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Dietary Chloride Deficiency Syndrome: Pathophysiology, History, and Systematic Literature Review
Metabolic alkalosis may develop as a consequence of urinary chloride (and sodium) wasting, excessive loss of salt in the sweat, or intestinal chloride wasting, among other causes. There is also a likely underrecognized association between poor salt intake and the mentioned electrolyte and acid–base...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7696598/ https://www.ncbi.nlm.nih.gov/pubmed/33182508 http://dx.doi.org/10.3390/nu12113436 |
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author | Signorelli, Giulia C. Bianchetti, Mario G. Jermini, Luca M. M. Agostoni, Carlo Milani, Gregorio P. Simonetti, Giacomo D. Lava, Sebastiano A. G. |
author_facet | Signorelli, Giulia C. Bianchetti, Mario G. Jermini, Luca M. M. Agostoni, Carlo Milani, Gregorio P. Simonetti, Giacomo D. Lava, Sebastiano A. G. |
author_sort | Signorelli, Giulia C. |
collection | PubMed |
description | Metabolic alkalosis may develop as a consequence of urinary chloride (and sodium) wasting, excessive loss of salt in the sweat, or intestinal chloride wasting, among other causes. There is also a likely underrecognized association between poor salt intake and the mentioned electrolyte and acid–base abnormality. In patients with excessive loss of salt in the sweat or poor salt intake, the maintenance of metabolic alkalosis is crucially modulated by the chloride–bicarbonate exchanger pendrin located on the renal tubular membrane of type B intercalated cells. In the late 1970s, recommendations were made to decrease the salt content of foods as part of an effort to minimize the tendency towards systemic hypertension. Hence, the baby food industry decided to remove added salt from formula milk. Some weeks later, approximately 200 infants (fed exclusively with formula milks with a chloride content of only 2–4 mmol/L), were admitted with failure to thrive, constipation, food refusal, muscular weakness, and delayed psychomotor development. The laboratory work-up disclosed metabolic alkalosis, hypokalemia, hypochloremia, and a reduced urinary chloride excretion. In all cases, both the clinical and the laboratory features remitted in ≤7 days when the infants were fed on formula milk with a normal chloride content. Since 1982, 13 further publications reported additional cases of dietary chloride depletion. It is therefore concluded that the dietary intake of chloride, which was previously considered a “mendicant” ion, plays a crucial role in acid–base and salt balance. |
format | Online Article Text |
id | pubmed-7696598 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-76965982020-11-29 Dietary Chloride Deficiency Syndrome: Pathophysiology, History, and Systematic Literature Review Signorelli, Giulia C. Bianchetti, Mario G. Jermini, Luca M. M. Agostoni, Carlo Milani, Gregorio P. Simonetti, Giacomo D. Lava, Sebastiano A. G. Nutrients Review Metabolic alkalosis may develop as a consequence of urinary chloride (and sodium) wasting, excessive loss of salt in the sweat, or intestinal chloride wasting, among other causes. There is also a likely underrecognized association between poor salt intake and the mentioned electrolyte and acid–base abnormality. In patients with excessive loss of salt in the sweat or poor salt intake, the maintenance of metabolic alkalosis is crucially modulated by the chloride–bicarbonate exchanger pendrin located on the renal tubular membrane of type B intercalated cells. In the late 1970s, recommendations were made to decrease the salt content of foods as part of an effort to minimize the tendency towards systemic hypertension. Hence, the baby food industry decided to remove added salt from formula milk. Some weeks later, approximately 200 infants (fed exclusively with formula milks with a chloride content of only 2–4 mmol/L), were admitted with failure to thrive, constipation, food refusal, muscular weakness, and delayed psychomotor development. The laboratory work-up disclosed metabolic alkalosis, hypokalemia, hypochloremia, and a reduced urinary chloride excretion. In all cases, both the clinical and the laboratory features remitted in ≤7 days when the infants were fed on formula milk with a normal chloride content. Since 1982, 13 further publications reported additional cases of dietary chloride depletion. It is therefore concluded that the dietary intake of chloride, which was previously considered a “mendicant” ion, plays a crucial role in acid–base and salt balance. MDPI 2020-11-09 /pmc/articles/PMC7696598/ /pubmed/33182508 http://dx.doi.org/10.3390/nu12113436 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Signorelli, Giulia C. Bianchetti, Mario G. Jermini, Luca M. M. Agostoni, Carlo Milani, Gregorio P. Simonetti, Giacomo D. Lava, Sebastiano A. G. Dietary Chloride Deficiency Syndrome: Pathophysiology, History, and Systematic Literature Review |
title | Dietary Chloride Deficiency Syndrome: Pathophysiology, History, and Systematic Literature Review |
title_full | Dietary Chloride Deficiency Syndrome: Pathophysiology, History, and Systematic Literature Review |
title_fullStr | Dietary Chloride Deficiency Syndrome: Pathophysiology, History, and Systematic Literature Review |
title_full_unstemmed | Dietary Chloride Deficiency Syndrome: Pathophysiology, History, and Systematic Literature Review |
title_short | Dietary Chloride Deficiency Syndrome: Pathophysiology, History, and Systematic Literature Review |
title_sort | dietary chloride deficiency syndrome: pathophysiology, history, and systematic literature review |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7696598/ https://www.ncbi.nlm.nih.gov/pubmed/33182508 http://dx.doi.org/10.3390/nu12113436 |
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