Multimedialna platforma wiedzy medycznej Internetowa Księgarnia Medyczna Kalendarium Konferencji
Endokrynologia Polska
MENU
Shortcuts Submit an article Author Guidelines Polish Society of Endocrinology Reviewers 2023 Redeem voucher

open access

Vol 69, No 2 (2018)
Case report
Submitted: 2017-02-08
Accepted: 2017-04-24
Published online: 2018-02-08
View PDF Download PDF file
Get Citation

Milk-alkali syndrome (MAS) as a complication of the treatment of hypoparathyroidism — a case study

Agata Skwarek, Janusz Pachucki, Tomasz Bednarczuk, Zuzanna Żurecka, Michał Popow, Agnieszka Kondracka1, Zbigniew Bartoszewicz1
DOI: 10.5603/EP.a2018.0015
·
Pubmed: 29442351
·
Endokrynol Pol 2018;69(2):200-204.
Affiliations
  1. Department of Internal Medicine and Endocrinology, Medical University of Warsaw, Warsaw, Poland, Poland

open access

Vol 69, No 2 (2018)
Case report
Submitted: 2017-02-08
Accepted: 2017-04-24
Published online: 2018-02-08

Abstract

Milk-alkali syndrome (MAS), characterized by renal failure, metabolic alkalosis and hypercalcemia, is a severe and life-threatening complication of the treatment of hypoparathyroidism. The clinical course is often sudden and is not preceded by any prodromal symptoms. Occurrence does not depend on the duration of hypoparathyroidism treatment, although it is closely related to the applied therapy, especially the dose of calcium carbonate and active vitamin D preparations. Drugs influencing the glomerular filtration rate (angiotensin receptor blockers, sartans, aldosterone receptor antagonists, thiazide diuretics), lack of adequate routine control, changing the calcium carbonate supplementation, dehydration, a diet rich in pH-basic foods (i.e. vegetarian diet), pregnancy and other associated conditions are listed among the factors triggering MAS. A higher calcium carbonate dose is directly associated with an increased risk of milk-alkali syndrome. In case of a high calcium demand it is necessary to control renal function and monitor the level of calcium in the serum more frequently, aiming for the lower end of the reference range. If MAS has been confirmed or if there are alarming neurological symptoms suggestive of hypercalcemia, the patient must be sent to the hospital immediately. Treatment of MAS involves: discontinuation of calcium and vitamin D supplementation, and intravenous infusion of normal saline solution to eliminate volume deficiencies and to achieve forced diuresis while maintaining proper fluid balance. As soon as there is improvement in the patient’s clinical condition, it is necessary to begin the treatment of comorbidities increasing the risk of renal failure or alkalosis (i.e. vomiting, diarrhea).

Abstract

Milk-alkali syndrome (MAS), characterized by renal failure, metabolic alkalosis and hypercalcemia, is a severe and life-threatening complication of the treatment of hypoparathyroidism. The clinical course is often sudden and is not preceded by any prodromal symptoms. Occurrence does not depend on the duration of hypoparathyroidism treatment, although it is closely related to the applied therapy, especially the dose of calcium carbonate and active vitamin D preparations. Drugs influencing the glomerular filtration rate (angiotensin receptor blockers, sartans, aldosterone receptor antagonists, thiazide diuretics), lack of adequate routine control, changing the calcium carbonate supplementation, dehydration, a diet rich in pH-basic foods (i.e. vegetarian diet), pregnancy and other associated conditions are listed among the factors triggering MAS. A higher calcium carbonate dose is directly associated with an increased risk of milk-alkali syndrome. In case of a high calcium demand it is necessary to control renal function and monitor the level of calcium in the serum more frequently, aiming for the lower end of the reference range. If MAS has been confirmed or if there are alarming neurological symptoms suggestive of hypercalcemia, the patient must be sent to the hospital immediately. Treatment of MAS involves: discontinuation of calcium and vitamin D supplementation, and intravenous infusion of normal saline solution to eliminate volume deficiencies and to achieve forced diuresis while maintaining proper fluid balance. As soon as there is improvement in the patient’s clinical condition, it is necessary to begin the treatment of comorbidities increasing the risk of renal failure or alkalosis (i.e. vomiting, diarrhea).

Full Text:

View PDF Download PDF file
Get Citation

Keywords

MAS, hypercalcemia, hypoparathyroidism, alkalinisation, hypercalciuria, milk alkali syndrome, metabolic alkalosis, renal failure, active vitamin D

About this article
Title

Milk-alkali syndrome (MAS) as a complication of the treatment of hypoparathyroidism — a case study

Journal

Endokrynologia Polska

Issue

Vol 69, No 2 (2018)

Article type

Case report

Pages

200-204

Published online

2018-02-08

Page views

3461

Article views/downloads

2623

DOI

10.5603/EP.a2018.0015

Pubmed

29442351

Bibliographic record

Endokrynol Pol 2018;69(2):200-204.

