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Daniel F Kelly - One of the best experts on this subject based on the ideXlab platform.

  • american association of clinical endocrinologists and american college of endocrinology disease state clinical review a neuroendocrine approach to patients with traumatic brain injury
    Endocrine Practice, 2015
    Co-Authors: Nicholas A Tritos, Kevin C J Yuen, Daniel F Kelly
    Abstract:

    ABSTRACT Objective: Traumatic brain injury (TBI) is now recognized as a major public health concern in the United States and is associated with substantial morbidity and mortality in both children and adults. Several lines of evidence indicate that TBI-induced Hypopituitarism is not infrequent in TBI survivors and may contribute to the burden of illness in this population. The goal of this article is to review the published data and propose an approach for the neuroendocrine evaluation and management of these patients. Methods: To identify pertinent articles, electronic literature searches were conducted using the following keywords: “traumatic brain injury,” “pituitary,” “Hypopituitarism,” “growth hormone deficiency,” “hypogonadism,” “hypoadrenalism,” and “hypothyroidism.” Relevant articles were identified and considered for inclusion in the present article. Results: TBI-induced Hypopituitarism appears to be more common in patients with severe TBI. However, patients with mild TBI or those with repeated, ...

  • pituitary hormonal loss and recovery after transsphenoidal adenoma removal
    Neurosurgery, 2008
    Co-Authors: Nasrin Fatemi, Joshua R Dusick, Carlos A Mattozo, David L Mcarthur, Pejman Cohan, John Boscardin, Christina Wang, Ronald S Swerdloff, Daniel F Kelly
    Abstract:

    OBJECTIVE: Transsphenoidal adenomectomy carries the possibility of new pituitary failure and recovery. Herein, we present rates and determinants of postoperative hormonal status. METHODS: All consecutive patients who underwent endonasal transsphenoidal adenoma removal over an 8-year period were analyzed. Those with previous sellar radiotherapy were excluded. Pre- and postoperative hormonal status (at least 3 mo after surgery) were determined and correlated with clinical parameters using a multivariate statistical model. RESULTS: Of 444 patients (median age 45 years, 75% macroadenoma, 19% with multiple operations), 9 had preoperative panHypopituitarism. Of the remaining 435 patients, new Hypopituitarism occurred in 5.5% of patients (anterior loss in 5%; permanent diabetes insipidus in 2.1%; including 2 patients who had total hypophysectomy). Of 346 patients with preoperative hormonal dysfunction, 170 (49%) had improved function. "Stalk compression" hyperprolactinemia resolved in 73% of 133 patients; recovery of at least 1 other anterior axis (excluding isolated hypogonadism associated with "stalk compression" hyperprolactinemia) occurred in 24% of 209 patients. Multivariate analysis showed that new Hypopituitarism was most strongly associated with larger tumor diameter (P = 0.04). Of 223 patients with an endocrine-inactive adenoma, new Hypopituitarism was seen in 0, 7.2, and 13.6% of patients with tumor diameters of <20, 20 to 29, and ≥30 mm, respectively (P = 0.005). Multivariate analysis revealed that resolution of Hypopituitarism was related to younger age (39 versus 52 years, P < 0.0001), absence of an intraoperative cerebrospinal fluid leak and, in patients with an endocrine-inactive adenoma, absence of systemic hypertension (24% versus 6%, P = 0.009). CONCLUSION: After transsphenoidal adenomectomy, new unplanned Hypopituitarism occurs in approximately 5% of patients, whereas improved hormonal function occurs in 50% of patients. The likelihood of new hormonal loss or recovery appears to depend on several factors. New Hypopituitarism occurs most commonly in patients with tumors larger than 20 mm in size, whereas hormonal recovery is most likely to occur in younger, nonhypertensive patients and those without an intraoperative cerebrospinal fluid leak.

