Pub Date : 2025-05-01DOI: 10.1016/j.beem.2025.101995
Canan Sehit Kara, Zuleyha Karaca
Traumatic brain injury (TBI) during sports activities may lead to dysfunction of the pituitary gland. Even mild TBIs have been shown to have the potential to induce pituitary dysfunction. The clinical picture of pituitary dysfunction subsequent to TBIs may mimic the post-TBI period itself. Pituitary hormone deficiencies may improve or new ones may be observed over time. For this reason, hypopituitarism should be considered both during the acute phase and in the recovery period. The most prevalent pituitary hormone deficiency that follows a sports injury is growth hormone (GH) deficiency. Despite the established knowledge regarding the deleterious consequences of GH deficiency in the athletes, the efficacy of replacement therapy remains controversial. Concurrently, given the potential for GH to be utilised for doping purposes, a consensus on the monitoring of these patients remains elusive. There is a necessity for further systematic and large-scale studies on the epidemiology, pathophysiological mechanisms, screening algorithms, and prevention strategies related to sports-related pituitary dysfunction.
{"title":"Pituitary dysfunction due to sports injuries","authors":"Canan Sehit Kara, Zuleyha Karaca","doi":"10.1016/j.beem.2025.101995","DOIUrl":"10.1016/j.beem.2025.101995","url":null,"abstract":"<div><div>Traumatic brain injury (TBI) during sports activities may lead to dysfunction of the pituitary gland. Even mild TBIs have been shown to have the potential to induce pituitary dysfunction. The clinical picture of pituitary dysfunction subsequent to TBIs may mimic the post-TBI period itself. Pituitary hormone deficiencies may improve or new ones may be observed over time. For this reason, hypopituitarism should be considered both during the acute phase and in the recovery period. The most prevalent pituitary hormone deficiency that follows a sports injury is growth hormone (GH) deficiency. Despite the established knowledge regarding the deleterious consequences of GH deficiency in the athletes, the efficacy of replacement therapy remains controversial. Concurrently, given the potential for GH to be utilised for doping purposes, a consensus on the monitoring of these patients remains elusive. There is a necessity for further systematic and large-scale studies on the epidemiology, pathophysiological mechanisms, screening algorithms, and prevention strategies related to sports-related pituitary dysfunction.</div></div>","PeriodicalId":8810,"journal":{"name":"Best practice & research. Clinical endocrinology & metabolism","volume":"39 3","pages":"Article 101995"},"PeriodicalIF":6.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143789332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-01DOI: 10.1016/j.beem.2025.102003
Eibhlín Marie Lonergan, Amar Agha
Hypopituitarism is a common manifestation of traumatic brain injury. The focus of much of the literature to date has been on the post-acute phase of injury. However, a small number of authors have systematically examined the prevalence of and risk factors for post-traumatic hypopituitarism in the immediate post-injury phase and reported on proposed screening methods, diagnostic investigations, and appropriate treatments of acute anterior and posterior hypopituitarism. It is paramount to promptly identify and treat acute post-traumatic hypopituitarism, particularly adrenocorticotropic hormone or cortisol deficiency and disorders of arginine vasopressin secretion, in order to reduce patient morbidity and mortality.
