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journal article Mar 27, 2014

GLCCI1 variant accelerates pulmonary function decline in patients with asthma receiving inhaled corticosteroids

Y. Izuhara H. Matsumoto ORCID Y. KANEMITSU K. Izuhara Y. Tohda T. Horiguchi H. Kita K. Kuwabara K. Tomii K. Otsuka M. Fujimura N. Ohkura K. Tomita A. Yokoyama H. Ohnishi Y. Nakano ORCID T. Oguma S. Hozawa T. Nagasaki I. Ito H. Inoue T. Tajiri T. Iwata ORCID J. Ono S. Ohta M. Tamari T. Hirota T. Yokoyama A. Niimi M. Mishima
Allergy Vol. 69 No. 5 pp. 668-673 · Wiley
View at Publisher Save 10.1111/all.12400
Abstract
AbstractBackgroundIn steroid‐naive patients with asthma, several gene variants are associated with a short‐term response to inhaled corticosteroid (ICS) treatment; this has mostly been observed in Caucasians. However, not many studies have been conducted for other ethnicities. Here, we aimed to determine the relationship between the annual decline in forced expiratory flow volume in one second (FEV1) and the variant of the glucocorticoid‐induced transcript 1 gene (GLCCI1) in Japanese patients with asthma receiving long‐term ICS treatment, taking into account the effect of high serum periostin levels, a known association factor of pulmonary function decline and a marker of refractory eosinophilic/Th2 inflammation.MethodsIn this study, 224 patients with asthma receiving ICS treatment for at least 4 years were enrolled. The effects of single‐nucleotide polymorphisms (SNPs) in GLCCI1, stress‐induced phosphoprotein 1 (STIP1), and T gene on the decline in FEV1 of 30 ml/year or greater were determined.ResultsBesides the known contributing factors, that is, the most intensive treatment step, ex‐smoking, and high serum periostin levels (≥95 ng/ml), the GG genotype of GLCCI1 rs37973, and not other SNPs, was independently associated with a decline in FEV1 of 30 ml/year or greater. When patients were stratified according to their serum periostin levels, the GG genotype of rs37973 was significantly associated with blood eosinophilia (≥250/μl) in the high serum periostin group.ConclusionsA GLCCI1 variant is a risk factor of pulmonary function decline in Japanese patients with asthma receiving long‐term ICS treatment. Thus, GLCCI1 may be associated with response to ICS across ethnicities.
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Metrics
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Citations
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References
Details
Published
Mar 27, 2014
Vol/Issue
69(5)
Pages
668-673
License
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Authors
Y
Y. Izuhara

Department of Respiratory Medicine Graduate School of Medicine Kyoto University Kyoto Japan

H
H. Matsumoto

Department of Respiratory Medicine Graduate School of Medicine Kyoto University Kyoto Japan; Kinki Hokuriku Airway Disease Conference (KiHAC) Osaka Japan

Y
Y. KANEMITSU

Department of Respiratory Medicine Graduate School of Medicine Kyoto University Kyoto Japan; Kinki Hokuriku Airway Disease Conference (KiHAC) Osaka Japan

K
K. Izuhara

Division of Medical Biochemistry Department of Biomolecular Sciences Saga Medical School Saga Japan

Y
Y. Tohda

Kinki Hokuriku Airway Disease Conference (KiHAC) Osaka Japan; Department of Respiratory Medicine and Allergology Faculty of Medicine Kinki University Osaka Japan

T
T. Horiguchi

Kinki Hokuriku Airway Disease Conference (KiHAC) Osaka Japan; Department of Respiratory Internal Medicine Fujita Health University Second Educational Hospital Aichi Japan

H
H. Kita

Kinki Hokuriku Airway Disease Conference (KiHAC) Osaka Japan; Department of Respiratory Medicine Takatsuki Red Cross Hospital Osaka Japan

K
K. Kuwabara

Kinki Hokuriku Airway Disease Conference (KiHAC) Osaka Japan; Department of Respiratory Internal Medicine Fujita Health University Second Educational Hospital Aichi Japan

K
K. Tomii

Kinki Hokuriku Airway Disease Conference (KiHAC) Osaka Japan; Department of Respiratory Medicine Kobe City Medical Center General Hospital Hyogo Japan