  • pituitary hormonal loss and recovery after transsphenoidal adenoma removal
    Neurosurgery, 2008
    Co-Authors: Nasrin Fatemi, Joshua R Dusick, Carlos A Mattozo, David L Mcarthur, Pejman Cohan, John Boscardin, Christina Wang, Ronald S Swerdloff, Daniel F Kelly
    Abstract:

    OBJECTIVE: Transsphenoidal adenomectomy carries the possibility of new pituitary failure and recovery. Herein, we present rates and determinants of postoperative hormonal status. METHODS: All consecutive patients who underwent endonasal transsphenoidal adenoma removal over an 8-year period were analyzed. Those with previous sellar radiotherapy were excluded. Pre- and postoperative hormonal status (at least 3 mo after surgery) were determined and correlated with clinical parameters using a multivariate statistical model. RESULTS: Of 444 patients (median age 45 years, 75% macroadenoma, 19% with multiple operations), 9 had preoperative panHypopituitarism. Of the remaining 435 patients, new Hypopituitarism occurred in 5.5% of patients (anterior loss in 5%; permanent diabetes insipidus in 2.1%; including 2 patients who had total hypophysectomy). Of 346 patients with preoperative hormonal dysfunction, 170 (49%) had improved function. "Stalk compression" hyperprolactinemia resolved in 73% of 133 patients; recovery of at least 1 other anterior axis (excluding isolated hypogonadism associated with "stalk compression" hyperprolactinemia) occurred in 24% of 209 patients. Multivariate analysis showed that new Hypopituitarism was most strongly associated with larger tumor diameter (P = 0.04). Of 223 patients with an endocrine-inactive adenoma, new Hypopituitarism was seen in 0, 7.2, and 13.6% of patients with tumor diameters of <20, 20 to 29, and ≥30 mm, respectively (P = 0.005). Multivariate analysis revealed that resolution of Hypopituitarism was related to younger age (39 versus 52 years, P < 0.0001), absence of an intraoperative cerebrospinal fluid leak and, in patients with an endocrine-inactive adenoma, absence of systemic hypertension (24% versus 6%, P = 0.009). CONCLUSION: After transsphenoidal adenomectomy, new unplanned Hypopituitarism occurs in approximately 5% of patients, whereas improved hormonal function occurs in 50% of patients. The likelihood of new hormonal loss or recovery appears to depend on several factors. New Hypopituitarism occurs most commonly in patients with tumors larger than 20 mm in size, whereas hormonal recovery is most likely to occur in younger, nonhypertensive patients and those without an intraoperative cerebrospinal fluid leak.

Felipe F Casanueva - One of the best experts on this subject based on the ideXlab platform.

  • Hypopituitarism after traumatic brain injury
    Endocrinology and Metabolism Clinics of North America, 2015
    Co-Authors: E Fernandezrodriguez, Felipe F Casanueva, Ignacio Bernabeu, Ana I Castro
    Abstract:

    The prevalence of Hypopituitarism after traumatic brain (TBI) injury is widely variable in the literature; a meta-analysis determined a pooled prevalence of anterior Hypopituitarism of 27.5%. Growth hormone deficiency is the most prevalent hormone insufficiency after TBI; however, the prevalence of each type of pituitary deficiency is influenced by the assays used for diagnosis, severity of head trauma, and time of evaluation. Recent studies have demonstrated improvement in cognitive function and cognitive quality of life with substitution therapy in GH-deficient patients after TBI.

  • manifesto for the current understanding and management of traumatic brain injury induced Hypopituitarism
    Journal of Endocrinological Investigation, 2011
    Co-Authors: Fatih Tanriverdi, Gianluca Aimaretti, Alberto M Pereira, A Agha, Felipe F Casanueva, Fahrettin Kelestimur, M Klose, Brent E Masel, Vesna Popovic, H J Schneider
    Abstract:

    Traumatic brain injury (TBI)-induced Hypopituitarism remains a relevant medical problem, because it may affect a significant proportion of the population. In the last decade important studies have been published investigating pituitary dysfunction after TBI. Recently, a group of experts gathered and revisited the topic of TBI-induced Hypopituitarism. During the 2-day meeting, the main issues of this topic were presented and discussed, and current understanding and management of TBI-induced Hypopituitarism are summarized here.

