Milk-Alkali Syndrome Medication

  • Author: R Hal Scofield, MD; Chief Editor: George T Griffing, MD   more...
 
Updated: Jan 6, 2012
 

Medication Summary

The primary therapy for hypercalcemia in milk-alkali syndrome is intravenous volume replacement with isotonic sodium chloride solution. When ingestion of calcium carbonate has stopped, the pathophysiologic stimulus for hypercalcemia is no longer present. Hypercalcemia in this setting usually is rapidly corrected. Loss of calcium from urine can be increased with the use of a loop diuretic, but this therapy cannot be started until intravascular volume has been replenished. Renal dialysis has been used in a few patients, as has intravenous infusion of pamidronate.

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Diuretics, Loop

Class Summary

Diuretics induce calciuresis. In patients with severe hypercalcemia, the individual typically is volume depleted, which means that volume should be replaced with saline prior to institution of diuretic therapy.

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Furosemide (Lasix)

 

Furosemide inhibits the resorption of sodium and chloride in the loop of Henle and the proximal and distal tubules of the kidney. Its onset of action is rapid after an intravenous dose.

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Calcium Metabolism Modifiers

Class Summary

These agents decrease the movement of calcium from bone to serum. Bisphosphonates are analogues of inorganic pyrophosphate and act by binding to hydroxyapatite in bone matrix, thereby inhibiting the dissolution of crystals. They prevent osteoclast attachment to the bone matrix and osteoclast recruitment and viability.

The newer bisphosphonates are not completely free of the risk of causing a mineralization defect, but their safe therapeutic window is much wider. They clearly are more potent than etidronate in reducing disease activity and normalizing alkaline phosphatase levels.

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Pamidronate (Aredia)

 

Pamidronate's main action is to inhibit the resorption of bone. The mechanism by which this inhibition occurs is not fully known. The drug is adsorbed onto calcium pyrophosphate crystals and may block the dissolution of these crystals, also known as hydroxyapatite, which are an important mineral component of bone. There is also evidence that pamidronate directly inhibits osteoclasts.

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Zoledronate (Reclast, Zometa)

 

Zoledronate inhibits bone resorption. It inhibits osteoclastic activity and induces osteoclastic apoptosis

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Contributor Information and Disclosures
Author

R Hal Scofield, MD  Professor, Department of Medicine, Section of Endocrinology, Associate Dean for Clinical and Translational Research, University of Oklahoma College of Medicine; Associate Member, Arthritis and Immunology Program, Oklahoma Medical Research Foundation

R Hal Scofield, MD is a member of the following medical societies: American Association of Immunologists, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American College of Rheumatology, American Diabetes Association, American Federation for Medical Research, Endocrine Society, and Oklahoma State Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Thuy-Trang Nguyen  University of Louisville School of Medicine

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD  Professor of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Additional Contributors

Romesh Khardori, MD, PhD, FACP Former Professor, Department of Medicine, Former Chief, Division of Endocrinology, Metabolism, and Molecular Medicine, Southern Illinois University School of Medicine

Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, and Endocrine Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References

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The hospital course of a patient with milk-alkali syndrome who, during treatment, developed symptomatic hypocalcemia with a markedly elevated serum parathyroid hormone level (PTH). Thirty days after discharge, the calcium and PTH levels were normal.
Table. Summary of 65 Consecutively Reported Adult Patients With Milk-Alkali Syndrome*
Mean Age51 Years (Range, 24-95 y)
Sex35 men and 43 women
Calcium sourceCalcium carbonate in all but 1
Ingestion of bicarbonateIn 7 patients
Ingestion of milkIn 20 patients (plus one who ate yogurt)
Mean serum calcium15.1mg/dL (3.75mmol/L) (range, 11.1-27.5mg/dL)
High serum phosphorusIn 12 patients
Permanent renal insufficiencyIn 20 of 57 patients eligible for evaluation
Parathyroid explorationIn 3 patients
Hypocalcemia with treatmentIn 16 patients
*These data are derived from the 7 patients reported, plus the 28 reviewed in Beall and Scofield, 1995,[6] as well as additional patients reported by Gibbs and Lee, 1992;[9] Nakanishi et al, 1992[10] ; Brandwein and Sigman, 1994[11] ; Campbell et al, 1994[12] ; Duthie et al, 1995[13] ; Spital and Freedman, 1995[14] ; Fiorino, 1996[15] ; Lin et al, 1996[16] ; Muldowney and Mazbar, 1996[17] ; Sulkin and Krentz, 1999[18] ;



Camidge and Peaston, 2000[19] ; George and Clark, 2000[20] ; Vanpee et al, 2000[21] ; Liu et al, 2002[22] ; Robertson, 2002[23] ; Morton, 2002[24] ; Kleinig and Torpy, 2004[2] ; Picolos et al, 2005[7] ; Gordon et al, 2005[25] ; Addington et al, 2006[5] ; Verburg et al, 2006[26] ; Ennen and Magann, 2006[27] ; Caruso et al, 2007[28] ; Dinnerstein et al, 2007[29] ; Javid et al, 2007; Kaklamanos and Perros, 2007[30] ; Shah et al, 2007[31] ; Irtiza-Ali et al, 2008[3] ; and Jousten and Guffens, 2008.[4]



Two of the patients were pregnant.



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