milk-alkali syndrome

ミルク・アルカリ症候群

WordNet

1. exploit as much as possible; "I am milking this for all its worth"
2. add milk to; "milk the tea"
3. take milk from female mammals; "Cows need to be milked every morning"
4. a white nutritious liquid secreted by mammals and used as food by human beings
5. any of several nutritive milklike liquids
6. produced by mammary glands of female mammals for feeding their young
7. a Cypriot monetary unit equal to one thousandth of a pound
8. a unit of length equal to one thousandth of an inch; used to specify thickness (e.g., of sheets or wire)
9. an angular unit used in artillery; equal to 1/6400 of a complete revolution
10. a pattern of symptoms indicative of some disease
11. a complex of concurrent things; "every word has a syndrome of meanings"
12. the syllable naming the third (mediant) note of any major scale in solmization
13. a mixture of soluble salts found in arid soils and some bodies of water; detrimental to agriculture

PrepTutorEJDIC

1. (雌の哺乳(ほにゅう)動物が分泌する)乳,(特に食料としての)『牛乳』,『ミルク』 / (植物の)乳汁,乳剤,乳液 / 〈牛など〉‘の'乳をしぼる / 〈情報など〉‘を'引き出す;(…を)〈人〉‘から'しぼり取る《+『名』+『of』+『名』》 / (毒を)〈蛇〉‘から'抜き取る《+『名』+『of』+『名』》 / 〈牛などが〉乳を出す
2. ミル(1000分の1インチ)
3. (疾患の徴候となる一群の)症徴候,症候群 / (事件・社会的状態などのパターンを示す)徴候形態
4. ミ(全音階の第3音)
5. アルカリ,塩基

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/03/06 23:10:00」(JST)

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[Wiki en表示]

milk-alkali syndrome
Classification and external resources
ICD-9	275.42
DiseasesDB	8215
MedlinePlus	000332
eMedicine	med/1477

In medicine, milk-alkali syndrome, also called Burnett's syndrome in honor of Charles Hoyt Burnett (1913–1967), the American physician who first described it, is characterized by hypercalcemia caused by repeated ingestion of calcium and absorbable alkali (such as calcium carbonate, or milk and sodium bicarbonate). If untreated, milk-alkali syndrome may lead to metastatic calcification and renal failure.

It was most common in the early 20th century, but there has been a recent increase in the number of cases reported.

Pathophysiology

The name "milk-alkali syndrome" derives from when patients would take in excessive amounts of milk and antiacids to control their dyspepsia, leading to overingestion of two key ingredients that lead to the disorder, excess calcium and excess base. Ingesting over two grams of elemental calcium per day produces this disorder in susceptible individuals. Gastrointestinal absorption of such a large amount of calcium leads to hypercalcemia. This inhibits parathyroid hormone secretion by the parathyroid gland and may also lead to diabetes insipidus. The body's attempt to rid itself of the excess base in the urine may cause bicarbonaturia and subsequent hypovolemia due to transport of sodium ions to accompany the bicarbonate.^{[citation needed]}

Hypovolemia may increase the reabsorption of calcium and bicarbonate in the proximal convoluted tubules of the kidney. Elevated bicarbonate levels in the blood raises the pH, producing an alkalemia. In this state, excess bicarbonate eventually begins to reach the distal convoluted tubule, leading to sodium retention in the lumen, an effect similar to the action of thiazide diuretics, hence increasing lumen positivity and driving calcium through the passive calcium channels to bind intracellular calbindin. Finally, because of the decreased intracellular sodium, there is an increased driving force for the basolateral Na+/Ca++ antiporter, thus facilitating calcium reabsorption. Basically, hypovolemia is the culprit that prevents correction of the hypercalcemia.^{[citation needed]}

A simpler mechanism: Increased calcium intake causes a hypercalcemia in individuals who maintain an elevated fractional absorption of calcium even with increased calcium intake. The hypercalcemia does two things: 1. It prevents PTH release and 2. It causes a Nephrogenic Diabetes Insipidus (where the tubules are less responsive to ADH). The decreased PTH results in an increased reclamation of bicarbonate by the proximal tubule, causing an alkalosis. [It is known that the increased PTH of primary hyperparathyroidism is a cause of Type II (proximal) Renal Tubular Acidosis which is characterized by a decreased bicarbonate reclamation in the PCT.] The NDI leads to water loss and hypovolemia which result in activation of Renin-Angiotensin-Aldosterone System and lead of a contraction alkalosis due to the high aldosterone levels. Both things result in Alkalosis and the hypovolemia further exacerbates the hypercalcemia keeping the cycle going.^{[citation needed]}

