Abstract:GH deficiency is the most common pituitary deficit 1 and 3 years after TBI. In patients with mild and moderate TBI, pituitary function improves over time in a considerable number of patients, but it may also worsen rarely over the 3-year period. In patients with severe TBI, ACTH and GH deficiencies at 1st year evaluation persist at 3rd year.
“…This prevalence of hypopituitarism is much lower compared with the prevalence rates reported in the majority of the previous studies (15-90%) (6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18). This might be explained by the use of different endocrine tests and cutoff values (19).…”
Section: Discussioncontrasting
confidence: 49%
“…The available cohort studies investigating the prevalence of pituitary insufficiency report a percentage ranging from 15 to 90% (6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18). There are several explanations for this remarkably wide range in reported prevalence, including differences in inclusion criteria and duration of follow-up since TBI (short-versus longterm follow-up), and the use of different tests, and cutoff values (19).…”
Objective: Hypopituitarism after traumatic brain injury (TBI) is considered to be a prevalent condition. However, prevalence rates differ considerably among reported studies, due to differences in definitions, endocrine assessments of hypopituitarism, and confounding factors, such as timing of evaluation and the severity of the trauma. Aim: To evaluate the prevalence of hypopituitarism in a large cohort of TBI patients after long-term follow-up using a standardized endocrine evaluation. Study design: Cross-sectional study.
Patients and methods:We included 112 patients with TBI, hospitalized for at least 3 days and duration of follow-up O1 year after TBI from five (neurosurgical) referral centers. Evaluation of pituitary function included fasting morning hormone measurements and insulin tolerance test (nZ90) or, when contraindicated, ACTH stimulation and/or CRH stimulation tests and a GH releasing hormonearginine test (nZ22). Clinical evaluation included quality of life questionnaires. Results: We studied 112 patients (75 males), with median age 48 years and mean body mass index (BMI) 26.7G4.8 kg/m 2 . Mean duration of hospitalization was 11 (3-105), and 33% of the patients had a severe trauma (Glasgow Coma Scale !9) after TBI. The mean duration of follow-up was 4 (1-12) years. Hypopituitarism was diagnosed in 5.4% (6/112) of patients: severe GH deficiency (nZ3), hypogonadism (nZ1), adrenal insufficiency (nZ2). Patients diagnosed with pituitary insufficiency had significantly higher BMI (PZ0.002). Conclusion: In this study, the prevalence of hypopituitarism during long-term follow-up after TBI was low. Prospective studies are urgently needed to find reliable predictive tools for the identification of patients with a significant pre-test likelihood for hypopituitarism after TBI.
“…This prevalence of hypopituitarism is much lower compared with the prevalence rates reported in the majority of the previous studies (15-90%) (6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18). This might be explained by the use of different endocrine tests and cutoff values (19).…”
Section: Discussioncontrasting
confidence: 49%
“…The available cohort studies investigating the prevalence of pituitary insufficiency report a percentage ranging from 15 to 90% (6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18). There are several explanations for this remarkably wide range in reported prevalence, including differences in inclusion criteria and duration of follow-up since TBI (short-versus longterm follow-up), and the use of different tests, and cutoff values (19).…”
Objective: Hypopituitarism after traumatic brain injury (TBI) is considered to be a prevalent condition. However, prevalence rates differ considerably among reported studies, due to differences in definitions, endocrine assessments of hypopituitarism, and confounding factors, such as timing of evaluation and the severity of the trauma. Aim: To evaluate the prevalence of hypopituitarism in a large cohort of TBI patients after long-term follow-up using a standardized endocrine evaluation. Study design: Cross-sectional study.
Patients and methods:We included 112 patients with TBI, hospitalized for at least 3 days and duration of follow-up O1 year after TBI from five (neurosurgical) referral centers. Evaluation of pituitary function included fasting morning hormone measurements and insulin tolerance test (nZ90) or, when contraindicated, ACTH stimulation and/or CRH stimulation tests and a GH releasing hormonearginine test (nZ22). Clinical evaluation included quality of life questionnaires. Results: We studied 112 patients (75 males), with median age 48 years and mean body mass index (BMI) 26.7G4.8 kg/m 2 . Mean duration of hospitalization was 11 (3-105), and 33% of the patients had a severe trauma (Glasgow Coma Scale !9) after TBI. The mean duration of follow-up was 4 (1-12) years. Hypopituitarism was diagnosed in 5.4% (6/112) of patients: severe GH deficiency (nZ3), hypogonadism (nZ1), adrenal insufficiency (nZ2). Patients diagnosed with pituitary insufficiency had significantly higher BMI (PZ0.002). Conclusion: In this study, the prevalence of hypopituitarism during long-term follow-up after TBI was low. Prospective studies are urgently needed to find reliable predictive tools for the identification of patients with a significant pre-test likelihood for hypopituitarism after TBI.
