New guidelines address hypopituitarism in TBI

New guidelines on traumatic brain injury and neuroendocrine dysfunction ask clinicians to be mindful that hypopituitarism in TBI survivors can develop following injuries classified as mild and can be slow to develop.

The guidelines – published online May 7, 2015,in Endocrine Reviews (doi:10.1210/er.2014-1065) and based on a review of 16 studies conducted between 2014 and 2011 – emphasize early detection and treatment of hypopituitarism in adults with TBI; recognition can be difficult because symptoms can progress slowly and be nonspecific. Deficiencies in pituitary hormones have been linked to elevated cardiovascular, metabolic, and cognitive risks, though studies in TBI populations are scant.About 12% of people with TBI will show persistent neuroendocrine dysfunction on repeat testing, according to Dr. Fatih Tanriverdi of Erciyes University in Kayseri, Turkey, and his associates. Although growth hormone (GH) deficiencies are the most common type of hormone deficiency after TBI, adrenocorticotropic hormone (ACTH), gonadotropins (FSH and LH), and thyroid-stimulating hormone (TSH) can all be diminished.

Dr. Tanriverdi and his colleagues noted that much more research is needed to determine the precise pathways by which TBI can cause pituitary dysfunction and whether hormone replacement can bring about functional or cognitive improvement in TBI patients with deficiencies. In addition to severity of injury, genetic factors, inflammation, and autoimmunity appear to bear on the risk of hypopituitarism after TBI, they said.

The guidelines recommend routine screening and early treatment for people with complicated mild TBI – a Glasgow coma score of 13-15 with some abnormalities on CT or MRI, hospitalization longer than 24 hours, or acute pituitary hormonal changes after injury – and for moderate and severe TBI. People with uncomplicated mild TBI (GCS of 13-15 but no screening abnormalities) are considered at low risk of developing pituitary dysfunction and do not need to be followed.

Patients with complicated mild TBI should be screened for ACTH deficiency immediately after injury and at hospital discharge and treated if necessary. At 6 months they should be reassessed for ACTH, TSH, and FSH/LH deficiencies and treated with hormone replacement therapy as needed. At a year post injury, patients should be assessed for GH deficiency and treated for this as well, if necessary, with annual clinical and hormonal evaluations continuing 5 years.

If no hormone deficiencies are found at 12 months, patients should still be reassessed annually through the fif^th year for hypopituitarism, as hormone deficiencies can still develop.

Patients with moderate and severe TBI should be assessed and treated according to the same algorithm, the guidelines say, except that they do not require further screening beyond 1 year in the absence of symptoms. Patients should instead be coached to recognize symptoms of hypopituitarism and present for screening if symptoms appear.The guideline authors did not report outside funding and disclosed no conflicts of interest related to their recommendations.

New guidelines on traumatic brain injury and neuroendocrine dysfunction ask clinicians to be mindful that hypopituitarism in TBI survivors can develop following injuries classified as mild and can be slow to develop.

The guidelines – published online May 7, 2015,in Endocrine Reviews (doi:10.1210/er.2014-1065) and based on a review of 16 studies conducted between 2014 and 2011 – emphasize early detection and treatment of hypopituitarism in adults with TBI; recognition can be difficult because symptoms can progress slowly and be nonspecific. Deficiencies in pituitary hormones have been linked to elevated cardiovascular, metabolic, and cognitive risks, though studies in TBI populations are scant.About 12% of people with TBI will show persistent neuroendocrine dysfunction on repeat testing, according to Dr. Fatih Tanriverdi of Erciyes University in Kayseri, Turkey, and his associates. Although growth hormone (GH) deficiencies are the most common type of hormone deficiency after TBI, adrenocorticotropic hormone (ACTH), gonadotropins (FSH and LH), and thyroid-stimulating hormone (TSH) can all be diminished.

Dr. Tanriverdi and his colleagues noted that much more research is needed to determine the precise pathways by which TBI can cause pituitary dysfunction and whether hormone replacement can bring about functional or cognitive improvement in TBI patients with deficiencies. In addition to severity of injury, genetic factors, inflammation, and autoimmunity appear to bear on the risk of hypopituitarism after TBI, they said.