The understanding of this mechanism led to the development of a simple and elegant treatment for hypercalcemia.^{[citation needed]} The first and most important step is intravenous infusion of normal saline to restore the intravascular volume, which reverses the calcium and bicarbonate retention in the PCT.^{[citation needed]} Then a loop diuretic is used, but only after the volume replacement is complete, otherwise volume contraction would result, which would further exacerbate the hypercalcemia.^{[citation needed]} The loop diuretics inhibit the Na-K-2Cl symporter and hence eliminate passive diffusion of potassium into the lumen via the ROMK channel. This effectively removes the net positive charge from the lumen, one of the main driving forces for calcium reabsorption via the paracellular pathway. In addition, loop diuretics increase the flow of luminal contents, which helps flush the calcium to the distal nephron.^{[citation needed]}

Clinical

Effects due to hypercalcemia caused by Primary Hyperparathyroidism may be remembered by the mnemonic bones, stones, groans and psychiatric overtones [ or moans ] while sitting on a "throne.^{[citation needed]} Milk alkali syndrome is a cause of secondary hyperparathyroidism. This means an increased risk of kidney stones due to the hypercalcemia, but not bone fractures as bone is not being resorped, anorexia, vomiting, constipation, weakness, abdominal pain and a host of psychiatric effects, including depression, fatigue and altered mental status.^{[citation needed]} Thus, a level of serum calcium must be obtained, but a full workup must include total/ionized calcium, albumin, phosphate, PTH, PTHrP, vitamin D and TSH. In addition, evaluation of hypercalcemia must include an ECG, which may show a short QT interval.^{[citation needed]}

References

External links

• eMedicine.com - Milk-Alkali Syndrome ([1]).

UpToDate Contents

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• 1. ミルク・アルカリ症候群 the milk alkali syndrome
• 2. 高カルシウム血症の原因 etiology of hypercalcemia
• 3. 高カルシウム血症への診断的アプローチ diagnostic approach to hypercalcemia
• 4. 代謝性アルカローシスの原因 causes of metabolic alkalosis
• 5. 皮膚石灰沈着症：病院および患者の評価 calcinosis cutis etiology and patient evaluation

English Journal

• Cinacalcet attenuates hypercalcemia observed in mice bearing either Rice H-500 Leydig cell or C26-DCT colon tumors.

• Colloton M, Shatzen E, Wiemann B, Starnes C, Scully S, Henley C, Martin D.SourceDepartment of Metabolic Disorders, Amgen, Inc., Thousand Oaks, CA 91320, United States.
• European journal of pharmacology.Eur J Pharmacol.2013 Jul 15;712(1-3):8-15. doi: 10.1016/j.ejphar.2013.04.013. Epub 2013 Apr 23.
• Excessive secretion of parathyroid hormone-related protein (PTHrP) by tumors stimulates bone resorption and increases renal tubular reabsorption of calcium, resulting in hypercalcemia of malignancy. We investigated the ability of cinacalcet, an allosteric modulator of the calcium-sensing receptor, t
• PMID 23623934

• [Renal ultrasound in fat necrosis].

• Tizki S, Lasry F, Elftoiki FZ, Hadj Khalifa H, Itri M, Khadir K, Benchikhi H.SourceUnité de néphrologie pédiatrique, pédiatrie III, hôpital d'enfants Abderrahim-Harouchi, CHU Ibn Rochd, rue El Faidouzi, Casablanca, Maroc. Electronic address: samira.tizki@gmail.com.
• Archives de pédiatrie : organe officiel de la Sociéte française de pédiatrie.Arch Pediatr.2013 Jul;20(7):768-71. doi: 10.1016/j.arcped.2013.04.022. Epub 2013 May 29.
• Subcutaneous fat necrosis is an uncommon disease that may be complicated with potentially fatal hypercalcemia or with nephrocalcinosis. We report on the case of a patient with a history of significant perinatal asphyxia, hospitalized for a urinary tract infection. Lesions of subcutaneous fat necrosi
• PMID 23726682

• New insights in regulation of calcium homeostasis.