Keywords

MAS
hypercalcemia
hypoparathyroidism
alkalinisation
hypercalciuria
milk alkali syndrome
metabolic alkalosis
renal failure
active vitamin D

Authors

Agata Skwarek
Janusz Pachucki
Tomasz Bednarczuk
Zuzanna Żurecka
Michał Popow
Agnieszka Kondracka
Zbigniew Bartoszewicz

References (17)
  1. Medarov BI. Milk-alkali syndrome. Mayo Clin Proc. 2009; 84(3): 261–267.
    CrossRefPubMed
  2. Kolnick L, Harris BD, Choma DP, et al. Hypercalcemia in pregnancy: a case of milk-alkali syndrome. J Gen Intern Med. 2011; 26(8): 939–942.
    CrossRefPubMed
  3. Endres DB. Investigation of hypercalcemia. Clin Biochem. 2012; 45(12): 954–963.
    CrossRefPubMed
  4. Kallas M, Green F, Hewison M, et al. Rare causes of calcitriol-mediated hypercalcemia: a case report and literature review. J Clin Endocrinol Metab. 2010; 95(7): 3111–3117.
    CrossRefPubMed
  5. Cusano NE, Rubin MR, Sliney J, et al. Mini-review: new therapeutic options in hypoparathyroidism. Endocrine. 2012; 41(3): 410–414.
    CrossRefPubMed
  6. Nijenhuis T, Hoenderop JGJ, Bindels RJM. TRPV5 and TRPV6 in Ca(2+) (re)absorption: regulating Ca(2+) entry at the gate. Pflugers Arch. 2005; 451(1): 181–192.
    CrossRefPubMed
  7. van de Graaf SFJ, Hoenderop JGJ, Bindels RJM. Regulation of TRPV5 and TRPV6 by associated proteins. Am J Physiol Renal Physiol. 2006; 290(6): F1295–F1302.
    CrossRefPubMed
  8. Hulter H HN. Effects and interrelationships of PTH, Ca2+, vitamin D, and Pi in acid-base homeostasis. Am J Physiol. 1985; 248(6 Pt 2): F739–F752.
    CrossRefPubMed
  9. Arnett TR. Extracellular pH regulates bone cell function. J Nutr. 2008; 138(2): 415S–418S.
    PubMed
  10. Fleet JC, Schoch RD. Molecular mechanisms for regulation of intestinal calcium absorption by vitamin D and other factors. Crit Rev Clin Lab Sci. 2010; 47(4): 181–195.
    CrossRefPubMed
  11. Christakos S, Ajibade DV, Dhawan P, et al. Vitamin D: metabolism. Endocrinol Metab Clin North Am. 2010; 39(2): 243–253.
    CrossRefPubMed
  12. Block GA, Hulbert-Shearon TE, Levin NW, et al. Association of serum phosphorus and calcium x phosphate product with mortality risk in chronic hemodialysis patients: a national study. Am J Kidney Dis. 1998; 31(4): 607–617.
    PubMed
  13. Lemos R, Ramos E, Legati A, et al. Update and Mutational Analysis ofSLC20A2: A Major Cause of Primary Familial Brain Calcification. Human Mutation. 2015; 36(5): 489–495.
    CrossRef
  14. Virkki LV, Biber J, Murer H, et al. Phosphate transporters: a tale of two solute carrier families. Am J Physiol Renal Physiol. 2007; 293(3): F643–F654.
    CrossRefPubMed
  15. Picard N, Capuano P, Stange G, et al. Acute parathyroid hormone differentially regulates renal brush border membrane phosphate cotransporters. Pflugers Arch. 2010; 460(3): 677–687.
    CrossRefPubMed
  16. Cui L, Houston DA, Farquharson C, et al. Characterisation of matrix vesicles in skeletal and soft tissue mineralisation. Bone. 2016; 87: 147–158.
    CrossRefPubMed
  17. Austin LA, Heath H. Calcitonin: physiology and pathophysiology. N Engl J Med. 1981; 304(5): 269–278.
    CrossRefPubMed

Regulations

Important: This website uses cookies. More >>

The cookies allow us to identify your computer and find out details about your last visit. They remembering whether you've visited the site before, so that you remain logged in - or to help us work out how many new website visitors we get each month. Most internet browsers accept cookies automatically, but you can change the settings of your browser to erase cookies or prevent automatic acceptance if you prefer.

Via MedicaWydawcą jest  VM Media Group sp. z o.o., Grupa Via Medica, ul. Świętokrzyska 73, 80–180 Gdańsk

tel.:+48 58 320 94 94, faks:+48 58 320 94 60, e-mail:  viamedica@viamedica.pl