Clinical and diagnostic approach to patients with hypopituitarism due to traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), and ischemic stroke (IS)

Abstract

The hypothalamic-pituitary dysfunction attributable to traumatic brain injury (TBI), aneurysmal subarachnoid hemorrhage (SAH), and ischemic stroke (IS) has been lately highlighted. The diagnosis of TBI-induced-hypopituitarism, defined as a deficient secretion of one or more pituitary hormones, is made similarly to the diagnosis of classical hypopituitarism because of hypothalamic/pituitary diseases. Hypopituitarism is believed to contribute to TBI-associated morbidity and to functional and cognitive final outcome, and quality-of-life impairment. Each pituitary hormone must be tested separately, since there is a variable pattern of hormone deficiency among patients with TBI-induced-hypopituitarism. Similarly, the SAH and IS may lead to pituitary dysfunction although the literature in this field is limited. The drive to diagnose hypopituitarism is the suspect that the secretion of one/more pituitary hormone may be subnormal. This suspicion can be based upon the knowledge that the patient has an appropriate clinical context in which hypopituitarism can be present, or a symptom known as caused by hypopituitarism. Hypopituitarism should be diagnosed as a combination of low peripheral and inappropriately normal/low pituitary hormones although their basal evaluation may be not distinctive due to pulsatile, circadian, or situational secretion of some hormones. Evaluation of the somatotroph and corticotroph axes require dynamic stimulation test (ITT for both axes, GHRH + arginine test for somatotroph axis) in order to clearly separate normal from deficient responses.

Assessment of the role of intracranial hypertension and stress on hippocampal cell apoptosis and hypothalamic-pituitary dysfunction after TBI

“…Hypopituitarism is a severe complication induced by TBI that causes affective disorder, cognitive dissonance, and physical symptoms; e.g., depression, anxiety, memory and concentration deficits, and fatigue 5 . In recent years, there has been an increasing amount of strong evidence that suggests that patients with TBI are at considerable risk of dysfunction of the hypothalamic-pituitary axis, and this risk is associated with morbidity and possibly mortality 6–9 . Furthermore, clinical trials have demonstrated that treatment with replacement hormones is convenient and physiologically relevant 9, 10 .…”

“…Furthermore, clinical trials have demonstrated that treatment with replacement hormones is convenient and physiologically relevant 9, 10 . According to one report, the incidence of hypothalamic-pituitary dysfunction induced by TBI is 5.4% to 90% 6 . Mechanisms have been suggested regarding the factors of hypopituitarism caused by TBI, including primary injury to the hypothalamic–pituitary axis and/or to its blood supply and secondary damage caused by oxidative stress or compression of the hypothalamic–pituitary structure by cerebral edema, cerebral hemorrhage, and intracranial hypertension 4, 11–14 .…”

Less known aspects of central hypothyroidism: Part 1 – Acquired etiologies

“…TBI leading to hospitalization has an incidence of 100–350 per 100,000 in the general population [15], [16], [17], [18], [19]. Relatively few cases are fatal; most individuals survive long-term, some of whom continue to suffer from non-specific symptoms such as depression, fatigue, sexual disturbances, cognitive deficits and sleep disorders [20], [21]. More recent studies have reported a high prevalence of chronic anterior pituitary hormone deficiency following TBI with an estimated frequency of more than 25% (approximately 5% for CH) (Table 1) [17].…”

Advances in understanding hypopituitarism

“…Thus, hypopituitarism seems to be less frequent in stroke patients than in patients after TBI or SAH 54 . Despite the impact of stroke on morbidity and mortality, research on hypopituitarism after stroke has been very limited in recent years 55 . Moreover, hypopituitarism may rarely occur after infectious diseases like encephalitis or meningitis 56 , 57 and should be considered in these patients presenting with an unusual course.…”