The natural history of post-traumatic hypopituitarism: implications for assessment and treatment

At 12 months after TBI, substantial rates of pituitary hormone deficiencies remain, ranging from 13% to 50%, with growth hormone deficiency the most common hormonal deficit.

“At the end of 12 months, there were still substantial rates of pituitary hormone deficiencies, ranging from 13% to 50%, of which growth hormone deficiency was the most common hormonal deficit.”

In these studies, pituitary hormone evaluations were performed only at one time point during the acute phase of TBI.

“It is important to note that, in these studies, pituitary hormone evaluations were performed only at one time point during the acute phase of TBI (15, 149, 150).”

Most pituitary hormonal changes (particularly FSH/LH, growth hormone, and TSH deficiencies) are transient and recover within 3-12 months of injury.

“Prospective studies evaluating pituitary function have demonstrated that most pituitary hormonal changes (particularly FSH/LH, growth hormone, and thyroid-stimulating hormone [TSH] deficiencies) are transient and recover within 3–12 months of injury.16,26,43–45”

The somatotrophs and gonadotrophs, located in the area perfused by long hypophyseal portal vessels, are the most frequent hormonal deficiencies after TBI; however, in some studies ACTH deficiency is the most common or second most common hormonal deficiency after TBI.

“The somatotrophs and gonadotrophs, which are located in the area of the pituitary perfused by long hypophyseal portal vessels, are the most frequent hormonal deficiencies after TBI (15, 18, 27, 29, 150, 160); however, in some studies ACTH deficiency (corticotrophs are located in the territory supplied by the short portal vessels) is the most common or second most common hormonal deficiency after”

The possible mechanisms of transient acute hypopituitarism could be due to direct mechanical injury, hypotension, reversible edema formation, increased ICP, and hypoperfusion due to reversible vasospasm; however, none of these mechanisms have been clearly demonstrated in clinical or experimental studies.

“The possible mechanisms of transient acute hypopituitarism could be due to direct mechanical injury (ie, hypothalamus, stalk, pituitary, or long portal vessels injury would do not cause pituitary infarction), hypotension, reversible edema formation, increased ICP, and hypoperfusion due to reversible vasospasm; however, none of these mechanisms have been clearly demonstrated in either clinical or”

Most prospective studies have demonstrated that the presence of acute anterior pituitary deficiencies after head trauma does not typically predict chronic hypopituitarism, and most of the acute changes are transient.

“Most prospective studies have demonstrated that the presence of acute anterior pituitary deficiencies after head trauma does not typically predict chronic hypopituitarism, and most of the acute changes are transient.”

At 12 months after TBI, substantial rates of some pituitary hormone deficiency remain, ranging from 13% to 50%, with GHD the most common hormonal deficit.

“At the end of 12 months, there were still substantial rates of some pituitary hormone deficiency ranging from 13 to 50%, of which GHD was the most common hormonal deficit.”

Six major prospective studies (five including patients with mild, moderate, or severe TBI) investigating pituitary function during the acute phase and 12 months later have been published.

“So far, six major prospective studies (five including patients with mild, moderate, or severe TBI) investigating pituitary function during the and 12 months later have been published.9,15,16,43–45”

Prospective studies have demonstrated dynamic characteristics of hypopituitarism in isolated and multiple pituitary deficiencies and in improvement (recovery) or worsening (new-onset deficiencies) of pituitary function.

“These prospective studies demonstrated the dynamic characteristics of hypopituitarism in isolated and multiple pituitary deficiencies as well as in the improvement (recovery) or worsening (new onset hormonal deficiencies) of pituitary function.”

Dynamic hormonal changes were defined mainly in the first 6 months but could be seen after 6 months.

“The dynamic hormonal changes were defined mainly in the first 6 months but could be seen after 6 months.9,15,16,43–45”

Based on prospective clinical studies, significant percentages of acute pituitary hormonal deficiencies are transient and recover after 3 to 12 months of injury.

“Based on the prospective clinical studies, significant percentages of the acute pituitary hormonal deficiencies are transient and recover after 3 to 12 months of injury (15, 25, 149 -151).”

Six major prospective studies have investigated pituitary function during the first 3 months of TBI and 12 months later.

“published investigating pituitary function during the first 3 months of TBI and 12 months later (15, 27, 149 -151, 181).”

Most pituitary hormonal changes (especially FSH/LH, GH, and TSH deficiencies) are transient and recover within 3 to 12 months after TBI.

“Based on the prospective studies evaluating pituitary function, most pituitary hormonal changes (especially FSH/LH, GH, and TSH deficiencies) are transient and recover within 3 to 12 months after injury (15, 25, 149 -151).”

Dynamic hormonal changes occur mainly in the first 6 months but can be seen after 6 months.

“The dynamic hormonal changes were defined mainly in the first 6 months but could be seen after 6 months (15, 27, 149 -151, 181).”

Prospective studies show dynamic properties of hypopituitarism in isolated and multiple pituitary deficiencies as well as in improvement (recovery) or worsening (new-onset hormonal deficiencies) of pituitary function.

“These prospective studies showed the dynamic properties of hypopituitarism in isolated and multiple pituitary deficiencies as well as in the improvement (recovery) or worsening (new-onset hormonal deficiencies) of pituitary function.”

Early GH deficiency post TBI can be transient.

“Early GH deficiency post TBI can be transient (36).”