Cystic fibrosis transmembrane conductance regulator function, not TAS2R38 gene haplotypes, predict sinus surgery in children and young adults with cystic fibrosis.


Journal

International forum of allergy & rhinology
ISSN: 2042-6984
Titre abrégé: Int Forum Allergy Rhinol
Pays: United States
ID NLM: 101550261

Informations de publication

Date de publication:
06 2020
Historique:
received: 19 11 2019
revised: 06 02 2020
accepted: 11 02 2020
pubmed: 14 4 2020
medline: 12 8 2021
entrez: 14 4 2020
Statut: ppublish

Résumé

Chronic rhinosinusitis symptomatology begins in early childhood individuals with cystic fibrosis (CF). Cystic fibrosis transmembrane conductance regulator (CFTR) function contributes to sinus development and disease. Genetic variants of the bitter taste receptor TAS2R38 have been suggested to contribute to sinus disease severity in individuals without CF. Our objective was to explore whether functional TAS2R38 haplotypes and CFTR function are associated with sinus disease or the need for sinus surgery in individuals with CF. We conducted a retrospective study using prospectively collected data from the CF Twin-Sibling Study. The function of CFTR was assessed via chloride conductance. Genotyping of the TAS2R38 gene identified patients who were homozygous for the functional haplotype, heterozygous, or homozygous for nonfunctional haplotypes. Clustered multivariate logistic regression was performed, controlling for sex and family relationship. A total of 1291 patients were evaluated. Patients with ≤1% CFTR function were 1.56 times more likely to require sinus surgery than those with >1% CFTR function (p = 0.049). CFTR function did not correlate significantly with the presence of sinus disease (p = 0.30). In addition, there were no statistically significant differences in diagnosis of sinus disease or need for sinus surgery between patients with functional and nonfunctional TAS2R38 haplotypes. CFTR function correlates with need for sinus surgery, whereas TAS2R38 function does not appear to contribute to sinus disease or the need for sinus surgery in patients with CF.

Sections du résumé

BACKGROUND
Chronic rhinosinusitis symptomatology begins in early childhood individuals with cystic fibrosis (CF). Cystic fibrosis transmembrane conductance regulator (CFTR) function contributes to sinus development and disease. Genetic variants of the bitter taste receptor TAS2R38 have been suggested to contribute to sinus disease severity in individuals without CF. Our objective was to explore whether functional TAS2R38 haplotypes and CFTR function are associated with sinus disease or the need for sinus surgery in individuals with CF.
METHODS
We conducted a retrospective study using prospectively collected data from the CF Twin-Sibling Study. The function of CFTR was assessed via chloride conductance. Genotyping of the TAS2R38 gene identified patients who were homozygous for the functional haplotype, heterozygous, or homozygous for nonfunctional haplotypes. Clustered multivariate logistic regression was performed, controlling for sex and family relationship.
RESULTS
A total of 1291 patients were evaluated. Patients with ≤1% CFTR function were 1.56 times more likely to require sinus surgery than those with >1% CFTR function (p = 0.049). CFTR function did not correlate significantly with the presence of sinus disease (p = 0.30). In addition, there were no statistically significant differences in diagnosis of sinus disease or need for sinus surgery between patients with functional and nonfunctional TAS2R38 haplotypes.
CONCLUSION
CFTR function correlates with need for sinus surgery, whereas TAS2R38 function does not appear to contribute to sinus disease or the need for sinus surgery in patients with CF.

Identifiants

pubmed: 32282124
doi: 10.1002/alr.22548
pmc: PMC7266728
mid: NIHMS1574894
doi:

Substances chimiques

CFTR protein, human 0
Receptors, G-Protein-Coupled 0
taste receptors, type 2 0
Cystic Fibrosis Transmembrane Conductance Regulator 126880-72-6

Types de publication

Journal Article Observational Study Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Twin Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

748-754

Subventions

Organisme : NHLBI NIH HHS
ID : P01 HL114471
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL114800
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL128475
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR003017
Pays : United States

Informations de copyright

© 2020 ARS-AAOA, LLC.

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Auteurs

Nicholas M Dalesio (NM)

Division of Pediatric Anesthesia/Critical Care Medicine, Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, MD.
Department of Otolaryngology/Head & Neck Surgery, Johns Hopkins University, Baltimore, MD.

Melis A Aksit (MA)

McKusick-Nathans Institute of the Department of Genetic Medicine, Johns Hopkins University, Baltimore, MD.

Kwangmi Ahn (K)

Genetic Epidemiology Research Branch, National Institute of Mental Health, Bethesda, MD.

Karen S Raraigh (KS)

McKusick-Nathans Institute of the Department of Genetic Medicine, Johns Hopkins University, Baltimore, MD.

Joseph M Collaco (JM)

Department of Pediatric Pulmonology, Johns Hopkins University, Baltimore, MD.

Sharon McGrath-Morrow (S)

Department of Pediatric Pulmonology, Johns Hopkins University, Baltimore, MD.

Pamela L Zeitlin (PL)

Department of Pediatrics, National Jewish Health, Denver, CO.

Steven S An (SS)

Department of Pharmacology, Rutgers-Robert Wood Johnson Medical School, The State University of New Jersey, Piscataway, NJ.
Rutgers Institute for Translational Medicine and Science, New Brunswick, NJ.

Garry R Cutting (GR)

McKusick-Nathans Institute of the Department of Genetic Medicine, Johns Hopkins University, Baltimore, MD.

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