hypophosphatemia

低リン血症

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2019/07/28 04:15:48」(JST)

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Not to be confused with hyperphosphatemia (high levels in the blood).

Hypophosphatemia
Other names	Low blood phosphate, phosphate deficiency
Phosphate group chemical structure
Specialty	Endocrinology
Symptoms	Weakness, trouble breathing, loss of appetite
Complications	Seizures, coma, rhabdomyolysis, softening of the bones
Causes	Alcoholism, refeeding in those with malnutrition, hyperventilation, diabetic ketoacidosis, burns, certain medications
Diagnostic method	Blood phosphate < 0.81 mmol/L (2.5 mg/dL)
Treatment	Based on the underlying cause, phosphate
Frequency	2% (people in hospital)

Hypophosphatemia is an electrolyte disorder in which there is a low level of phosphate in the blood. Symptoms may include weakness, trouble breathing, and loss of appetite. Complications may include seizures, coma, rhabdomyolysis, or softening of the bones.

Causes include alcoholism, refeeding in those with malnutrition, diabetic ketoacidosis, burns, hyperventilation, and certain medications. It may also occur in the setting of hyperparathyroidism, hypothyroidism, and Cushing syndrome. It is diagnosed based on a blood phosphate concentration of less than 0.81 mmol/L (2.5 mg/dL). When levels are below 0.32 mmol/L (1.0 mg/dL) it is deemed to be severe.

Treatment depends on the underlying cause. Phosphate may be given by mouth or by injection into a vein. Hypophosphatemia occurs in about 2% of people within hospital and 70% of people in the intensive care unit (ICU).

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 blood cell dysfunction, causing worsening of infections.
• Instability of cell membranes due to low adenosine triphosphate (ATP) levels – This may cause rhabdomyolysis with increased serum levels of creatine phosphokinase, and also hemolytic anemia.
• Increased affinity for oxygen in the blood caused by decreased production of 2,3-bisphosphoglyceric acid.
• Large pulp chambers in the teeth.

Causes

• 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. 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.
• Metabolic acidosis
• 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 gastrointestinal 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 non-nutritional 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.

Hypophosphatemia decreases 2,3-diphosphoglycerate (2,3-DPG) causing a left shift in the oxyhemoglobin curve.

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 of phosphorus from the extracellular to the intracellular space. This can be seen in treatment of diabetic ketoacidosis, refeeding, short-term increases in cellular demand (e.g. hungry bone syndrome) and acute respiratory alkalosis.

Diagnosis

Hypophosphatemia is diagnosed by measuring the concentration of phosphate in the blood. Concentrations of phosphate less than 0.81 mmol/L (2.5 mg/dL) are considered diagnostic of hypophosphatemia, though additional tests may be needed to identify the underlying cause of the disorder.

Treatment

Standard intravenous preparations of potassium phosphate are available and are routinely used in malnourished people and alcoholics. Supplementation by mouth is also useful where no intravenous treatment are available. Historically one of the first demonstrations of this was in people in concentration camp 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

• X-linked hypophosphatemia

External links

Classification	D ICD-10: E83.3 ICD-9-CM: 275.3 MeSH: D017674 DiseasesDB: 6503
External resources	MedlinePlus: 000307 eMedicine: med/1135 Patient UK: Hypophosphatemia

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

• Electrolyte Imbalance in Patients with Sheehan's Syndrome.

• Lim CH1, Han JH1, Jin J1, Yu JE1, Chung JO2, Cho DH1, Chung DJ1, Chung MY1.
• Endocrinology and metabolism (Seoul, Korea).Endocrinol Metab (Seoul).2015 Oct 20. [Epub ahead of print]
• BACKGROUND: We investigated the prevalence of electrolyte imbalance and the relationship between serum electrolyte and anterior pituitary hormone levels in patients with Sheehan's syndrome.METHODS: In a retrospective study, we investigated 78 patients with Sheehan's syndrome. We also included 95 nor
• PMID 26485467

• A LC-MS method to quantify tenofovir urinary concentrations in treated patients.

