Evidence map›Paper›PMID 41521526›Full record

ArticleThe Journal of clinical endocrinology and metabolism2026

GH Response to Glucagon in Transition: Role of Body Mass Index and Etiology in Childhood-onset GH Deficiency.

Daniela Fava, Stefano Parodi, Alessia Angelelli, Caterina Tedesco, Flavia Napoli, Anna Elsa Maria Allegri, Giuseppa Patti, Roberto Gastaldi, Chiara Santucci, Barbara Vanorio and 10 more

Abstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 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

20 authors.

Daniela FavaDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa 16132, Italy.ORCID 0000-0002-0128-6501
Stefano ParodiEpidemiology and Biostatistics Unit, Scientific Directorate, IRCCS Istituto Giannina Gaslini, Genoa 16147, Italy.ORCID 0000-0002-9193-1622
Alessia AngelelliDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa 16132, Italy.
Caterina TedescoPediatric Endocrinology Unit, Department of Pediatrics, IRCCS Istituto Giannina Gaslini, Genoa 16147, Italy.
Flavia NapoliPediatric Endocrinology Unit, Department of Pediatrics, IRCCS Istituto Giannina Gaslini, Genoa 16147, Italy.ORCID 0000-0003-3567-6118
Anna Elsa Maria AllegriPediatric Endocrinology Unit, Department of Pediatrics, IRCCS Istituto Giannina Gaslini, Genoa 16147, Italy.
Giuseppa PattiDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa 16132, Italy.
Roberto GastaldiPediatric Endocrinology Unit, Department of Pediatrics, IRCCS Istituto Giannina Gaslini, Genoa 16147, Italy.ORCID 0000-0002-2157-1158
Chiara SantucciDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa 16132, Italy.
Barbara VanorioDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa 16132, Italy.
Claudia CaridiDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa 16132, Italy.
Nadia Gabriella MaioranoDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa 16132, Italy.
Rosa FumoDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa 16132, Italy.
Marta PanciroliDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa 16132, Italy.
Alessandro NaimDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa 16132, Italy.
Alessandro StefaniDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa 16132, Italy.
Elena Lucia De RoseDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa 16132, Italy.
Erica DataPediatric Endocrinology Unit, Department of Pediatrics, IRCCS Istituto Giannina Gaslini, Genoa 16147, Italy.
Mohamad MaghnieDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa 16132, Italy.ORCID 0000-0002-7183-5238
Natascia Di IorgiDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health, University of Genoa, Genoa 16132, Italy.ORCID 0000-0002-4492-4585

Funding

Italian Ministry of Health
6 · The paper itself

Abstract

contextThe glucagon stimulation test (GST) is increasingly used as an alternative to the insulin tolerance test for diagnosing persistent GH deficiency (GHD) during transition, though its accuracy and appropriate cutoff values are still uncertain.

objectiveTo investigate the GH response to GST in transitional-age patients with childhood-onset GHD (CO-GHD), with a focus on the influence of body mass index (BMI) and the underlying etiology. PATIENTS AND

methodsA total of 180 patients with CO-GHD (median age 17.39 years) underwent GST. They were grouped based on the number of pituitary deficiencies and magnetic resonance imaging findings into isolated GHD (n = 80), organic moderate GHD (1-2 deficiencies with congenital or acquired anomalies, n = 63), and organic severe GHD (≥3 deficiencies with complex central nervous system abnormalities, n = 37). Additionally, patients were classified by BMI as normal weight, overweight, or obesity, according to age-appropriate BMI criteria. Childhood cancer survivors (CCS) accounted for 42% of the cohort.

resultsPeak GH response to GST showed a significant inverse association with the severity of pituitary dysfunction (P < .001) and an inverse correlation with BMI SD score (ρ = -0.46, P < .001). However, adjusting by disease group strongly reduced the impact of BMI on the GST response. When stratified by etiology or CCS status, GH peaks were primarily influenced by hypothalamic-pituitary damage with BMI showing a minimal effect.

conclusionThe GST provides valuable insights into GH deficiency in transitional-age patients with CO-GHD. GH response is primarily influenced by the severity of pituitary dysfunction, with BMI playing a minimal role once adjusted for etiology.

Indexed as

Body Mass IndexGlucagonHuman Growth HormoneHypopituitarismAdolescentAdultAge of OnsetChildChild, PreschoolFemaleHumansMaleYoung AdultGlucagonHuman Growth Hormonebrain tumorschildren cancer survivorscongenital hypopituitarismGH deficiencyglucagontransitionyoung adults

Identifiers

PMID41521526
PMCPMC13183450

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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.