• Felsenfeld A, Rodriguez M, Levine B.SourceaDepartment of Medicine, VA Greater Los Angeles Healthcare System and the David Geffen School of Medicine at UCLA, Los Angeles, California, USA bServicio de Nefrologia, REDINREN, IMIBIC, Hospital Universitario Reina Sofia, Cordoba, Spain.
• Current opinion in nephrology and hypertension.Curr Opin Nephrol Hypertens.2013 Jul;22(4):371-6. doi: 10.1097/MNH.0b013e328362141e.
• PURPOSE OF REVIEW: Regulation of calcium homeostasis during a lifetime is a complex process reflecting a balance among intestinal calcium absorption, bone calcium influx and efflux, and renal calcium excretion. Perturbations can result in hypocalcemia or hypercalcemia and adaptations in calcium hand
• PMID 23736839

Japanese Journal

• Calcium-Alkali Syndrome-Like Symptoms Manifested by Daily Alphacalcidol and Thiazide

• Satoh Fumie,Okado Tomokazu,Iwamoto Mari,Akita Wataru,Wakabayashi Mai,Ohta Akihito,Sohara Eisei,Noda Yumi,Rai Tatemitsu,Uchida Shinichi,Sasaki Sei
• Internal Medicine 49(9), 2010
• … Laboratory examination revealed hypercalcemia, metabolic alkalosis, and kidney injury, similar to the traditional milk-alkali syndrome. … Recently, it has been recommended the term "milk-alkali syndrome" be replaced by "calcium-alkali syndrome", which broadens the definition of the condition. …
• NAID 130000251882

Related Links

• Milk-Alkali Syndrome - Diseases & Conditions - Medscape ...

Milk-alkali syndrome is caused by the ingestion of large amounts of calcium and absorbable alkali, with resulting hypercalcemia. If unrecognized and untreated, milk-alkali syndrome can lead to metastatic calcification and renal failure. This syndrome was originally recognized in the 1920s during ...

• Milk-alkali syndrome: MedlinePlus Medical Encyclopedia

Milk-alkali syndrome is a condition in which there is a high level of calcium in the body (hypercalcemia). This causes a shift in the body's acid/base balance toward alkaline (metabolic alkalosis). As a result, there can be ...

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★リンクテーブル★

リンク元	「高カルシウム血症」「ミルク・アルカリ症候群」
関連記事	「mi」「alkali」「syndrome」「milk」

「高カルシウム血症」

　　[★]

英

hypercalcemia

同

高Ca血症

関

カルシウム、低カルシウム血症

研修医当直御法度 症例帳 p.32

• 組織へのカルシウム蓄積を引き起こしうる (BPT.27)

病因

• 1. 原発性副甲状腺機能亢進症(甲状腺腺腫などによるPTHの分泌亢進)
• 2. 腫瘍に随伴

• 2-1. 肺の扁平上皮癌、成人性Ｔ細胞白血病→PTH関連蛋白(PTHrP)の分泌
• 2-2. 腫瘍の骨転移により、破骨細胞が骨破壊。

• 3. サルコイドーシス、肉芽細胞→異所性1,25(OH)2D3が発生する。

• 肉芽の構成成分であるマクロファージがビタミンD3を産生？

• 4. サイアザイド系利尿薬や骨粗しょう症の薬として1,25(OH)2D3製剤。

• 4-1. サイアザイド系利尿薬

• チアジド系利尿薬の慢性使用により体液量が減少し、近位尿細管での再吸収が亢進するため (GOO.755)　？？
• チアジド系利尿薬自体のDCTでの作用による；NCCTを阻害すると細胞内のNa濃度低下、これにより側底膜でのNa+-Ca2+交換系が亢進することでCa2+の再吸収↑ (GOO.755) 　→　ループ利尿薬と違ってチアジド系利尿薬ははCaを排泄しない！！ see.利尿薬

• 5. 家族性低Ca尿性高Ca血症
• 6. その他(リチウム？？？？ (ICU.558))

ECGP.223

• 7. ビタミンA, ビタミンDの中毒
• 8. 腎不全
• 9. 副腎不全

USMLEより

• Caused by calcium ingestion (milk-alkali syndrome), hyperparathyroid, hyperthyroid, iatrogenic (thiazides), multiple myeloma, Paget's disease, Addison's disease, Neoplasms, Zollinger-Ellison syndrome, Excess vitamin D, Excess vitamin A, sarcoidosis.

