Milk-Alkali Syndrome Treatment & Management

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

Approach Considerations

Mild hypercalcemia

The only care required is discontinuation of calcium carbonate or reduction of the dose to no more than 1200-1500mg of elemental calcium daily. In most patients, calcium supplementation should be changed to a form of calcium other than calcium carbonate. Thus, absorbable alkali is avoided.

Severe hypercalcemia

The patient should be admitted to the hospital. Saline diuresis, produced by infusion of large volumes of intravenous isotonic sodium chloride solution, is the treatment of choice. Further calciuresis can be induced by treatment with intravenous loop diuretics, although the utility of loop diuretics for hypercalcemia has been questioned.[34]

The typical patient is volume depleted; therefore, volume should be replaced with saline prior to institution of diuretic therapy. Care should be taken to not induce volume depletion with the diuretics, because this may worsen the hypercalcemia.

Calcium carbonate should be stopped to resolve the pathophysiology that produced the hypercalcemia. As stated previously, however, patients with milk-alkali syndrome may become transiently hypocalcemic during treatment with intravenous saline and intravenous diuretics.

Because laboratory studies such as PTH measurements will not have returned to normal when therapy is instituted, the serum calcium level must be monitored closely.

Pamidronate has been used successfully in the treatment of hypercalcemia secondary to milk-alkali syndrome. However, treatment of milk-alkali syndrome with bisphosphonates was associated with hypocalcemia in one series; 6 of 11 patients with milk-alkali syndrome developed treatment-induced hypocalcemia, with 5 of the 6 patients having received bisphosphonates,[7] while in the author’s series of 6 patients, none of whom received bisphosphonate, only 1 developed hypocalcemia.[6]

Treatment-related hypocalcemia

If hypocalcemia develops in the course of treatment, this usually can be treated with oral calcium supplementation. A calcium source without absorbable alkali, such as calcium citrate, is preferred. Rarely, intravenous calcium might be required to treat severe hypocalcemia.

Diet and activity

A low-calcium, low-phosphorus diet is required during hypercalcemia. No activity restrictions are necessary.

Consultations

Consultation with a nephrologist may be needed with severe renal disease and/or severe hypercalcemia, because dialysis sometimes is required. Consultation with an endocrinologist may be needed for interpretation of PTH and other laboratory studies.

Transfer

Occasionally, dialysis may be required with severe renal impairment. With elevated serum calcium and phosphorus levels, dialysis may be needed to urgently lower these parameters. This may prevent ectopic calcification.

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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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