Acute and long‐term pituitary insufficiency in traumatic brain injury: a prospective single‐centre study

Abstract

Long-term hypopituitarism was frequent only in severe TBI. During the 3-12 months follow-up, recovery but no new insufficiencies were recorded, indicating manifest hypothalamic or pituitary damage already a few months postinjury. Very early hormone alterations were not associated to long-term post-traumatic hypopituitarism. Clinicians should, nonetheless, be aware of potential ACTH deficiency in the early post-traumatic period.

Early endocrine alterations reflect prolonged stress and relate to 1-year functional outcome in patients with severe brain injury

“…Similar endocrine alterations have been reported both in patients with brain injury (4,5,6) and in patients with other causes of acute and severe illness (24). Although in some cases endocrine alterations may be attributed to primary or secondary injury to the hypothalamus or pituitary gland, acute severe illness involves major stress to the organism, and increased ACTH, cortisol, GH and prolactin concentrations, together with low testosterone and low triiodothyronine syndrome, have all been described as being part of important adaptive responses in the early phases following trauma, surgery and severe medical illness (24).…”

“…The lower four panels in Fig. 1 show the prevalence of elevated stress hormones 12 nmol/l (1.0-28.0) 9.9 nmol/l (0.2-17.5) FT 4 14.2 pmol/l (6.9-19.1) 14.7 pmol/l (9.7-26.4) (i.e. concentrations above the upper normal reference limit), including elevated prolactin (49% of the TBI patients and 50% of the non-TBI patients), IGF1 (26% of the TBI patients and 36% of the non-TBI patients), basal cortisol (5% of the TBI patients and 4% of the non-TBI patients) and 30 min cortisol (34% of the TBI patients and 29% of the non-TBI patients).…”

“…Therefore, routine pituitary assessment in the early phases (e.g. within a year) after acquired brain injury should be limited to patients that present with typical clinical features suggestive of hypopituitarism (4,7). …”

The Case of Hypopituitarism in Traumatic Brain Injury

“…However, individual data showed no obvious relationship between early and late pituitary dysfunctions. We (Klose et al, 2007b) described acute hormone alterations in 76% of 46 patients, with patients suffering the most severe TBI exhibiting the highest prevalence of alterations mimicking hypogonadotropic hypogonadism, central hypothyroidism, hyperprolactinaemia, and increased HPA-activity, all in agreement with the alterations seen in non-pituitary critical illness (Fig. 1).…”

“…The temporal relationship between TBI and hypopituitarism is poorly understood. Longitudinal studies examining TBI patients at variable time points from the acute phase to years after the trauma, have reported transient, permanent, and de novo deficiencies all through the time span (Agha et al, 2005a;Kleindienst et al, 2009;Klose et al, 2007b;Tanriverdi et al, 2006). Part of this variation may be ascribed to diagnostic difficulties, including those caused by the stress of severe illness, but may also in some cases be related to medication effects, and lack of test re-test reproducibility.…”