Milk-alkali syndrome pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shakiba Hassanzadeh, MD[2]

Overview

The exact pathogenesis of milk-alkali syndrome is unknown. Hypercalcemia in milk-alkali syndrome involves several mechanisms including: intestinal absorption of calcium is increased, bone buffering of calcium becomes saturated, and renal excretion of calcium is decreased. Several factors that increase bicarbonate reabsorption and contribute to the alkalosis in milk-alkali syndrome include: volume depletion due to increased sodium and free water excretion caused by increased calcium intake, suppression of PTH, direct tubular effects of calcium and other factors that cause volume depletion or alkalosis such as vomiting or thiazide use.

Pathophysiology

  • The exact pathogenesis of milk-alkali syndrome is unknown.
  • Consumption of excessive amounts of calcium and absorbable alkali causes milk-alkali syndrome.[1]

Pathogenesis

The pathogenesis of milk-alkali syndrome involves the kidneys, bones, and intestines.[2]

Hypercalcemia
Metabolic Alkalosis

Histopathology

References

  1. 1.0 1.1 1.2 Medarov BI (2009). "Milk-alkali syndrome". Mayo Clin Proc. 84 (3): 261–7. doi:10.1016/S0025-6196(11)61144-0. PMC 2664604. PMID 19252114.
  2. Arroyo M, Fenves AZ, Emmett M (2013). "The calcium-alkali syndrome". Proc (Bayl Univ Med Cent). 26 (2): 179–81. doi:10.1080/08998280.2013.11928954. PMC 3603742. PMID 23543983.
  3. 3.0 3.1 3.2 3.3 Felsenfeld AJ, Levine BS (2006). "Milk alkali syndrome and the dynamics of calcium homeostasis". Clin J Am Soc Nephrol. 1 (4): 641–54. doi:10.2215/CJN.01451005. PMID 17699269.
  4. 4.0 4.1 Riccardi D, Brown EM (2010). "Physiology and pathophysiology of the calcium-sensing receptor in the kidney". Am J Physiol Renal Physiol. 298 (3): F485–99. doi:10.1152/ajprenal.00608.2009. PMC 2838589. PMID 19923405.
  5. Picolos MK, Lavis VR, Orlander PR (2005). "Milk-alkali syndrome is a major cause of hypercalcaemia among non-end-stage renal disease (non-ESRD) inpatients". Clin Endocrinol (Oxf). 63 (5): 566–76. doi:10.1111/j.1365-2265.2005.02383.x. PMID 16268810.
  6. Fiorino AS (1996). "Hypercalcemia and alkalosis due to the milk-alkali syndrome: a case report and review". Yale J Biol Med. 69 (6): 517–23. PMC 2589043. PMID 9436295.
  7. BURNETT CH, COMMONS RR (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. doi:10.1056/NEJM194905192402001. PMID 18126919.
  8. WERMER P, KUSCHNER M, RILEY EA (1953). "Case reports; reversible metastatic calcification associated with excessive milk and alkali intake". Am J Med. 14 (1): 108–15. doi:10.1016/0002-9343(53)90362-3. PMID 13016590.
  9. HOLTEN C, LUNDBAEK K (1955). "Renal insufficiency and severe calcinosis due to excessive alkali-intake". Acta Med Scand. 151 (3): 177–83. doi:10.1111/j.0954-6820.1955.tb10281.x. PMID 14375805.
  10. DUFAULT FX, TOBIAS GJ (1954). "Potentially reversible renal failure following excessive calcium and alkali intake in peptic ulcer therapy". Am J Med. 16 (2): 231–6. doi:10.1016/0002-9343(54)90339-3. PMID 13124355.
  11. SCHOLZ DA, KEATING FR (1955). "Milk-alkali syndrome; review of eight cases". AMA Arch Intern Med. 95 (3): 460–8. doi:10.1001/archinte.1955.00250090098012. PMID 14349424.
  12. RANDALL RE, STRAUSS MB, McNEELY WF (1961). "The milk-alkali synfcmme". Arch Intern Med. 107: 163–81. doi:10.1001/archinte.1961.03620020013003. PMID 13739449.
  13. 13.0 13.1 Junor BJ, Catto GR (1976). "Renal biopsy in the milk-alkali syndrome". J Clin Pathol. 29 (12): 1074–6. doi:10.1136/jcp.29.12.1074. PMC 476303. PMID 1010876.