Evidence map›Paper›PMID 42095177›Full record

ReviewFrontiers in endocrinology2026

Endocrine-related osteoporosis: the state of the art.

Iacopo Chiodini, Agostino Gaudio, Luigi Gennari, Domenico Rendina, Alfredo Scillitani, Fabio Vescini, Alberto Falchetti

Abstract readReview
In one paragraph

Review in Frontiers in endocrinology, 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

7 authors.

Iacopo ChiodiniDepartment of Medical Biotechnology and Translational Medicine, University of Milan, Milan, Italy.
Agostino GaudioDepartment of Clinical and Experimental Medicine, University of Catania, Catania, Italy.
Luigi GennariDepartment of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy.
Domenico RendinaDepartment of Clinical Medicine and Surgery, Federico II University, Naples, Italy.
Alfredo ScillitaniUnit of Endocrinology, Ospedale "Casa Sollievo della Sofferenza", San Giovanni Rotondo, Foggia, Italy.
Fabio VesciniDepartment of Oncology, University of Udine, Udine, Italy.
Alberto FalchettiEndocrinology Unit, Azienda Sanitaria-Universitaria Friuli Centrale, P.O. Santa Maria della Misericordia, Udine, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Endocrine-related secondary osteoporosis (ERSOP) comprises disorders in which bone fragility results from hormonal abnormalities other than age-related or menopausal hypogonadism. Its prevalence is underestimated, and timely recognition is essential because many forms improve or reverse when the underlying endocrine disturbance is corrected. Objective: This Review highlights the evolving concepts, unmet needs, and research opportunities in ERSOP, with focus on hypercortisolism, primary aldosteronism, male hypogonadism, hypercalciuria, and FGF23-dependent phosphate-wasting disorders. Recent findings: Mild autonomous cortisol secretion (MACS) is increasingly recognized as a contributor to fracture risk even at near-normal cortisol levels.Primary aldosteronism promotes skeletal fragility via mineralocorticoid receptor activation, oxidative stress, hypercalciuria, and secondary hyperparathyroidism.Male hypogonadism is a major driver of bone loss, and optimal fracture prevention may require combined hormonal and anti-osteoporotic therapy.Differentiating PTH-dependent from PTH-independent hypercalciuria is crucial for management.FGF23-mediated phosphate-wasting disorders impair mineralization and may respond to targeted therapy, including burosumab. Conclusion: ERSOP should be considered in patients with atypical osteoporosis phenotypes, including men, younger adults, and individuals with normal BMD but fragility fractures. Optimal care requires structured endocrine assessment, correction of the primary disorder, and integration with bone-specific therapy where appropriate.

Indexed as

Endocrine System DiseasesOsteoporosisAnimalsFibroblast Growth Factor-23HumansHypogonadismMaleFGF23 protein, humanFibroblast Growth Factor-23FGF23-dependent phosphate-wasting disordershypercalciuriahypercortisolismhyperparathyroidismmale hypogonadismprimary aldosteronismsecondary osteoporosis

Identifiers

PMID42095177
PMCPMC13138963

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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.