• Calcium ingestion
• Hyperparathyroid/Hyperthyroid
• Iatrogenic
• Multiplemyeloma
• Paget's disease
• Addison's disease
• Neoplasms
• Zollinger-Ellison syndrome: ZES単独ではなく、MEN Iによるparathyroid tumorに続発した病態
• Excessive vitamin D
• Excessive vitamin A
• Sarcoidosis

定義

• 血清カルシウムが正常上限を超える場合。

• 疑い：常に≧10.3 mg/dl
• 確実：≧10.5 mg/dl

↑

基準値

• 血清総Ca 8.6-10.1 mg/dl(臨床検査法提要第32版)
• 血清Caイオン 1.15-1.30 mmmol/l(臨床検査法提要第32版), 4.6-5.1 mg/dl

症候

軽度(11-11.5 mg/dL)：通常は無症状。(HIM.285)

重度(>12-13 mg/dL)：傾眠、昏迷、昏睡、消化器症状が出現。(HIM.285)

• 精神・神経症状：錯乱、昏迷、昏睡。イライラ感、うつ傾向(QB.D-339)
• 消化器：食欲不振、悪心・嘔吐、便秘。膵炎、消化性潰瘍。腹部膨満(腸管運動抑制による(QB.D-339))

• 消化性潰瘍：高カルシウム血症は胃酸分泌を促進する
• 急性膵炎：高カルシウム血症は膵液の分泌を亢進する。(YN.B-78)　←　過剰に出ちゃうと炎症が起こってしまうらしい

• 泌尿器：多尿、腎結石(血清Ca 12mg/dLでできやすくなるらしい)　←　多尿は浸透圧利尿による(ICU.558)

• 急性腎不全

• 腎不全は一般的に低カルシウム血症となるが、高カルシウム血症に起因する腎不全は例外。

→高カルシウム血症性腎症 hypercalcemic nephropathy

• 腎の石灰化→髄質に蓄積→尿細管圧迫→尿濃縮力障害　←　続発性尿崩症の原因？？？

• 高カルシウム血症は腎の濃縮力を低下させる(HIM.286)　←　腎集合管におけるADHの作用を阻害(QB.D-339)

• 心血管：血管収縮による高血圧(出典不明！！)。徐脈、房室ブロック、QT短縮(HIM.284)。　←　YN.D-147には血圧上昇、ICU.558には低血圧とある。
• 筋　：筋力低下、筋痛
• 全身：易疲労感

• 異所性石灰化 red eye　強膜にカルシウムが沈着
• 多尿による脱水、高血圧、徐脈

心電図

EAB.114 SP.94,524

• QT短縮、ST短縮　←　活動電位持続時間が短縮したことを示す。QRS幅については延長する場合もある(EAB.114)

• ↑細胞外カルシウム濃度→↑内向きカルシウム電流(↑流入速度)→さらに脱分極するように思えるが↑外向きカリウム電流により打ち消される→正味、カルシウムの移動が無くなるまでの時間が早まる→↓活動電位持続時間

• PR間隔延長？？

高カルシウム血症→QT短縮：　←高カリウム血症

低カルシウム血症→QT延長：　←低カリウム血症　低マグネシウム血症

治療

• 症状が出たときか、症状無く血清Ca 14mg/dL以上の場合(ICU.558)

生理食塩水

• 1. 細胞外液の補充
• 2. ナトリウム利尿によるカルシウム排泄の促進

高カルシウム血症の鑑別

		尿中のCa排泄	PTH	PTHrP	1,25(OH)2D3
原発性甲状腺機能亢進症	↑	↑	↓	→　or　↑
腫瘍のPTH関連蛋白分泌	↑	↓	↑	↓
	 腫瘍の骨破壊	↑	↓	↓	↓
	 肉芽腫症		↓	↓	↓	→　or　↑

参考

• http://akimichi.homeunix.net/~emile/aki/html/medical/endocrine/node52.html

国試

• 102G052

「ミルク・アルカリ症候群」

　　[★]

英

milk-alkali syndrome

同

バーネット症候群 Burnett syndrome Burnett's syndrome、アルカローシス症候群 alkalosis syndrome

関

高カルシウム血症

「mi」

　　[★]

mi-, mio-

• conb form

• より小さい、より少ない。劣った

• ex.

• miosis 縮瞳

？

MI

　 　

「alkali」

　　[★]

• アルカリ

関

alkaline

　 　

「syndrome」

　　[★]

• n.

• 症候群

　 　 　

「milk」

　　[★]