Should anterior pituitary function be tested during follow-up of all patients presenting at the emergency department because of traumatic brain injury?

Abstract

Context: A wide range (15-56%) of prevalences of anterior pituitary insufficiency are reported in patients after traumatic brain injury (TBI). However, different study populations, study designs, and diagnostic procedures were used. No data are available on emergency-department-based cohorts of TBI patients. Objective: To assess the prevalence of pituitary dysfunction in an emergency-department-based cohort of TBI patients using strict endocrinological diagnostic criteria. Methods: Of all the patients presenting in the emergency department with TBI over a 2-year period, 516 matched the inclusion criteria. One hundred and seven patients (77 with mild TBI and 30 with moderate/severe TBI) agreed to participate. They were screened for anterior pituitary insufficiency by GHRH-arginine testing, evaluation of fasting morning hormone levels (cortisol, TSH, free thyroxine, FSH, LH, and 17b-estradiol or testosterone), and menstrual history 3-30 months after TBI. Abnormal screening results were defined as low peak GH to GHRH-arginine, or low levels of any of the end-organ hormones with low or normal pituitary hormone levels. Patients with abnormal screening results were extensively evaluated, including additional hormone provocation tests (insulin tolerance test, ACTH stimulation test, and repeated GHRH-arginine test) and assessment of free testosterone levels. Results: Screening results were abnormal in 15 of 107 patients. In a subsequent extensive endocrine evaluation, anterior pituitary dysfunction was diagnosed in only one patient (partial hypocortisolism). Conclusion: By applying strict diagnostic criteria to an emergency-department-based cohort of TBI patients, it was shown that anterior pituitary dysfunction is rare (!1%). Routine pituitary screening in unselected patients after TBI is unlikely to be cost-effective.

Low prevalence of hypopituitarism after traumatic brain injury: a multicenter study

“…This may result in higher prevalence rates when patients with a more severe degree of trauma are included. Conversely, prevalence rates of hypopituitarism may decrease when patients with only minor traumas are included (35).…”

The Case of Hypopituitarism in Traumatic Brain Injury

“…They confirmed that part of the variation indeed seemed to be caused by differences in study design, diagnostic procedures, and other confounding factors such as BMI, prohibiting simple generalization from the original studies. In general, a lower prevalence of posttraumatic hypopituitarism tended to be recorded in studies using the ITT for the evaluation of the GH reserve (Kelly et al, 2000;Klose et al, 2007a;Kokshoorn et al, 2011), and in the studies using confirmatory tests (Agha et al, 2004;Klose et al, 2007a;LealCerro et al, 2005;van der Eerden et al, 2010). Table 2 a-d illustrates the relationship between diagnostic stringency and reported prevalence of GH, ACTH, LH/FSH and TSH deficiencies.…”

“…Over the last 10 years, the field has received increased attention and chronic anterior pituitary hormone deficiency has been reported with a prevalence ranging from 1% and up to 83% (Table 1). The results from most studies have suggested that persistent posttraumatic hypopituitarism might be a more common complication in TBI than previously believed, although some studies have failed to show such high occurrence rates (Kokshoorn et al, 2011;van der Eerden et al, 2010). The diversity of the reported prevalences of chronic anterior pituitary hormone deficiency is likely to be explained by differences in study populations, study designs, and diagnostic procedures.…”

“…Trauma severity varied considerably among the studies (Table 1). In general, a lower prevalence of posttraumatic hypopituitarism tended to be recorded in studies recruiting less severely injured patients (Kokshoorn et al, 2011;van der Eerden et al, 2010), and indicators of increased trauma severity was also suggested to be associated with development of hypopituitarism by some (Bavisetty et al, 2008;Bondanelli et al, 2004;Kelly et al, 2000;Klose et al, 2007a;Schneider et al, 2008), while not by others (Agha et al, 2004;Aimaretti et al, 2005;Leal-Cerro et al, 2005). In 22 TBI patients Kelly et al (Kelly et al, 2000) identified injury severity in terms of an initial Glasgow Coma Scale score (GCS) of less than 10, diffuse brain swelling and hypoxia/hypotension as risk factors of posttraumatic hypopituitarism.…”

“…Not unanticipated, those studies applying the lowest cut-offs tended to report lower prevalences of gonadotropin deficiency. Furthermore, studies following the general recommendation of repeated sampling in case of a low or low normal testosterone concentration, reported lower prevalences of gonadotropin deficiency (Klose et al, 2007a;van der Eerden et al, 2010), which is probably due to the low test-retest reproducibility (Bhasin et al, 2010;Brambilla et al, 2007) of testosterone measurements. Although the diagnosis of secondary hypothyroidism is challenging, the studies used very similar definitions, with cut-offs mostly differing according to the local reference ranges applied (Table 1d).…”