Research Reports - Pituitary deficiency following traumatic brain injury in early childhood

Georgian Med News. 2015 Jul-Aug;(244-245):62-71

Soliman A(1), Adel A(1), Soliman N(1), Elalaily R(1), De Sanctis V(1)

Aims of review - the intent of the current manuscript is to critically review the
studies on pituitary gland dysfunction in early childhood following traumatic
brain injury (TBI), in comparison with those in adults. Search of the literature:
The MEDLINE database was accessed through PubMed in April 2015. Results were
restricted to the past 15 years and English language of articles. Both transient
and permanent hypopituitarisms are not uncommon after TBI. Early after the TBI,
pituitary dysfunction/s differ than those occurring after few weeks and months.
Growth hormone deficiency (GHD) and alterations in puberty are the most common.
After the one to more years of TBI, pituitary dysfunction tends to improve in
some patients but may deteriorate in others. GH deficiency as well as
Hypogonadism and thyroid dysfunction are the most common permanent lesions. Many
of the symptoms of these endocrine defects can pass unnoticed because of the
psychomotor defects associated with the TBI like depression and apathy.
Unfortunately pituitary dysfunction appear to negatively affect
psycho-neuro-motor recovery as well as growth and pubertal development of
children and adolescents after TBI. Therefore, the current review highlights the
importance of closely following patients, especially children and adolescents for
growth and other symptoms and signs suggestive of endocrine dysfunction. In
addition, all should be screened serially for possible endocrine disturbances
early after the TBI as well as few months to a year after the injury. Risk
factors for pituitary dysfunction after TBI include relatively serious TBI
(Glasgow Coma Scale score < 10 and MRI showing damage to the hypothalamic
pituitary area), diffuse brain swelling and the occurrence of hypotensive and/or
hypoxic episodes.IN CONCLUSION: There is a considerable risk of developing
pituitary dysfunction after TBI in children and adolescents. These patients
should be clinically followed and screened for these abnormalities according to
an agreed protocol of investigations. Further multicenter and multidisciplinary
prospective studies are required to explore in details the occurrence of
permanent pituitary dysfunction after TBI in larger numbers of children with TBI.
This requires considerable organisation and communication between many
disciplines such as neurosurgery, neurology, endocrinology, rehabilitation and
developmental paediatrics.

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