Evidence map›Paper›PMID 27649075›Full record

ArticlePloS one2016

Analysis of BCLI, N363S and ER22/23EK Polymorphisms of the Glucocorticoid Receptor Gene in Adrenal Incidentalomas.

Giuseppe Reimondo, Iacopo Chiodini, Soraya Puglisi, Anna Pia, Valentina Morelli, Darko Kastelan, Salvatore Cannavo, Paola Berchialla, Daniela Giachino, Paola Perotti and 5 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

9 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  3. Article
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  5. Article
  6. Pathophysiology of Mild Hypercortisolism: From the Bench to the Bedside.International journal of molecular sciences · 2022
    Review
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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 5 institutions in 2 countries.

Giuseppe ReimondoInternal Medicine 1, Department of Clinical and Biological Sciences, University of Turin, San Luigi Gonzaga Hospital, Orbassano, Italy.
Iacopo ChiodiniUnit of Endocrinology and Metabolic Diseases, Fondazione IRCCS Cà Granda-Ospedale Maggiore Policlinico, Milano Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy.
Soraya PuglisiEndocrine Unit, Department of Clinical and Experimental Medicine, University of Messina, Policlinico G. Martino Hospital, Messina, Italy.
Anna PiaInternal Medicine 1, Department of Clinical and Biological Sciences, University of Turin, San Luigi Gonzaga Hospital, Orbassano, Italy.
Valentina MorelliUnit of Endocrinology and Metabolic Diseases, Fondazione IRCCS Cà Granda-Ospedale Maggiore Policlinico, Milano Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy.
Darko KastelanDepartment of Endocrinology, University Hospital Zagreb, Zagreb, Croatia.
Salvatore CannavoEndocrine Unit, Department of Clinical and Experimental Medicine, University of Messina, Policlinico G. Martino Hospital, Messina, Italy.
Paola BerchiallaStatistical Unit, Department of Clinical and Biological Sciences, University of Turin, San Luigi Gonzaga, Hospital, Orbassano, Italy.
Daniela GiachinoMedical Genetics, Department of Clinical and Biological Sciences, University of Turin, San Luigi Gonzaga Hospital, Orbassano, Italy.
Paola PerottiInternal Medicine 1, Department of Clinical and Biological Sciences, University of Turin, San Luigi Gonzaga Hospital, Orbassano, Italy.
Alessandra CuccurulloMedical Genetics, Department of Clinical and Biological Sciences, University of Turin, San Luigi Gonzaga Hospital, Orbassano, Italy.
Piero PaccottiInternal Medicine 1, Department of Clinical and Biological Sciences, University of Turin, San Luigi Gonzaga Hospital, Orbassano, Italy.
Paolo Beck-PeccozUnit of Endocrinology and Metabolic Diseases, Fondazione IRCCS Cà Granda-Ospedale Maggiore Policlinico, Milano Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy.
Mario De MarchiMedical Genetics, Department of Clinical and Biological Sciences, University of Turin, San Luigi Gonzaga Hospital, Orbassano, Italy.
Massimo TerzoloInternal Medicine 1, Department of Clinical and Biological Sciences, University of Turin, San Luigi Gonzaga Hospital, Orbassano, Italy.
University of Turin · ITOspedale San Luigi Gonzaga · ITUniversity of Milan · ITUniversity of Messina · ITUniversity Hospital Centre Zagreb · HR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

contextPatients with adrenal incidentalomas (AI) may experience detrimental consequences due to a minimal cortisol excess sustained by adrenal adenoma. SNPs of the glucocorticoid receptor gene (NR3C1) modulate individual sensitivity to glucocorticoids and may interfere with the clinical presentation.

objectiveTo compare the frequency of N363S, ER22/23EK and BclI SNPs in patients with AI with the general population and to evaluate whether these SNPs are linked to consequences of cortisol excess.

settingMulticentric, retrospective analysis of patients referred from 2010 to 2014 to 4 centers (Orbassano, Milano, Messina [Italy] and Zagreb [Croatia]). PATIENTS: 411 patients with AI; 153 males and 258 females and 186 from blood donors. MAIN OUTCOMES MEASURES: All patients and controls were genotyped for BclI, N363S and ER22/23EK and SNPs frequency was associated with clinical and hormonal features.

resultsSNP frequency was: SNP frequency was: N363S 5.4% (MAF 0.027), BclI 54.7% (MAF 0.328), ER22/23EK 4.4% (MAF 0.022), without any significant difference between patients and controls. N363S was more frequent in hypertensive patients (p = 0.03) and was associated with hypertension (p = 0.015) in patients with suppressed cortisol after the 1-mg DST.

conclusionsOur results demonstrate that SNPs of the glucocorticoid receptor gene do not play a pathogenetic role for AI. The impact of any single SNP on the phenotypic expression of minimal cortisol excess is limited and their analysis does not provide additional data that may be exploited for patient management.

Indexed as

Polymorphism, Single NucleotideAdrenal Gland NeoplasmsAdrenal GlandsAdultAgedAged, 80 and overFemaleHumansHydrocortisoneHypertensionMaleMiddle AgedReceptors, GlucocorticoidHydrocortisoneNR3C1 protein, humanReceptors, Glucocorticoid

Identifiers

PMID27649075
PMCPMC5029814
OpenAlexW2523189911

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.