{"title":"Neuroendocrine changes during the acute phase following traumatic brain injury","authors":"Eibhlín Marie Lonergan, Amar Agha","doi":"10.1016/j.beem.2025.102003","DOIUrl":"10.1016/j.beem.2025.102003","url":null,"abstract":"<div><div>Hypopituitarism is a common manifestation of traumatic brain injury. The focus of much of the literature to date has been on the post-acute phase of injury. However, a small number of authors have systematically examined the prevalence of and risk factors for post-traumatic hypopituitarism in the immediate post-injury phase and reported on proposed screening methods, diagnostic investigations, and appropriate treatments of acute anterior and posterior hypopituitarism. It is paramount to promptly identify and treat acute post-traumatic hypopituitarism, particularly adrenocorticotropic hormone or cortisol deficiency and disorders of arginine vasopressin secretion, in order to reduce patient morbidity and mortality.</div></div>","PeriodicalId":8810,"journal":{"name":"Best practice & research. Clinical endocrinology & metabolism","volume":"39 3","pages":"Article 102003"},"PeriodicalIF":6.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144060842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-01DOI: 10.1016/j.beem.2025.101996
Catherine D. Zhang , Adriana G. Ioachimescu
Traumatic brain injury (TBI) is a global health problem with rising incidence. In many patients, pituitary hormone deficiencies after TBI are transient; however, in some cases, they can persist or develop in the chronic phase. Post-traumatic hypopituitarism has a variable clinical course, reflecting its complex pathophysiology and incompletely understood risk factors. The diagnosis can be challenging, because symptoms of hypopituitarism may overlap with other TBI manifestations. Confirmatory endocrine testing is often required for diagnosis. Untreated chronic hypopituitarism can adversely affect physical, neurocognitive, and psychosocial rehabilitation; body composition; glucose metabolism; bone metabolism; and quality of life. Screening for hypopituitarism is recommended after moderate or severe TBI and for selected patients with mild TBI and suggestive clinical symptoms. Management requires an individualized multidisciplinary approach and consideration of endocrine pathology. In this review, we discuss the clinical manifestations and current management standards for hypopituitarism in adults with TBI.
{"title":"Clinical manifestations and treatment of hypopituitarism due to traumatic brain injury","authors":"Catherine D. Zhang , Adriana G. Ioachimescu","doi":"10.1016/j.beem.2025.101996","DOIUrl":"10.1016/j.beem.2025.101996","url":null,"abstract":"<div><div>Traumatic brain injury (TBI) is a global health problem with rising incidence. In many patients, pituitary hormone deficiencies after TBI are transient; however, in some cases, they can persist or develop in the chronic phase. Post-traumatic hypopituitarism has a variable clinical course, reflecting its complex pathophysiology and incompletely understood risk factors. The diagnosis can be challenging, because symptoms of hypopituitarism may overlap with other TBI manifestations. Confirmatory endocrine testing is often required for diagnosis. Untreated chronic hypopituitarism can adversely affect physical, neurocognitive, and psychosocial rehabilitation; body composition; glucose metabolism; bone metabolism; and quality of life. Screening for hypopituitarism is recommended after moderate or severe TBI and for selected patients with mild TBI and suggestive clinical symptoms. Management requires an individualized multidisciplinary approach and consideration of endocrine pathology. In this review, we discuss the clinical manifestations and current management standards for hypopituitarism in adults with TBI.</div></div>","PeriodicalId":8810,"journal":{"name":"Best practice & research. Clinical endocrinology & metabolism","volume":"39 3","pages":"Article 101996"},"PeriodicalIF":6.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144032101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-01DOI: 10.1016/j.beem.2025.102015
Richard D. Batson , Joshua Z. Goldenberg , Ryan S. Wexler , Traver Wright , Eunisse Chua , Alissya Yuen , Michael Freeman , Tamara L. Wexler , Walter High Jr. , Brent E. Masel , Randall J. Urban , Kevin C.J. Yuen
Background
Post-traumatic hypopituitarism (PTHP), including growth hormone deficiency (GHD), is a prevalent and underdiagnosed complication of traumatic brain injury (TBI), resulting in substantial morbidity. Emerging evidence suggests that recombinant human growth hormone (rhGH) therapy may provide benefit for patients with confirmed GHD, and also those with growth hormone insufficiency (GHI), abnormal growth hormone secretion (AGHS), or Brain Injury Associated Fatigue and Altered Cognition (BIAFAC), even when peak growth hormone response to growth hormone stimulation testing is above traditional GHD diagnostic cutoffs in these patients.
Objective
To conduct a scoping review evaluating the effects of rhGH in adults with TBI, including those classified as GHD, GHI, AGHS, or BIAFAC, on clinical, functional, and neurobiological outcomes.
Methods
A comprehensive search of PubMed/MEDLINE was performed using a peer-reviewed search strategy. Studies were screened in duplicate. Eligible studies included clinical trials, observational studies, and case series, reporting rhGH use in adults with a history of TBI, with or without GHD. Outcomes included quality of life, neuropsychological performance, physical functioning, biochemical markers, and neuroimaging data.
