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Permanent hypopituitarism is rare after structural traumatic brain injury in early childhood
Natasha L Heather1, Craig Jefferies, Paul L Hofman
1Liggins Institute, University of Auckland, Private Bag 92019, Auckland, New Zealand.
Insights
Permanent hypopituitarism is rare in young children following traumatic brain injury (TBI). This study found no cases of hypopituitarism after structural TBI, regardless of injury cause.
Area of Science:
- Pediatric Endocrinology
- Neuroscience
- Trauma Surgery
Background:
- Traumatic brain injury (TBI) in early childhood can affect pituitary function.
- Assessing the incidence of permanent hypopituitarism post-TBI is crucial for this vulnerable population.
Purpose of the Study:
- To determine the incidence of permanent hypopituitarism in young children after structural traumatic brain injury (TBI).
Main Methods:
- Cross-sectional study with longitudinal follow-up of 198 children post-structural TBI.
- Dynamic testing of growth hormone (GH) and adrenocorticotropic hormone (ACTH) pituitary function.
- Evaluation included puberty staging, thyroid function, IGF-I, and cortisol levels.
Main Results:
- No cases of permanent hypopituitarism were recorded in 198 pediatric TBI survivors.
- Subnormal GH or cortisol responses were observed but did not indicate permanent deficiency.
- Precocious puberty occurred at a rate consistent with the general population.
Conclusions:
- Permanent hypopituitarism is uncommon after structural TBI in early childhood.
- Both inflicted and accidental TBI showed a low incidence of pituitary dysfunction.
- Precocious puberty was the sole identified pituitary abnormality, not exceeding background rates.
Background:
We sought to determine the incidence of permanent hypopituitarism in a potentially high-risk group: young children after structural traumatic brain injury (TBI).
Methods:
We conducted a cross-sectional study with longitudinal follow-up. Dynamic tests of pituitary function (GH and ACTH) were performed in all subjects and potential abnormalities critically evaluated. Puberty was clinically staged; baseline thyroid function, prolactin, IGF-I, serum sodium, and osmolality were compared with age-matched data. Diagnosis of GH deficiency was based on an integrated assessment of stimulated GH peak (<5 μg/liter suggestive of deficiency), IGF-I, and growth pattern. ACTH deficiency was diagnosed based on a subnormal response to two serial Synacthen tests (peak cortisol <500 nmol/liter) and a metyrapone test.
Results:
We studied 198 survivors of structural TBI sustained in early childhood (112 male, age at injury 1.7 ± 1.5 yr) 6.5 ± 3.2 yr after injury. Sixty-four of the injuries (33%) were inflicted and 134 (68%) accidental. Two participants had developed precocious puberty, which is within the expected background population rate. Peak stimulated GH was subnormal in 16 participants (8%), in the context of normal IGF-I and normal growth. Stimulated peak cortisol was low in 17 (8%), but all had normal ACTH function on follow-up. One participant had a transient low serum T(4). Therefore, no cases of hypopituitarism were recorded.
Conclusion:
Permanent hypopituitarism is rare after both inflicted and accidental structural TBI in early childhood. Precocious puberty was the only pituitary hormone abnormality found, but the prevalence did not exceed that of the normal population.
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