• Simiele M1, Carcieri C2, De Nicolò A1, Ariaudo A1, Sciandra M1, Calcagno A1, Bonora S1, Di Perri G1, D'Avolio A3.
• Journal of pharmaceutical and biomedical analysis.J Pharm Biomed Anal.2015 Oct 10;114:8-11. doi: 10.1016/j.jpba.2015.05.001. Epub 2015 May 8.
• Tenofovir disoproxil fumarate is a prodrug of tenofovir used in the treatment of HIV and HBV infections: it is the most used antiretroviral worldwide. Tenofovir is nucleotidic HIV reverse trascriptase inhibitor that showed excellent long-term efficacy and tolerability. However renal and bone complic
• PMID 25997174

• Risk factors for refeeding hypophosphatemia in Japanese inpatients with anorexia nervosa.

• Kameoka N1, Iga JI1, Tamaru M1, Tominaga T1, Kubo H1, Watanabe SY1, Sumitani S1, Tomotake M1, Ohmori T1.
• The International journal of eating disorders.Int J Eat Disord.2015 Oct 8. doi: 10.1002/eat.22472. [Epub ahead of print]
• OBJECTIVE: Refeeding in patients with anorexia nervosa (AN) is associated with a risk of refeeding syndrome, which is a disruption in metabolism with a variety of features including hypophosphatemia. We evaluated the risk factors for refeeding hypophosphatemia (RH) during nutritional replenishment i
• PMID 26446402

Japanese Journal

• 症例 AdefovirによるFanconi症候群から低リン血症性骨軟化症をきたした1例

• 今井 実,伊古田 明美,糸島 早織 [他]
• 内科 114(5), 879-882, 2014-11
• NAID 40020243659

• O-68 低リン血症合併の劇症肝炎に対し血漿交換・HDFが奏功した一例(肝・胆・膵,一般演題16,第35回日本アフェレシス学会学術大会)

• 前川 洋,高橋 正倫,手島 一陽,新井 雅裕,中尾 彰秀,根岸 康介
• 日本アフェレシス学会雑誌 33(Supplement), 186, 2014-09-26
• NAID 110009874580

• 症例報告 アデホビル長期投与中にFanconi症候群による低リン血性骨軟化症を発症したB型慢性肝炎の1例

• 石川 和真,宮西 浩嗣,保木 寿文 [他]
• 肝臓 55(3), 162-169, 2014-03
• NAID 40020025392

Related Pictures

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★リンクテーブル★

リンク元	「低リン血症」「リン」「hypophosphatemic」「hypophosphataemic」「hypophosphataemia」
拡張検索	「X-linked hypophosphatemia」「familial hypophosphatemia」

「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

[show details]

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/

「リン」

　　[★]

英

phosphorus P

関

serum phosphorus level

分子量

• 30.973762 u (wikipedia)
• 単体で化合物としてはP4、淡黄色を帯びた半透明の固体、所謂黄リンで毒性が高い。分子量124.08。

基準値

血清中のリンおよびリン化合物(リン酸イオンなどとして存在)を無機リン(P)として定量した値。

• (serum)phosphorus, inorganic 2.5–4.3 mg/dL(HIM.Appendix)
• 2.5-4.5 mg/dL (QB)

代謝

• リンは経口的に摂取され、小腸から吸収され、細胞内に取り込まれる。
• 骨形成とともに骨に取り込まれる。
• 腎より排泄される。

尿細管での分泌・再吸収

近位尿細管	70%
遠位尿細管	20%

排泄：10%

尿細管における再吸収の調節要素

• パラサイロイドホルモン PTH：排泄↑
• カルシトニン：吸収↑
• ビタミンD：吸収↑

臨床検査

無機リンとして定量される。

• 血清や尿(蓄尿)で定量される。

基準範囲

血清

• 基準範囲：2.5-4.5mg/dL

• 小児：4-7mg/dL
• 閉経後女性は一般集団より0.3mg/dL高値となる

尿

• 基準範囲：1g/日

測定値に影響を与える要因

• 食事。食前に測定するのが好ましい。

臨床関連

• 高リン酸血症 高リン血症
• 低リン酸血症 低リン血症 hypophosphatemia

参考

• 1. wikiepdia

http://ja.wikipedia.org/wiki/%E3%83%AA%E3%83%B3

「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

「hypophosphataemia」

　　[★] 低リン血症、低リン酸血症

関

hypophosphataemic、hypophosphatemia、hypophosphatemic

「X-linked hypophosphatemia」

　　[★] X連鎖性低リン酸血症

関

hypophosphatemic rickets、vitamin D-resistant rickets、X-linked dominant hypophosphatemic rickets、X-linked hypophosphatemic rickets

「familial hypophosphatemia」

　　[★] 家族性低リン酸血症

関

hyperphosphaturia、phosphaturia