Results
Eleven studies met inclusion criteria: two double-blind, randomized, placebo-controlled trials; one double-blind, randomized, placebo-controlled crossover study; one double-blind, non-randomized, placebo-controlled trial; two non-randomized controlled trials; three retrospective cohort studies; and two open-label, single-arm trials.
Across the studies reviewed, the researchers reported improvements in insulin-like growth factor-1 (IGF-1) levels, fatigue, mood, physical performance, and cognition. Structural and functional neuroimaging changes following rhGH were also reported, including increased cortical thickness and gray matter volume, and improved functional connectivity of somatosensory networks. Symptomatic improvement as well as improvements in objective measures were described among patients who did not meet diagnostic cut-point criteria for GHD.
Conclusion
Evidence suggests that rhGH may confer benefit in a broad range of symptomatic TBI patients, including those with peak growth hormone values in ranges overlapping with normal, healthy controls. Larger, controlled studies are warranted to validate these findings and inform clinical guidelines.
{"title":"Outcomes of recombinant growth hormone therapy in the traumatic brain injury population: A scoping review","authors":"Richard D. Batson , Joshua Z. Goldenberg , Ryan S. Wexler , Traver Wright , Eunisse Chua , Alissya Yuen , Michael Freeman , Tamara L. Wexler , Walter High Jr. , Brent E. Masel , Randall J. Urban , Kevin C.J. Yuen","doi":"10.1016/j.beem.2025.102015","DOIUrl":"10.1016/j.beem.2025.102015","url":null,"abstract":"<div><h3>Background</h3><div>Post-traumatic hypopituitarism (PTHP), including growth hormone deficiency (GHD), is a prevalent and underdiagnosed complication of traumatic brain injury (TBI), resulting in substantial morbidity. Emerging evidence suggests that recombinant human growth hormone (rhGH) therapy may provide benefit for patients with confirmed GHD, and also those with growth hormone insufficiency (GHI), abnormal growth hormone secretion (AGHS), or Brain Injury Associated Fatigue and Altered Cognition (BIAFAC), even when peak growth hormone response to growth hormone stimulation testing is above traditional GHD diagnostic cutoffs in these patients.</div></div><div><h3>Objective</h3><div>To conduct a scoping review evaluating the effects of rhGH in adults with TBI, including those classified as GHD, GHI, AGHS, or BIAFAC, on clinical, functional, and neurobiological outcomes.</div></div><div><h3>Methods</h3><div>A comprehensive search of PubMed/MEDLINE was performed using a peer-reviewed search strategy. Studies were screened in duplicate. Eligible studies included clinical trials, observational studies, and case series, reporting rhGH use in adults with a history of TBI, with or without GHD. Outcomes included quality of life, neuropsychological performance, physical functioning, biochemical markers, and neuroimaging data.</div></div><div><h3>Results</h3><div>Eleven studies met inclusion criteria: two double-blind, randomized, placebo-controlled trials; one double-blind, randomized, placebo-controlled crossover study; one double-blind, non-randomized, placebo-controlled trial; two non-randomized controlled trials; three retrospective cohort studies; and two open-label, single-arm trials.</div><div>Across the studies reviewed, the researchers reported improvements in insulin-like growth factor-1 (IGF-1) levels, fatigue, mood, physical performance, and cognition. Structural and functional neuroimaging changes following rhGH were also reported, including increased cortical thickness and gray matter volume, and improved functional connectivity of somatosensory networks. Symptomatic improvement as well as improvements in objective measures were described among patients who did not meet diagnostic cut-point criteria for GHD.</div></div><div><h3>Conclusion</h3><div>Evidence suggests that rhGH may confer benefit in a broad range of symptomatic TBI patients, including those with peak growth hormone values in ranges overlapping with normal, healthy controls. Larger, controlled studies are warranted to validate these findings and inform clinical guidelines.</div></div>","PeriodicalId":8810,"journal":{"name":"Best practice & research. Clinical endocrinology & metabolism","volume":"39 3","pages":"Article 102015"},"PeriodicalIF":6.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144337338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-01DOI: 10.1016/j.beem.2025.102001
