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The clinical consequences of sucrase-isomaltase deficiency

Primary sucrase-isomaltase deficiency, originally thought to be a homozygous recessive disorder, has been found to have numerous genetic variants that alone or in combination (compound heterozygosity) express varying degrees of clinical illness, most commonly causing chronic diarrhea, abdominal pain...

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Detalles Bibliográficos
Autor principal: Cohen, Stanley A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4746203/
https://www.ncbi.nlm.nih.gov/pubmed/26857124
http://dx.doi.org/10.1186/s40348-015-0028-0
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author Cohen, Stanley A.
author_facet Cohen, Stanley A.
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description Primary sucrase-isomaltase deficiency, originally thought to be a homozygous recessive disorder, has been found to have numerous genetic variants that alone or in combination (compound heterozygosity) express varying degrees of clinical illness, most commonly causing chronic diarrhea, abdominal pain, and bloating. These symptoms are also present with secondary sucrase-isomaltase deficiency. Recent investigations are providing evidence that sucrase-isomaltase deficiency is more prevalent and of greater clinical significance than previously suspected. Further research is required to correlate the specific genotypes and phenotypes with their clinical expressions and to determine the most appropriate treatment algorithm for these patients.
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spelling pubmed-47462032016-02-19 The clinical consequences of sucrase-isomaltase deficiency Cohen, Stanley A. Mol Cell Pediatr Mini Review Primary sucrase-isomaltase deficiency, originally thought to be a homozygous recessive disorder, has been found to have numerous genetic variants that alone or in combination (compound heterozygosity) express varying degrees of clinical illness, most commonly causing chronic diarrhea, abdominal pain, and bloating. These symptoms are also present with secondary sucrase-isomaltase deficiency. Recent investigations are providing evidence that sucrase-isomaltase deficiency is more prevalent and of greater clinical significance than previously suspected. Further research is required to correlate the specific genotypes and phenotypes with their clinical expressions and to determine the most appropriate treatment algorithm for these patients. Springer Berlin Heidelberg 2016-02-08 /pmc/articles/PMC4746203/ /pubmed/26857124 http://dx.doi.org/10.1186/s40348-015-0028-0 Text en © Cohen. 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Mini Review
Cohen, Stanley A.
The clinical consequences of sucrase-isomaltase deficiency
title The clinical consequences of sucrase-isomaltase deficiency
title_full The clinical consequences of sucrase-isomaltase deficiency
title_fullStr The clinical consequences of sucrase-isomaltase deficiency
title_full_unstemmed The clinical consequences of sucrase-isomaltase deficiency
title_short The clinical consequences of sucrase-isomaltase deficiency
title_sort clinical consequences of sucrase-isomaltase deficiency
topic Mini Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4746203/
https://www.ncbi.nlm.nih.gov/pubmed/26857124
http://dx.doi.org/10.1186/s40348-015-0028-0
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