The guidelines recommend routine screening and early treatment for people with complicated mild TBI – a Glasgow coma score of 13-15 with some abnormalities on CT or MRI, hospitalization longer than 24 hours, or acute pituitary hormonal changes after injury – and for moderate and severe TBI. People with uncomplicated mild TBI (GCS of 13-15 but no screening abnormalities) are considered at low risk of developing pituitary dysfunction and do not need to be followed.

Patients with complicated mild TBI should be screened for ACTH deficiency immediately after injury and at hospital discharge and treated if necessary. At 6 months they should be reassessed for ACTH, TSH, and FSH/LH deficiencies and treated with hormone replacement therapy as needed. At a year post injury, patients should be assessed for GH deficiency and treated for this as well, if necessary, with annual clinical and hormonal evaluations continuing 5 years.

If no hormone deficiencies are found at 12 months, patients should still be reassessed annually through the fif^th year for hypopituitarism, as hormone deficiencies can still develop.

Patients with moderate and severe TBI should be assessed and treated according to the same algorithm, the guidelines say, except that they do not require further screening beyond 1 year in the absence of symptoms. Patients should instead be coached to recognize symptoms of hypopituitarism and present for screening if symptoms appear.The guideline authors did not report outside funding and disclosed no conflicts of interest related to their recommendations.

New guidelines on traumatic brain injury and neuroendocrine dysfunction ask clinicians to be mindful that hypopituitarism in TBI survivors can develop following injuries classified as mild and can be slow to develop.

The guidelines – published online May 7, 2015,in Endocrine Reviews (doi:10.1210/er.2014-1065) and based on a review of 16 studies conducted between 2014 and 2011 – emphasize early detection and treatment of hypopituitarism in adults with TBI; recognition can be difficult because symptoms can progress slowly and be nonspecific. Deficiencies in pituitary hormones have been linked to elevated cardiovascular, metabolic, and cognitive risks, though studies in TBI populations are scant.About 12% of people with TBI will show persistent neuroendocrine dysfunction on repeat testing, according to Dr. Fatih Tanriverdi of Erciyes University in Kayseri, Turkey, and his associates. Although growth hormone (GH) deficiencies are the most common type of hormone deficiency after TBI, adrenocorticotropic hormone (ACTH), gonadotropins (FSH and LH), and thyroid-stimulating hormone (TSH) can all be diminished.

Dr. Tanriverdi and his colleagues noted that much more research is needed to determine the precise pathways by which TBI can cause pituitary dysfunction and whether hormone replacement can bring about functional or cognitive improvement in TBI patients with deficiencies. In addition to severity of injury, genetic factors, inflammation, and autoimmunity appear to bear on the risk of hypopituitarism after TBI, they said.

The guidelines recommend routine screening and early treatment for people with complicated mild TBI – a Glasgow coma score of 13-15 with some abnormalities on CT or MRI, hospitalization longer than 24 hours, or acute pituitary hormonal changes after injury – and for moderate and severe TBI. People with uncomplicated mild TBI (GCS of 13-15 but no screening abnormalities) are considered at low risk of developing pituitary dysfunction and do not need to be followed.

Patients with complicated mild TBI should be screened for ACTH deficiency immediately after injury and at hospital discharge and treated if necessary. At 6 months they should be reassessed for ACTH, TSH, and FSH/LH deficiencies and treated with hormone replacement therapy as needed. At a year post injury, patients should be assessed for GH deficiency and treated for this as well, if necessary, with annual clinical and hormonal evaluations continuing 5 years.

If no hormone deficiencies are found at 12 months, patients should still be reassessed annually through the fif^th year for hypopituitarism, as hormone deficiencies can still develop.

Patients with moderate and severe TBI should be assessed and treated according to the same algorithm, the guidelines say, except that they do not require further screening beyond 1 year in the absence of symptoms. Patients should instead be coached to recognize symptoms of hypopituitarism and present for screening if symptoms appear.The guideline authors did not report outside funding and disclosed no conflicts of interest related to their recommendations.