Chiara Mele , Lucrezia De Marchi , Rosa Pitino , Luisa Costantini , Beatrice Cavigiolo , Marina Caputo , Paolo Marzullo , Gianluca Aimaretti
Traumatic brain injury (TBI) is a leading cause of mortality and long-term disability, with its pathophysiology encompassing both primary mechanical damage and secondary neuroinflammatory, metabolic, and biochemical alterations. These complex mechanisms contribute to the observed heterogeneous clinical outcomes, including neuroendocrine dysfunctions, post-traumatic seizures, and disorders of consciousness (DoC). Thyroid hormones (THs) play essential roles in synaptic plasticity, neurogenesis and neuronal homeostasis, and the hypothalamic-pituitary-thyroid (HPT) axis has recently emerged as a potential acute and chronic modulator of neurological and functional recovery following TBI, thereby hinting at the potential involvement of THs in post-TBI outcomes. While evidence suggests that alterations in the HPT axis may influence susceptibility to seizures, progression of DoC, and rehabilitation outcomes, an increased blood-brain barrier permeability in concert with dysregulated deiodinase activity and expanding oxidative stress have all been proposed as mechanisms linking THs to post-TBI neurological complications. This review aims to summarize current evidence on the potential role of the thyrotropic axis in neurological and rehabilitation outcomes following TBI.
{"title":"The interplay between thyrotropic axis, neurological complications, and rehabilitation outcomes in patients with traumatic brain injury","authors":"Chiara Mele , Lucrezia De Marchi , Rosa Pitino , Luisa Costantini , Beatrice Cavigiolo , Marina Caputo , Paolo Marzullo , Gianluca Aimaretti","doi":"10.1016/j.beem.2025.102001","DOIUrl":"10.1016/j.beem.2025.102001","url":null,"abstract":"<div><div>Traumatic brain injury (TBI) is a leading cause of mortality and long-term disability, with its pathophysiology encompassing both primary mechanical damage and secondary neuroinflammatory, metabolic, and biochemical alterations. These complex mechanisms contribute to the observed heterogeneous clinical outcomes, including neuroendocrine dysfunctions, post-traumatic seizures, and disorders of consciousness (DoC). Thyroid hormones (THs) play essential roles in synaptic plasticity, neurogenesis and neuronal homeostasis, and the hypothalamic-pituitary-thyroid (HPT) axis has recently emerged as a potential acute and chronic modulator of neurological and functional recovery following TBI, thereby hinting at the potential involvement of THs in post-TBI outcomes. While evidence suggests that alterations in the HPT axis may influence susceptibility to seizures, progression of DoC, and rehabilitation outcomes, an increased blood-brain barrier permeability in concert with dysregulated deiodinase activity and expanding oxidative stress have all been proposed as mechanisms linking THs to post-TBI neurological complications. This review aims to summarize current evidence on the potential role of the thyrotropic axis in neurological and rehabilitation outcomes following TBI.</div></div>","PeriodicalId":8810,"journal":{"name":"Best practice & research. Clinical endocrinology & metabolism","volume":"39 3","pages":"Article 102001"},"PeriodicalIF":6.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144031997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-01DOI: 10.1016/j.beem.2025.102013
Aydin Sav , Grazia Menna , Carlo Serra , Erdem Söztutar , Uğur Türe
The pituitary gland, historically misconceived as a structure devoted to mucus excretion, has undergone centuries of anatomical and functional reinterpretation. From the ancient humoral theories of Galen to the molecular frameworks of modern embryology, this review offers a comprehensive historical and anatomical overview of the gland. Emphasis is placed on the evolution of terminology, the gland’s dual embryologic origin, intricate vascularization, and topographic organization within the sella turcica. Clarifying historical controversies and integrating developmental, surgical, and neuroendocrine perspectives, this work proposes a harmonized anatomical and terminological framework in accordance with modern neuroanatomical standards. This review aims to clarify the developed vascular structure and histology of the pituitary gland, which is responsible for the complex processes involved in traumatic brain injury (TBI).
