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Milk-alkali syndrome: a ‘quick ease’ or a ‘long-lasting problem’

SUMMARY: We report the case of a 65-year-old female who presented with symptomatic hypercalcaemia (corrected calcium of 4.57 mmol/L) with confusion, myalgias and abdominal discomfort. She had a concomitant metabolic alkalosis (pH 7.46, HCO(3)(-) 40 mmol/L, pCO(2) 54.6 mmHg). A history of significant...

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Autores principales: Wang, Mawson, Cho, Catherine, Gray, Callum, Chai, Thora Y, Daud, Ruhaida, Luttrell, Matthew
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Bioscientifica Ltd 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7274561/
https://www.ncbi.nlm.nih.gov/pubmed/32408269
http://dx.doi.org/10.1530/EDM-20-0028
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author Wang, Mawson
Cho, Catherine
Gray, Callum
Chai, Thora Y
Daud, Ruhaida
Luttrell, Matthew
author_facet Wang, Mawson
Cho, Catherine
Gray, Callum
Chai, Thora Y
Daud, Ruhaida
Luttrell, Matthew
author_sort Wang, Mawson
collection PubMed
description SUMMARY: We report the case of a 65-year-old female who presented with symptomatic hypercalcaemia (corrected calcium of 4.57 mmol/L) with confusion, myalgias and abdominal discomfort. She had a concomitant metabolic alkalosis (pH 7.46, HCO(3)(-) 40 mmol/L, pCO(2) 54.6 mmHg). A history of significant Quick-Eze use (a calcium carbonate based antacid) for abdominal discomfort, for 2 weeks prior to presentation, suggested a diagnosis of milk-alkali syndrome (MAS). Further investigations did not demonstrate malignancy or primary hyperparathyroidism. Following management with i.v. fluid rehydration and a single dose of i.v. bisphosphonate, she developed symptomatic hypocalcaemia requiring oral and parenteral calcium replacement. She was discharged from the hospital with stable biochemistry on follow-up. This case demonstrates the importance of a detailed history in the diagnosis of severe hypercalcaemia, with MAS representing the third most common cause of hypercalcaemia. We discuss its pathophysiology and clinical importance, which can often present with severe hypercalcaemia that can respond precipitously to calcium-lowering therapy. LEARNING POINTS: Milk-alkali syndrome is an often unrecognised cause for hypercalcaemia, but is the third most common cause of admission for hypercalcaemia. Calcium ingestion leading to MAS can occur at intakes as low as 1.0–1.5 g per day in those with risk factors. Early recognition of this syndrome can avoid the use of calcium-lowering therapy such as bisphosphonates which can precipitate hypocalcaemia.
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spelling pubmed-72745612020-06-10 Milk-alkali syndrome: a ‘quick ease’ or a ‘long-lasting problem’ Wang, Mawson Cho, Catherine Gray, Callum Chai, Thora Y Daud, Ruhaida Luttrell, Matthew Endocrinol Diabetes Metab Case Rep Insight into Disease Pathogenesis or Mechanism of Therapy SUMMARY: We report the case of a 65-year-old female who presented with symptomatic hypercalcaemia (corrected calcium of 4.57 mmol/L) with confusion, myalgias and abdominal discomfort. She had a concomitant metabolic alkalosis (pH 7.46, HCO(3)(-) 40 mmol/L, pCO(2) 54.6 mmHg). A history of significant Quick-Eze use (a calcium carbonate based antacid) for abdominal discomfort, for 2 weeks prior to presentation, suggested a diagnosis of milk-alkali syndrome (MAS). Further investigations did not demonstrate malignancy or primary hyperparathyroidism. Following management with i.v. fluid rehydration and a single dose of i.v. bisphosphonate, she developed symptomatic hypocalcaemia requiring oral and parenteral calcium replacement. She was discharged from the hospital with stable biochemistry on follow-up. This case demonstrates the importance of a detailed history in the diagnosis of severe hypercalcaemia, with MAS representing the third most common cause of hypercalcaemia. We discuss its pathophysiology and clinical importance, which can often present with severe hypercalcaemia that can respond precipitously to calcium-lowering therapy. LEARNING POINTS: Milk-alkali syndrome is an often unrecognised cause for hypercalcaemia, but is the third most common cause of admission for hypercalcaemia. Calcium ingestion leading to MAS can occur at intakes as low as 1.0–1.5 g per day in those with risk factors. Early recognition of this syndrome can avoid the use of calcium-lowering therapy such as bisphosphonates which can precipitate hypocalcaemia. Bioscientifica Ltd 2020-05-13 /pmc/articles/PMC7274561/ /pubmed/32408269 http://dx.doi.org/10.1530/EDM-20-0028 Text en © 2020 The authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. (http://creativecommons.org/licenses/by-nc-nd/4.0/) .
spellingShingle Insight into Disease Pathogenesis or Mechanism of Therapy
Wang, Mawson
Cho, Catherine
Gray, Callum
Chai, Thora Y
Daud, Ruhaida
Luttrell, Matthew
Milk-alkali syndrome: a ‘quick ease’ or a ‘long-lasting problem’
title Milk-alkali syndrome: a ‘quick ease’ or a ‘long-lasting problem’
title_full Milk-alkali syndrome: a ‘quick ease’ or a ‘long-lasting problem’
title_fullStr Milk-alkali syndrome: a ‘quick ease’ or a ‘long-lasting problem’
title_full_unstemmed Milk-alkali syndrome: a ‘quick ease’ or a ‘long-lasting problem’
title_short Milk-alkali syndrome: a ‘quick ease’ or a ‘long-lasting problem’
title_sort milk-alkali syndrome: a ‘quick ease’ or a ‘long-lasting problem’
topic Insight into Disease Pathogenesis or Mechanism of Therapy
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7274561/
https://www.ncbi.nlm.nih.gov/pubmed/32408269
http://dx.doi.org/10.1530/EDM-20-0028
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