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GLCCI1 rs37973: A potential genetic predictor of therapeutic response to inhaled corticosteroids in Chinese asthma patients.

Abstract Glucocorticoids are the primary anti-inflammatory therapy for asthma, but their effects are characterized by some interindividual variability that might have a genetic basis.We aimed to determine the relationship between pulmonary function change and the variant of the glucocorticoid-induced transcript 1 (GLCCI1) gene in patients with asthma receiving long-term ICS treatment, the association of GLCCI1 genotypes and the level of GLCCI1 expression and cytokines production.A total of 418 patients with asthma, including 25 individuals from 11 families with a history of asthma, were enrolled. The effects of single-nucleotide polymorphisms (SNPs) in GLCCI1 on changes in lung function in response to inhaled glucocorticoids were assessed. The expression levels of GLCCI1 mRNA and cytokines were also measured.The SNP rs37973 in GLCCI1 was independently associated with changes in forced expiratory volume at one second (FEV1) and FEV1%pred. Individuals homozygous for the wild-type allele who had a percent FEV1 change greater than 5% were more common than individuals homozygous for the rare allele. When patients were stratified according to genotype, GLCCI1 expression was enhanced upon administration of low-dose dexamethasone among patients with the rs37973 A allele; however, GG homozygotes required high-dose dexamethasone to achieve enhanced GLCCI1 expression. Furthermore, the levels of some cytokines were significantly reduced after glucocorticoid treatment in individuals with the AA and AG genotypes.The genetic variant rs37973 in GLCCI1 is associated with poorer clinical therapeutic response to inhaled glucocorticoids in a Chinese asthma population.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title medicine
Publication Year Start




PMID- 29384926
OWN - NLM
STAT- MEDLINE
DCOM- 20180209
LR  - 20180209
IS  - 1536-5964 (Electronic)
IS  - 0025-7974 (Linking)
VI  - 96
IP  - 52
DP  - 2017 Dec
TI  - GLCCI1 rs37973: A potential genetic predictor of therapeutic response to inhaled 
      corticosteroids in Chinese asthma patients.
PG  - e9442
LID - 10.1097/MD.0000000000009442 [doi]
AB  - Glucocorticoids are the primary anti-inflammatory therapy for asthma, but their
      effects are characterized by some interindividual variability that might have a
      genetic basis.We aimed to determine the relationship between pulmonary function
      change and the variant of the glucocorticoid-induced transcript 1 (GLCCI1) gene
      in patients with asthma receiving long-term ICS treatment, the association of
      GLCCI1 genotypes and the level of GLCCI1 expression and cytokines production.A
      total of 418 patients with asthma, including 25 individuals from 11 families with
      a history of asthma, were enrolled. The effects of single-nucleotide
      polymorphisms (SNPs) in GLCCI1 on changes in lung function in response to inhaled
      glucocorticoids were assessed. The expression levels of GLCCI1 mRNA and cytokines
      were also measured.The SNP rs37973 in GLCCI1 was independently associated with
      changes in forced expiratory volume at one second (FEV1) and FEV1%pred.
      Individuals homozygous for the wild-type allele who had a percent FEV1 change
      greater than 5% were more common than individuals homozygous for the rare allele.
      When patients were stratified according to genotype, GLCCI1 expression was
      enhanced upon administration of low-dose dexamethasone among patients with the
      rs37973 A allele; however, GG homozygotes required high-dose dexamethasone to
      achieve enhanced GLCCI1 expression. Furthermore, the levels of some cytokines
      were significantly reduced after glucocorticoid treatment in individuals with the
      AA and AG genotypes.The genetic variant rs37973 in GLCCI1 is associated with
      poorer clinical therapeutic response to inhaled glucocorticoids in a Chinese
      asthma population.
CI  - Copyright (c) 2017 The Authors. Published by Wolters Kluwer Health, Inc. All
      rights reserved.
FAU - Xu, Yuzhu
AU  - Xu Y
AD  - Department of Respiratory and Critical Care Medicine, National Clinical Research 
      Center of Respiratory Disease.
FAU - Wu, Hongxu
AU  - Wu H
AD  - Department of Respiratory and Critical Care Medicine, National Clinical Research 
      Center of Respiratory Disease.
FAU - Wu, Xiaojie
AU  - Wu X
AD  - Department of Respiratory and Critical Care Medicine, National Clinical Research 
      Center of Respiratory Disease.
FAU - Xu, Yongjian
AU  - Xu Y
AD  - Department of Respiratory and Critical Care Medicine, National Clinical Research 
      Center of Respiratory Disease.
FAU - Zhao, Jianping
AU  - Zhao J
AD  - Department of Respiratory and Critical Care Medicine, National Clinical Research 
      Center of Respiratory Disease.
FAU - Xie, Jungang
AU  - Xie J
AD  - Department of Respiratory and Critical Care Medicine, National Clinical Research 
      Center of Respiratory Disease.
FAU - Yu, Jun
AU  - Yu J
AD  - Department of Respiratory and Critical Care Medicine, National Clinical Research 
      Center of Respiratory Disease.
AD  - Department of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong
      University of Science and Technology, Wuhan 430030, China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Medicine (Baltimore)
JT  - Medicine
JID - 2985248R
RN  - 0 (Cytokines)
RN  - 0 (Glucocorticoids)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Glucocorticoid)
RN  - 0 (glucocorticoid-induced transcript 1 protein, human)
RN  - 7S5I7G3JQL (Dexamethasone)
SB  - AIM
SB  - IM
MH  - Administration, Inhalation
MH  - Adult
MH  - Asian Continental Ancestry Group/*genetics
MH  - Asthma/*drug therapy/*genetics
MH  - China
MH  - Cytokines/metabolism
MH  - Dexamethasone/therapeutic use
MH  - Female
MH  - Genotype
MH  - Glucocorticoids/*therapeutic use
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - Polymorphism, Single Nucleotide/*genetics
MH  - RNA, Messenger/metabolism
MH  - Receptors, Glucocorticoid/*genetics/metabolism
MH  - Treatment Outcome
MH  - Young Adult
EDAT- 2018/02/01 06:00
MHDA- 2018/02/10 06:00
CRDT- 2018/02/01 06:00
PHST- 2018/02/01 06:00 [entrez]
PHST- 2018/02/01 06:00 [pubmed]
PHST- 2018/02/10 06:00 [medline]
AID - 10.1097/MD.0000000000009442 [doi]
AID - 00005792-201712290-00034 [pii]
PST - ppublish
SO  - Medicine (Baltimore). 2017 Dec;96(52):e9442. doi: 10.1097/MD.0000000000009442.