{"title":"Anatomy of the pituitary gland","authors":"Aydin Sav , Grazia Menna , Carlo Serra , Erdem Söztutar , Uğur Türe","doi":"10.1016/j.beem.2025.102013","DOIUrl":"10.1016/j.beem.2025.102013","url":null,"abstract":"<div><div>The pituitary gland, historically misconceived as a structure devoted to mucus excretion, has undergone centuries of anatomical and functional reinterpretation. From the ancient humoral theories of Galen to the molecular frameworks of modern embryology, this review offers a comprehensive historical and anatomical overview of the gland. Emphasis is placed on the evolution of terminology, the gland’s dual embryologic origin, intricate vascularization, and topographic organization within the sella turcica. Clarifying historical controversies and integrating developmental, surgical, and neuroendocrine perspectives, this work proposes a harmonized anatomical and terminological framework in accordance with modern neuroanatomical standards. This review aims to clarify the developed vascular structure and histology of the pituitary gland, which is responsible for the complex processes involved in traumatic brain injury (TBI).</div></div>","PeriodicalId":8810,"journal":{"name":"Best practice & research. Clinical endocrinology & metabolism","volume":"39 3","pages":"Article 102013"},"PeriodicalIF":6.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144277034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-01DOI: 10.1016/j.beem.2025.102020
Ulla Feldt-Rasmussen , Marianne Christina Klose
One of the possible clinical complications following traumatic brain injury (TBI) is post-traumatic hypopituitarism. Severe TBI can disrupt the hypothalamus-pituitary-peripheral hormone axes, not only in the acute phase but also over the long term, potentially resulting in persistent pituitary dysfunction. Acute critical illness and its management can alter the normal adaptive response of the hypothalamus-pituitary axis through changes in metabolism, hormone binding, and hormone production. In the context of TBI, structural brain damage may further impair hypothalamus-pituitary function by directly disrupting its anatomical integrity. Diagnosing pituitary hormone imbalances in the acute phase after TBI is challenging, and the clinical significance remains debatable. However, adrenal insufficiency and ADH deficiency poses a life-threatening risk if left untreated and requires prompt intervention. Practical points are provided on how to recognize, avoid, and manage both over- and underdiagnosis of hypopituitarism in patients with TBI.
{"title":"Pathophysiology and diagnosis of neuroendocrine abnormalities in patients with traumatic brain injury","authors":"Ulla Feldt-Rasmussen , Marianne Christina Klose","doi":"10.1016/j.beem.2025.102020","DOIUrl":"10.1016/j.beem.2025.102020","url":null,"abstract":"<div><div>One of the possible clinical complications following traumatic brain injury (TBI) is post-traumatic hypopituitarism. Severe TBI can disrupt the hypothalamus-pituitary-peripheral hormone axes, not only in the acute phase but also over the long term, potentially resulting in persistent pituitary dysfunction. Acute critical illness and its management can alter the normal adaptive response of the hypothalamus-pituitary axis through changes in metabolism, hormone binding, and hormone production. In the context of TBI, structural brain damage may further impair hypothalamus-pituitary function by directly disrupting its anatomical integrity. Diagnosing pituitary hormone imbalances in the acute phase after TBI is challenging, and the clinical significance remains debatable. However, adrenal insufficiency and ADH deficiency poses a life-threatening risk if left untreated and requires prompt intervention. Practical points are provided on how to recognize, avoid, and manage both over- and underdiagnosis of hypopituitarism in patients with TBI.</div></div>","PeriodicalId":8810,"journal":{"name":"Best practice & research. Clinical endocrinology & metabolism","volume":"39 3","pages":"Article 102020"},"PeriodicalIF":6.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144518673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-01DOI: 10.1016/j.beem.2025.102006
Shumaila Hasan , Chris Uff
Traumatic brain injury (TBI) is not a singular event with finite boundaries, but a complex and evolving pathology. While the initial mechanical insult may be fleeting, its consequences can ripple across physiological systems for months or years. One of the most underappreciated yet clinically significant consequences is the disruption of the hypothalamic-pituitary axis (HPA). Neuroendocrine dysfunction after TBI can present in various forms—some subtle, others life-altering—affecting metabolic regulation, sexual health, psychological wellbeing, and rehabilitation potential. This review explores the pathophysiology and clinical implications of HPA dysfunction in TBI, highlighting current gaps in diagnosis and proposing an approach that recognises the chronic nature of these sequelae.
