Milk-alkali syndrome
5720556
221193575
2008-06-23T13:21:08Z
Arcadian
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{{Infobox_Disease |
Name = {{PAGENAME}} |
Image = |
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DiseasesDB = 8215 |
ICD10 = |
ICD9 = {{ICD9|275.42}} |
ICDO = |
OMIM = |
MedlinePlus = 000332 |
eMedicineSubj = med |
eMedicineTopic = 1477 |
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In [[medicine]], '''milk-alkali syndrome''', also called Burnett's syndrome in honour of 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.<ref name="pmid17483976">{{cite journal |author=Caruso JB, Patel RM, Julka K, Parish DC |title=Health-behavior induced disease: return of the milk-alkali syndrome |journal=J Gen Intern Med |volume=22 |issue=7 |pages=1053–5 |year=2007 |month=July |pmid=17483976 |doi=10.1007/s11606-007-0226-0 |url=http://dx.doi.org/10.1007/s11606-007-0226-0}}</ref><ref name="pmid16702792">{{cite journal |author=Beall DP, Henslee HB, Webb HR, Scofield RH |title=Milk-alkali syndrome: a historical review and description of the modern version of the syndrome |journal=Am. J. Med. Sci. |volume=331 |issue=5 |pages=233–42 |year=2006 |month=May |pmid=16702792 |doi= |url=http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?an=00000441-200605000-00001}}</ref>
==Pathophysiology==
Ingestion of over 2 g of elemental [[calcium]] per day may lead to this disorder. When a large quantity of [[calcium]] is ingested and absorbed by the GI tract, this leads to [[hypercalcemia]]. This inhibits production of [[Parathyroid hormone|PTH]] by the [[parathyroid gland]], and also causes [[diabetes insipidus]], which leads to [[hypovolemia|volume contraction]] and consequent increased calcium reabsorption at the [[Proximal tubule|PCT]]. Another [[homeostasis|homeostatic]] response to the volume contraction is increased reabsorption of [[bicarbonate]] in the PCT, hence maintaining the [[alkalosis]]. With the alkalosis, excess bicarb eventually begins to reach the [[Distal convoluted tubule|DCT]], 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. Thirdly, because of the decreased intracellular sodium, there is an increased driving force for the basolateral Na/Ca antiport, thus facilitating Ca transport back into the circulation.
The understanding of this mechanism led to the development of a simple yet elegant treatment for hypercalcemia. The first and most important step is [[Route of administration#Parenteral by injection or infusion|intravenous infusion]] of [[Saline (medicine)|normal saline]] to restore the intravascular volume, which reverses the calcium and bicarbonate retention in the PCT. 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. 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.
==Clinical==
Effects due to [[hypercalcemia]] may be remembered by ''bones'', ''stones'', ''groans'' and ''psychiatric undertones''. This means an increased risk of [[Kidney stones]], [[bone fractures]], [[anorexia (symptom)|anorexia]], [[vomiting]], [[constipation]] and a host of psychiatric effects, including weakness, fatigue and [[altered mental status]]. Thus, a level of [[serum]] [[calcium]] must be obtained, but a full workup must include total/ionized [[calcium]], [[human serum albumin|albumin]], [[phosphate]], [[PTH]], [[PTHrP]], [[vitamin D]] and [[TSH]]. In addition, evaluation of [[hypercalcemia]] must include an [[ECG]], which may show a short QT interval.
==Eponym==
It is named for [[Charles Hoyt Burnett]].<ref>{{WhoNamedIt|synd|4029}}</ref><ref>C. H. Burnett, R. R. Commons, Fuller Albright, J. E. Howard. Hypercalcemia without hypercalcuria or hyposphatemia, calcinosis and renal insufficiency. A syndrome following prolonged intake of milk and alkali. New England Journal of Medicine, Boston, 1949, 240: 787-794.</ref>
==References==
{{reflist}}
==External links==
* eMedicine.com - Milk-Alkali Syndrome ([http://www.emedicine.com/med/topic1477.htm]).
[[Category:Electrolyte disturbances]]
[[Category:Calcium]]
[[Category:Urinary system]]
[[Category:Diseases]]
[[Category:Kidney diseases]]
[[Category:Urology]]
{{Mineral metabolic pathology}}
[[de:Burnett-Syndrom]]