Evidence map›Paper›PMID 35120172›Full record

Observational studyPloS one2022

Adrenal suppression in patients with chronic obstructive pulmonary disease treated with glucocorticoids: Role of specific glucocorticoid receptor polymorphisms.

Pradeesh Sivapalan, Stina Willemoes Borresen, Josefin Eklöf, Marianne Klose, Freja S Holm, Ulla Feldt-Rasmussen, Maria Rossing, Niklas R Jørgensen, Rasmus L Marvig, Mohamad Isam Saeed and 5 more

Open access · goldAbstract readObservational Study
In one paragraph

Observational study in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.8field-weighted citation impact, top 27% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed, 6 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 3 institutions in 2 countries.

Pradeesh SivapalanSection of Respiratory Medicine, Department of Medicine, Herlev and Gentofte Hospital, University of Copenhagen, Hellerup, Denmark.ORCID 0000-0002-8620-3655
Stina Willemoes BorresenDepartment of Medical Endocrinology and Metabolism, Rigshospitalet, Copenhagen University Hospital.
Josefin EklöfSection of Respiratory Medicine, Department of Medicine, Herlev and Gentofte Hospital, University of Copenhagen, Hellerup, Denmark.
Marianne KloseDepartment of Medical Endocrinology and Metabolism, Rigshospitalet, Copenhagen University Hospital.
Freja S HolmSection of Respiratory Medicine, Department of Medicine, Herlev and Gentofte Hospital, University of Copenhagen, Hellerup, Denmark.
Ulla Feldt-RasmussenDepartment of Medical Endocrinology and Metabolism, Rigshospitalet, Copenhagen University Hospital.ORCID 0000-0002-5903-3355
Maria RossingCenter for Genomic Medicine, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark.
Niklas R JørgensenInstitute for Clinical Medicine, Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark.
Rasmus L MarvigCenter for Genomic Medicine, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark.ORCID 0000-0002-5267-3173
Mohamad Isam SaeedSection of Respiratory Medicine, Department of Medicine, Herlev and Gentofte Hospital, University of Copenhagen, Hellerup, Denmark.
Torgny WilckeSection of Respiratory Medicine, Department of Medicine, Herlev and Gentofte Hospital, University of Copenhagen, Hellerup, Denmark.
Niels SeersholmSection of Respiratory Medicine, Department of Medicine, Herlev and Gentofte Hospital, University of Copenhagen, Hellerup, Denmark.
Alexander G MathioudakisDivision of Infection, Immunity and Respiratory Medicine, University of Manchester, Manchester Academic Health Science Centre, Manchester, United Kingdom.ORCID 0000-0002-4675-9616
Jørgen VestboDivision of Infection, Immunity and Respiratory Medicine, University of Manchester, Manchester Academic Health Science Centre, Manchester, United Kingdom.
Jens-Ulrik Stæhr JensenSection of Respiratory Medicine, Department of Medicine, Herlev and Gentofte Hospital, University of Copenhagen, Hellerup, Denmark.
University of Copenhagen · DKCopenhagen University Hospital · DKManchester Academic Health Science Centre · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSingle-nucleotide polymorphisms (SNPs) of the glucocorticoid receptor (GR) gene NR3C1 have been associated with an altered sensitivity to glucocorticoids, and thus may alter the therapeutic effects of glucocorticoids. We investigated the prevalence of adrenal suppression after treatment with glucocorticoids and evaluated whether GR SNPs were associated with altered risks of adrenal suppression and metabolic disorders in patients with chronic obstructive pulmonary disease (COPD).

methodsIn an observational prospective cohort study, we recruited 78 patients with severe COPD receiving 5 days glucocorticoid treatment for an exacerbation of COPD. In total, 55% of these patients were also receiving regular inhaled corticosteroids (ICS). Adrenal function was evaluated with a corticotropin test 30 days after the exacerbation. Patients were genotyped for Bcl1, N363S, ER22/23EK, and 9β SNPs.

resultsThe prevalence of adrenal suppression (corticotropin-stimulated plasma-cortisol ≤ 420 nmol/L) 30 days after glucocorticoid treatment was 4/78 (5%). There was no difference between carriers and non-carriers of the polymorphisms (Bcl1, 9β, ER22/23K, and N363S) in corticotropin stimulated plasma-cortisol concentrations. In the haplotype analyses, we included the 50 patients who had a high-sensitivity (76%), a low-sensitivity (4%), or a wild-type (20%) GR haplotype. There was no difference in the frequency of adrenal suppression or metabolic disorders between the two stratified groups: (a) high-sensitivity (Bcl1 and/or N363S) haplotypes vs. (b) low-sensitivity (9β and/or ER22/23K) plus wild-type haplotypes (p > 0.05). Carriers of the high-sensitivity GR gene haplotype exhibited a steeper decline in stimulated P-cortisol with increased ICS dose (slope, -1.35 vs. 0.94; p = 0.17), compared to the group with low-sensitivity or wild-type haplotypes, respectively.

conclusionsIn total, 5% of patients exhibited insufficient adrenal function. The Bcl1 and N363S polymorphisms did not seem to increase the risk of glucocorticoid suppression or metabolic disorders in adults treated with glucocorticoids for COPD exacerbations.

Indexed as

GlucocorticoidsPolymorphism, Single NucleotidePulmonary Disease, Chronic ObstructiveReceptors, GlucocorticoidAdrenal GlandsAgedFemaleHaplotypesHumansHydrocortisoneMaleMiddle AgedProspective StudiesGlucocorticoidsHydrocortisoneNR3C1 protein, humanReceptors, Glucocorticoid

Identifiers

PMID35120172
PMCPMC8815987
OpenAlexW4210365304

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.