{"title":"Neuroendocrine dysfunction following traumatic brain injury: Current insights and emerging perspectives","authors":"Shumaila Hasan , Chris Uff","doi":"10.1016/j.beem.2025.102006","DOIUrl":"10.1016/j.beem.2025.102006","url":null,"abstract":"<div><div>Traumatic brain injury (TBI) is not a singular event with finite boundaries, but a complex and evolving pathology. While the initial mechanical insult may be fleeting, its consequences can ripple across physiological systems for months or years. One of the most underappreciated yet clinically significant consequences is the disruption of the hypothalamic-pituitary axis (HPA). Neuroendocrine dysfunction after TBI can present in various forms—some subtle, others life-altering—affecting metabolic regulation, sexual health, psychological wellbeing, and rehabilitation potential. This review explores the pathophysiology and clinical implications of HPA dysfunction in TBI, highlighting current gaps in diagnosis and proposing an approach that recognises the chronic nature of these sequelae.</div></div>","PeriodicalId":8810,"journal":{"name":"Best practice & research. Clinical endocrinology & metabolism","volume":"39 3","pages":"Article 102006"},"PeriodicalIF":6.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144217811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-05-01DOI: 10.1016/j.beem.2025.101997
Kursad Unluhizarci, Emre Urhan
During the last two decades traumatic brain injury (TBI) was also found as an important cause of hypopituitarism. Although the most common causes of TBI are traffic accidents and falls, others such as blast-related injuries, acts of violence and combative sports are also considered in the etiology. TBI may lead to transient or permanent pituitary dysfunction. The definition of TBI-induced hypopituitarism cover alterations in pituitary hormone levels which may occur even after five years of injury and characterised by hormonal deficiencies but rarely recovery of some hormones during the course of the disease. It has been shown that between 5 % and 70 % of the TBI patients suffer from hypopituitarism. This large variation in the prevalence may be explained by diverse diagnostic criteria used in different studies, different time points of interventions after TBI, severity of trauma etc. Patients with advanced age, low Glasgow Coma Scale, needing intensive care unit stay, presence of skull fractures, brain edema are particularly make patients vulnerable to TBI-induced hypopituitarism.
{"title":"Epidemiology and risk factors for hypopituitarism due to traumatic brain injury","authors":"Kursad Unluhizarci, Emre Urhan","doi":"10.1016/j.beem.2025.101997","DOIUrl":"10.1016/j.beem.2025.101997","url":null,"abstract":"<div><div>During the last two decades traumatic brain injury (TBI) was also found as an important cause of hypopituitarism. Although the most common causes of TBI are traffic accidents and falls, others such as blast-related injuries, acts of violence and combative sports are also considered in the etiology. TBI may lead to transient or permanent pituitary dysfunction. The definition of TBI-induced hypopituitarism cover alterations in pituitary hormone levels which may occur even after five years of injury and characterised by hormonal deficiencies but rarely recovery of some hormones during the course of the disease. It has been shown that between 5 % and 70 % of the TBI patients suffer from hypopituitarism. This large variation in the prevalence may be explained by diverse diagnostic criteria used in different studies, different time points of interventions after TBI, severity of trauma etc. Patients with advanced age, low Glasgow Coma Scale, needing intensive care unit stay, presence of skull fractures, brain edema are particularly make patients vulnerable to TBI-induced hypopituitarism.</div></div>","PeriodicalId":8810,"journal":{"name":"Best practice & research. Clinical endocrinology & metabolism","volume":"39 3","pages":"Article 101997"},"PeriodicalIF":6.1,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144062872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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