗性

尿からの排泄増加

• 副甲状腺機能亢進症
• ビタミンD欠乏、ビタミンD抵抗性
• 遺伝性低リン血症性くる病
• 腫瘍性骨軟化症
• 原発性副甲状腺機能亢進症
• 尿細管性アシドーシス
• ファンコニ症候群
• 薬剤性：アセタゾラミド、テノホビル、鉄剤注射、化学療法薬

臨床関連

リンは骨や歯を形成するのに不可欠な物質であり、血清リン酸の低下が持続すると骨石灰化障害を来す

• くる病
• 骨軟化症

参考

• Hypophosphatemia - Sandeep Sharma; Muhammad F. Hashmi; Danny Castro.

https://www.ncbi.nlm.nih.gov/books/NBK493172/

「hypophosphatemic」

　　[★]

• adj.

• 低リン血症の、低リン酸血症の、低リン血症性の

関

hypophosphataemia、hypophosphataemic、hypophosphatemia

「hypophosphataemic」

　　[★]

• adj.

• 低リン血症の、低リン酸血症の

関

hypophosphataemia、hypophosphatemia、hypophosphatemic