“…Nine studies used basal free thyroxine (FT 4 ) and TSH levels only. Within these studies, the cut-off value for decreased FT 4 varied between 8 and 12 pmol/l (2,5,7,11,14,18,19). In two studies, reference values were not reported (4, 10), one of which (Bushnik et al) reported the highest prevalence of secondary hypothyroidism.…”
Section: The Hypothalamus-pituitary-thyroid Axismentioning
confidence: 99%
“…In recent years, an increasing number of studies have reported the presence of pituitary insufficiency in patients who experienced traumatic brain injury (TBI) (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14). The prevalence of pituitary insufficiency after TBI appeared to be unexpectedly high (15,16).…”
Section: Introductionmentioning
confidence: 99%
“…In the other three studies, only a subset of the patients (those with subnormal basal cortisol levels) underwent stimulation with ACTH. The prevalence in these studies varied between 7 and 19% (weighted mean 10%) (11,12,14).…”
Objective: Traumatic brain injury (TBI) has emerged as an important cause of hypopituitarism. However, considerable variations in the prevalence of hypopituitarism are reported. These can partly be explained by severity of trauma and timing of hormonal evaluation, but may also be dependent on endocrine tests and criteria used for diagnosis of hypopituitarism. Methods: Systematic review of studies reporting prevalence of hypopituitarism in adults R1 year after TBI focusing on used (dynamic) tests and biochemical criteria. Results: We included data from 14 studies with a total of 931 patients. There was considerable variation in definition of hypopituitarism. Overall, reported prevalences of severe GH deficiency varied between 2 and 39%. Prevalences were 8-20% using the GHRH-arginine test (cutoff !9 mg/l), 11-39% using the glucagon test (cutoff 1-5 mg/l), 2% using the GHRH test (no cutoff), and 15-18% using the insulin tolerance test (ITT; cutoff !3 mg/l). Overall, the reported prevalence of secondary adrenal insufficiency had a broad range from 0 to 60%. This prevalence was 0-60% with basal cortisol (cutoff !220 or !440 nmol/l), 7-19% using the ACTH test, and 5% with the ITT as first test (cutoff !500 or !550 nmol/l). Secondary hypothyroidism was present in 0-19% (free thyroxine) or 5-15% (thyroid-releasing hormone stimulation). Secondary hypogonadism was present in 0-29%. Conclusion: The reported variations in the prevalence rates of hypopituitarism after TBI are in part caused by differences in definitions, endocrine assessments of hypopituitarism, and confounding factors. These methodological issues prohibit simple generalizations of results of original studies on TBI-associated hypopituitarism in the perspective of meta-analyses or reviews.
Mild traumatic brain injury (mTBI) has been linked to mental health disorders (MHDs) and pituitary function alterations. Due to the complex relationship of mTBI, the neuroendocrine system, and MHDs, we propose that neuroendocrine dysfunction (NED) may play a role in negative long-term health outcomes. The goal of this study was to determine if blast-concussed service members (SMs) have a stronger likelihood of developing NED. We hypothesized that NED either pre-or post-injury is associated with poor mental and physical health outcomes. Serum samples from the Armed Forces Health Surveillance Branch were obtained from concussed (n = 59) and nonconcussed (n = 72) SMs treated at the Concussion Restoration Care Center (CRCC) in Afghanistan. Serum was collected within 2 years prior to deployment and one or two times within 3 years following their CRCC visit. Samples were analyzed for luteinizing hormone (LH), testosterone, human growth hormone, cortisol, and prolactin to assess post-injury neuroendocrine function. Results indicate that SMs who incurred an mTBI exhibited long-term LH and testosterone deficiencies 3 years following injury compared to controls. Specifically, 47.6% of head-injured SMs displayed hypofunction in at least one of five hormones at 3 years post-injury. Anxiety disorders were the most common MHD observed in concussed SMs with hypopituitarism, while there was also a trend for SMs with chronic pituitary dysfunction to have MHD diagnoses. Findings indicate blast-related mTBI may be associated with long-term health outcomes following a period of incubation. Neuroendocrine screenings may increase treatment opportunities, inform rehabilitation strategies, and improve overall quality of life for patients. K E Y W O R D S concussion, military, neuroendocrine, pituitary, traumatic brain injury Published 2020. This article is a U.S. Government work and is in the public domain in the USA.| 1175 CIARLONE Et AL.
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