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| | '''For patient information page click [[{{PAGENAME}} (patient information)|here]]''' |
| {{Infobox_Disease | | | {{Infobox_Disease | |
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| eMedicineSubj = med |
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| eMedicineTopic = 1477 |
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| {{Search infobox}} | | {{Milk-alkali syndrome}} |
| {{SCC}} | | {{CMG}} {{SCC}} {{AE}} {{SHA}} |
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| ==Overview==
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| '''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]].
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| 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>
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| ==Pathophysiology==
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| The name "milk-alkali syndrome" derives from when patients would take in excessive amounts of milk and antacids 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 tract|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.
| | ==[[Milk-alkali syndrome overview|Overview]]== |
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| Hypovolemia may increase the reabsorption of calcium and [[bicarbonate]] in the [[proximal convoluted tubule]]s 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.
| | ==[[Milk-alkali syndrome historical perspective|Historical Perspective]]== |
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| 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.
| | ==[[Milk-alkali syndrome classification|Classification]]== |
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| ==Clinical== | | ==[[Milk-alkali syndrome pathophysiology|Pathophysiology]]== |
| Effects due to [[hypercalcemia]] may be remembered by ''bones'', ''stones'', ''groans'' and ''psychiatric overtones''. 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.
| | ==[[Milk-alkali syndrome causes|Causes]]== |
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| ==Eponym== | | ==[[Milk-alkali syndrome differential diagnosis|Differentiating Milk-alkali syndrome from other Diseases]]== |
| It is named for Charles Hoyt Burnett.<ref>{{WhoNamedIt|synd|4029}}</ref><ref>{{cite journal |author=Burnett CH, Commons RR, Albright F, Howard JE |title=Hypercalcemia without hypercalcuria or hypophosphatemia, calcinosis and renal insufficiency; a syndrome following prolonged intake of milk and alkali |journal=N. Engl. J. Med. |volume=240 |issue=20 |pages=787–94 |year=1949 |pmid=18126919 |doi= |url=}}</ref>
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| ==References== | | ==[[Milk-alkali syndrome epidemiology and demographics|Epidemiology and Demographics]]== |
| {{reflist}}
| | ==[[Milk-alkali syndrome risk factors|Risk Factors]]== |
| | ==[[Milk-alkali syndrome screening|Screening]]== |
| | ==[[Milk-alkali syndrome natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
| | ==Diagnosis== |
| | [[Milk-alkali syndrome diagnostic study of choice|Diagnostic Study of Choice]] |[[Milk-alkali syndrome history and symptoms|History and Symptoms]] | [[Milk-alkali syndrome physical examination|Physical Examination]] | [[Milk-alkali syndrome laboratory findings|Laboratory Findings]] |[[Milk-alkali syndrome electrocardiogram|Electrocardiogram]] |[[Milk-alkali syndrome x-ray|X-ray]] |[[Milk-alkali syndrome echocardiography and ultrasound|Echocardiography and Ultrasound]] | | [[Milk-alkali syndrome CT scan|CT Scan]] |[[Milk-alkali syndrome MRI|MRI]] | [[Milk-alkali syndrome other imaging findings|Other Imaging Findings]] | [[Milk-alkali syndrome other diagnostic studies|Other Diagnostic Studies]] |
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| ==External links== | | ==Treatment== |
| * eMedicine.com - Milk-Alkali Syndrome ([http://www.emedicine.com/med/topic1477.htm])
| | [[Milk-alkali syndrome medical therapy|Medical Therapy]] | [[Milk-alkali syndrome surgery|Surgery]] | [[Milk-alkali syndrome primary prevention|Primary Prevention]] |[[Milk-alkali syndrome secondary prevention| Secondary Prevention]]|[[Milk-alkali syndrome cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Milk-alkali syndrome future or investigational therapies|Future or Investigational Therapies]] |
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| {{Mineral metabolic pathology}} | | {{Mineral metabolic pathology}} |
| {{SIB}}
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| [[Category:Electrolyte disturbances]] | | [[Category:Electrolyte disturbances]] |