Milk-alkali syndrome
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| Milk-alkali syndrome Classification and external resources | |
| ICD-9 | 275.42 |
|---|---|
| DiseasesDB | 8215 |
| MedlinePlus | 000332 |
| eMedicine | med/1477 |
Editor-In-Chief: Steven C. Campbell, M.D., Ph.D., Professor of Surgery, Residency Program Director, Section of Urologic Oncology, Glickman Urological and Kidney Institute, Cleveland Clinic. You can email Dr. Campbell by clicking here. Office phone: 216-444-5595.
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Overview
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.[1][2]
Pathophysiology
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 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.
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.
The understanding of this mechanism led to the development of a simple yet elegant treatment for hypercalcemia. 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. 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 overtones. This means an increased risk of kidney stones, bone fractures, 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, 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.[3][4]
References
- ↑ Caruso JB, Patel RM, Julka K, Parish DC (July 2007). "Health-behavior induced disease: return of the milk-alkali syndrome". J Gen Intern Med 22 (7): 1053–5. doi:10.1007/s11606-007-0226-0. PMID 17483976.
- ↑ Beall DP, Henslee HB, Webb HR, Scofield RH (May 2006). "Milk-alkali syndrome: a historical review and description of the modern version of the syndrome". Am. J. Med. Sci. 331 (5): 233–42. PMID 16702792.
- ↑ synd/4029 at Who Named It
- ↑ Burnett CH, Commons RR, Albright F, Howard JE (1949). "Hypercalcemia without hypercalcuria or hypophosphatemia, calcinosis and renal insufficiency; a syndrome following prolonged intake of milk and alkali". N. Engl. J. Med. 240 (20): 787–94. PMID 18126919.
External links
- eMedicine.com - Milk-Alkali Syndrome ([2])
Mineral metabolic pathology (E83, 275) | |
|---|---|
| Mineral | Cu Wilson's disease/Menkes disease
Fe Haemochromatosis, Aceruloplasminemia, Atransferrinemia Zn Acrodermatitis enteropathica PO43− Hypophosphatemia/Hypophosphatasia Mg2+ Hypermagnesemia/Hypomagnesemia Ca2+ Hypercalcaemia/Hypocalcaemia/Disorders of calcium metabolism Biotin Biotinidase deficiency, Holocarboxylase synthetase deficiency |
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
