# Endocrine Dysfunctions After Pediatric Traumatic Brain Injury: Present Insights and Future Directions

**Authors:** Ignazio Cammisa, Elena Malavolta, Giorgio Sodero, Donato Rigante, Clelia Cipolla

PMC · DOI: 10.3390/children12111484 · Children · 2025-11-03

## TL;DR

Pediatric traumatic brain injury can lead to long-term endocrine problems, requiring ongoing monitoring and early treatment to improve recovery.

## Contribution

Highlights the underrecognized issue of post-traumatic endocrine dysfunction in children and advocates for structured surveillance and standardized protocols.

## Key findings

- Endocrine dysfunction after pediatric TBI affects growth, puberty, and metabolism, with prevalence ranging from 5 to 57%.
- Growth hormone deficiency is the most common endocrine abnormality, often persisting long after injury.
- Endocrine issues may appear months to years post-injury, complicating timely diagnosis and management.

## Abstract

Traumatic brain injury (TBI) in childhood is a major global health concern and a leading cause of morbidity and mortality in the pediatric population. Its incidence is rising worldwide, with early childhood and adolescence representing the most vulnerable age groups. Beyond acute neurological injury, post-traumatic endocrine dysfunction has emerged as an underrecognized but clinically significant sequela, with potential long-term consequences for growth, puberty, metabolism, and overall quality of life. The hypothalamic–pituitary axis (HPA) is uniquely vulnerable due to its anatomical and vascular characteristics, making pituitary cells—particularly somatotrophs and gonadotrophs—susceptible to ischemic, traumatic, and inflammatory damage. Reported prevalence of post-TBI pituitary dysfunction in children ranges from 5 to 57%, reflecting a deep heterogeneity in injury severity, diagnostic methods, and timing of evaluations. Growth hormone deficiency (GHD) is the most frequently reported abnormality, with presentations varying from transient to persistent forms. Gonadal axis disturbances, including hypogonadotropic hypogonadism and, less commonly, central precocious puberty, highlight the impact of TBI on pubertal development. Adrenal dysfunctions, though less frequent, may be life-threatening if unrecognized, while posterior pituitary disorders, such as diabetes insipidus, usually revealed acutely, are often transient. Importantly, many endocrine sequelae manifest months to years after the initial trauma, complicating a timely diagnosis. Current evidence underscores the need for structured, longitudinal endocrine surveillance after pediatric TBI, with baseline and follow-up assessments at defined intervals. Early recognition and intervention, including hormone replacement when appropriate, may improve neurocognitive recovery and overall rehabilitation outcomes. Future multicenter studies and standardized screening protocols should be considered essential to clarify incidence, natural history, and optimal management strategies for post-traumatic endocrine dysfunction in children.

## Linked entities

- **Diseases:** traumatic brain injury (MONDO:0858950), hypogonadotropic hypogonadism (MONDO:0018555), central precocious puberty (MONDO:0019165), diabetes insipidus (MONDO:0004782)

## Full-text entities

- **Diseases:** Endocrine Dysfunctions (MESH:D004700), trauma (MESH:D014947), neurological injury (MESH:D020196), Gonadal axis disturbances (MESH:C566610), GHD (MESH:D004393), ischemic (MESH:D002545), diabetes insipidus (MESH:D003919), Adrenal dysfunctions (MESH:D000307), central precocious puberty (MESH:D011629), hypogonadotropic hypogonadism (MESH:D007006), pituitary dysfunction (MESH:D010900), TBI (MESH:D000070642), inflammatory (MESH:D007249)

## Full text

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## Figures

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## References

66 references — full list in the complete paper: https://tomesphere.com/paper/PMC12651762/full.md

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Source: https://tomesphere.com/paper/PMC12651762