K
K. Otsuka

Department of Respiratory Medicine Graduate School of Medicine Kyoto University Kyoto Japan; Kinki Hokuriku Airway Disease Conference (KiHAC) Osaka Japan; Department of Respiratory Medicine Kobe City Medical Center General Hospital Hyogo Japan

M
M. Fujimura

Kinki Hokuriku Airway Disease Conference (KiHAC) Osaka Japan; Department of Respiratory Medicine, Cellular Transplantation Biology Kanazawa University Graduate School of Medicine Kanazawa Japan

N
N. Ohkura

Kinki Hokuriku Airway Disease Conference (KiHAC) Osaka Japan; Department of Respiratory Medicine, Cellular Transplantation Biology Kanazawa University Graduate School of Medicine Kanazawa Japan

K
K. Tomita

Kinki Hokuriku Airway Disease Conference (KiHAC) Osaka Japan; Department of Respiratory Medicine and Allergology Faculty of Medicine Kinki University Osaka Japan

A
A. Yokoyama

Kinki Hokuriku Airway Disease Conference (KiHAC) Osaka Japan; Department of Hematology and Respiratory Medicine Kochi University Kochi Japan

H
H. Ohnishi

Kinki Hokuriku Airway Disease Conference (KiHAC) Osaka Japan; Department of Hematology and Respiratory Medicine Kochi University Kochi Japan

Y
Y. Nakano

Kinki Hokuriku Airway Disease Conference (KiHAC) Osaka Japan; Division of Respiratory Medicine Department of Internal Medicine Shiga University of Medical Science Shiga Japan

T
T. Oguma

Kinki Hokuriku Airway Disease Conference (KiHAC) Osaka Japan; Division of Respiratory Medicine Department of Internal Medicine Shiga University of Medical Science Shiga Japan

S
S. Hozawa

Kinki Hokuriku Airway Disease Conference (KiHAC) Osaka Japan; Hiroshima Allergy and Respiratory Clinic Hiroshima Japan

T
T. Nagasaki

Department of Respiratory Medicine Graduate School of Medicine Kyoto University Kyoto Japan

I
I. Ito

Department of Respiratory Medicine Graduate School of Medicine Kyoto University Kyoto Japan

H
H. Inoue

Department of Respiratory Medicine Graduate School of Medicine Kyoto University Kyoto Japan

T
T. Tajiri

Department of Respiratory Medicine Graduate School of Medicine Kyoto University Kyoto Japan

T
T. Iwata

Department of Respiratory Medicine Graduate School of Medicine Kyoto University Kyoto Japan

J
J. Ono

Shino‐Test Corporation Kanagawa Japan

S
S. Ohta

Department of Laboratory Medicine Saga Medical School Saga Japan

M
M. Tamari

Laboratory for Respiratory and Allergic Diseases Core for Genomic Medicine Center for Integrative Medical Sciences Institute of Physical and Chemical Research (RIKEN) Yokohama Kanagawa Japan

T
T. Hirota

Laboratory for Respiratory and Allergic Diseases Core for Genomic Medicine Center for Integrative Medical Sciences Institute of Physical and Chemical Research (RIKEN) Yokohama Kanagawa Japan

T
T. Yokoyama

Department of Health Promotion National Institute of Public Health Wako Saitama Japan

A
A. Niimi

Department of Respiratory Medicine Graduate School of Medicine Kyoto University Kyoto Japan; Kinki Hokuriku Airway Disease Conference (KiHAC) Osaka Japan; Department of Medical Oncology and Immunology Nagoya City University School of Medical Sciences Aichi Japan

M
M. Mishima

Department of Respiratory Medicine Graduate School of Medicine Kyoto University Kyoto Japan; Kinki Hokuriku Airway Disease Conference (KiHAC) Osaka Japan

Cite This Article
Y. Izuhara, H. Matsumoto, Y. KANEMITSU, et al. (2014). GLCCI1 variant accelerates pulmonary function decline in patients with asthma receiving inhaled corticosteroids. Allergy, 69(5), 668-673. https://doi.org/10.1111/all.12400
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