Evidence map›Paper›PMID 42622938›Full record

ArticleJournal of endocrinological investigation2026

Lifelong congenital untreated isolated GH deficiency does not alter human leukocyte telomere length.

Ângela C Leal, Rodrigo T Calado, Martin Bidlingmaier, Júnia R O L Schweizer, Roberto Salvatori, Barbara A Santana, Jan Frystyk, Fabrícia Alvisi, Viviane C Campos, Elenilde G Santos and 13 more

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Article in Journal of endocrinological investigation, 2026. 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
–field-weighted citation impact
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.

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

23 authors.

Ângela C LealDivision of Endocrinology, Health Sciences Graduate Program, Federal University of Sergipe, Aracaju, Brazil.
Rodrigo T CaladoCentre for Cell-based Therapy, São Paulo Research Foundation (FAPESP), Ribeirao Preto, Brazil.
Martin BidlingmaierLudwig-Maximilians-Universität, Munich, Germany.
Júnia R O L SchweizerLudwig-Maximilians-Universität, Munich, Germany.
Roberto SalvatoriJohns Hopkins University, Baltimore, USA.
Barbara A SantanaCentre for Cell-based Therapy, São Paulo Research Foundation (FAPESP), Ribeirao Preto, Brazil.
Jan FrystykUniversity of Southern Denmark, Odense, Denmark.
Fabrícia AlvisiLaboratory of Molecular Biology and Immunology, University Hospital, Federal University of Sergipe, Aracaju, Brazil.
Viviane C CamposDivision of Endocrinology, Health Sciences Graduate Program, Federal University of Sergipe, Aracaju, Brazil.
Elenilde G SantosDivision of Endocrinology, Health Sciences Graduate Program, Federal University of Sergipe, Aracaju, Brazil.
Keila R Villar-GouyDivision of Endocrinology, Health Sciences Graduate Program, Federal University of Sergipe, Aracaju, Brazil.
Enaldo V MeloDivision of Endocrinology, Health Sciences Graduate Program, Federal University of Sergipe, Aracaju, Brazil.
Nathalie O SantanaDivision of Endocrinology, Health Sciences Graduate Program, Federal University of Sergipe, Aracaju, Brazil.
Francisco A PereiraDivision of Endocrinology, Health Sciences Graduate Program, Federal University of Sergipe, Aracaju, Brazil.
Carla R P OliveiraDivision of Endocrinology, Health Sciences Graduate Program, Federal University of Sergipe, Aracaju, Brazil.
Dulce A OliveiraDivision of Endocrinology, Health Sciences Graduate Program, Federal University of Sergipe, Aracaju, Brazil.
Higor D G CarvalhoDivision of Endocrinology, Health Sciences Graduate Program, Federal University of Sergipe, Aracaju, Brazil.
Luciana P S Diniz LeiteDivision of Endocrinology, Health Sciences Graduate Program, Federal University of Sergipe, Aracaju, Brazil.
Francisco J A de PaulaDepartment of Internal Medicine, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto, SP, Brazil.
Paula C L EliasDepartment of Internal Medicine, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto, SP, Brazil.
Angela SilvaLaboratory of Molecular Biology and Immunology, University Hospital, Federal University of Sergipe, Aracaju, Brazil.
Margaret de CastroDepartment of Internal Medicine, Ribeirao Preto Medical School, University of São Paulo, Ribeirao Preto, SP, Brazil.
Manuel H Aguiar-OliveiraDivision of Endocrinology, Health Sciences Graduate Program, Federal University of Sergipe, Aracaju, Brazil. herminio.endo@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTelomere shortening reflects cumulative cell replication and functions as a mitotic clock. It is influenced by age and body mass, as both increase the demand for cell proliferation. The GH/IGF-I axis plays a central role in cell proliferation. The Itabaianinha cohort in Brazil, with severe isolated congenital GH deficiency (IGHD) due to a homozygous mutation in the GHRH receptor gene (GHRHR), represents a unique human model of markedly reduced stature and body mass with preserved lifespan, extended healthspan, and normal brain aging. PURPOSE: To evaluate leukocyte telomere length (LTL) in individuals with untreated congenital IGHD and its association with the GH/IGF axis and metabolic parameters.

methodsLTL was assessed in 34 IGHD subjects homozygous for the GHRHR c.57 + 1G→A mutation (aged 24-89 years) and 36 controls homozygous for the wild-type allele (aged 26-79 years). LTL was measured by quantitative PCR using the telomere-to-single copy gene (T/S) ratio. T/S ratio Z-scores used the control-group mean and standard deviation. Circulating IGF-I, IGF-II, and metabolic parameters were evaluated.

resultsIGHD subjects had markedly reduced height and weight, while BMI was similar between groups. IGF-I and IGF-II levels were significantly lower in IGHD (p < 0.0001 for both). LTL did not differ between IGHD,0.96 (0.3), and controls),1.01 (0.4), and age-related telomere decline was comparable. Z-scores confirmed no deviation from expected values. LTL correlated modestly with IGF-II, but not with IGF-I or HOMA-IR.

conclusionLTL in individuals with untreated IGHD was like that of controls. Age-related LTL decline was also comparable between the groups.

Indexed as

GHRH receptor mutationInsulin-Like Growth Factor IInsulin-Like Growth Factor IIIsolated growth hormone deficiencyTelomere shortening

Identifiers

PMID42622938

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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.