  • antipituitary antibodies after traumatic brain injury is head trauma induced pituitary dysfunction associated with autoimmunity
    European Journal of Endocrinology, 2008
    Co-Authors: Fatih Tanriverdi, A A Sinisi, Elena Pane, Giuseppe Bellastella, Annamaria De Bellis, Antonio Bizzarro, Antonio Bellastella, Kursad Unluhizarci, Ahmet Selcuklu, Felipe F Casanueva
    Abstract:

    Objective: Traumatic brain injury (TBI) is a devastating public health problem that may result in Hypopituitarism. However, the mechanisms responsible for hypothalamic–pituitary dysfunction due to TBI are still unclear. Although the antibodies against neurons have been demonstrated in injured animal studies, investigations regarding the occurrence of antipituitary antibodies (APAs) in patients with TBI are lacking in the literature. In order to investigate whether autoimmune mechanisms could play a role in the pituitary dysfunction after TBI, we have planned this study aimed at investigating the presence of APA at the third year of TBI and association between the TBI-induced Hypopituitarism and APA. Patients and design: Twenty-nine (25 males and 4 females; age 36.5G2.3 years) patients who had completed a 3-year follow-up after TBI were included in the present study. APA and pituitary function were evaluated in all the patients 3 years after TBI; moreover, APAs were tested also in sera of 60 age-/sexmatched normal controls. The APAs were investigated by an indirect immunofluorescence method. Results: APAs were detected in 13 out of the 29 TBI patients (44.8%), but in none of the normal controls. Pituitary dysfunction development ratio was significantly higher in APA-positive patients (46.2%) when compared with APA-negative ones (12.5%; PZ0.04). There was a significant association between APA positivity and Hypopituitarism due to TBI (odds ratio: 2.25, 95% confidence intervals 1.1–4.6). Moreover, there was a significant positive correlation (rZ0.74, PZ0.004) between APA titer ratio and peak GH response to GHRHCGH related peptide (GHRP)-6 test, suggesting that high APA titers were associated with low GH response to GHRHCGHRP-6 test. Conclusions: This study shows for the first time the presence of the APA in TBI patients 3 years after head trauma. Moreover, present investigation indicates preliminary evidence that APA may be associated with the development of TBI-induced pituitary dysfunction, thus suggesting that autoimmunity may contribute in the development of TBI-induced Hypopituitarism. The presence of the association between APA and TBIinduced Hypopituitarism may provide a new point of view in this field and promote further clinical and experimental studies.

  • Hypopituitarism following traumatic brain injury
    Growth Hormone & Igf Research, 2005
    Co-Authors: Vera Popovic, Gianluca Aimaretti, Felipe F Casanueva, Ezio Ghigo
    Abstract:

    Recent studies have demonstrated that Hypopituitarism, and in particular growth hormone (GH) deficiency, is common among survivors of traumatic brain injury (TBI) tested several months or years following head trauma. In addition, it has been shown that post-traumatic neuroendocrine abnormalities occur early and with high frequency. These findings may have significant implications for the recovery and rehabilitation of patients with TBI. Although data emerging after 2000 demonstrate the relevance of the problem, in general there is a lack of awareness in the medical community about the incidence and clinical repercussions of the pathology. Most, but not all, head trauma associated with Hypopituitarism is the result of motor accidents. The subjects at risk are those who have suffered moderate-to severe head trauma although mild intensity trauma may precede Hypopituitarism also. Particular attention should be paid to this problem in children and adolescents. Onset of pituitary deficits can evolve over years following injury. For the assessment of the GH-IGF axis in TBI patients, plasma IGF-I concentrations, plus dynamic GH testing is indicated. Some degree of Hypopituitarism is found in 35-40% of TBI patients. Among multiple pituitary deficits, the most common ones were GHD and gonadotrophin deficiency. In most series 10-15% presented with severe GHD and 15% with partial GHD after stimulating GH secretion confirming that the most common isolated deficit is GHD. Psychometric evaluation together with neurocognitive testing shows variability of disability and the possibility that untreated TBI induced Hypopituitarism contributes to the chronic neurobehavioral problems seen in many head-injured patients warrants consideration. Preliminary data, from small pilot, open-label studies show that subjects treated with GH experience significant improvements in concentration, memory, depression, anxiety and fatigue. In conclusion, pituitary failure can occur even in minor head injuries and is poorly recognized.

Mehul T Dattani - One of the best experts on this subject based on the ideXlab platform.

  • genetic aspects of hypothalamic and pituitary gland development
    Handbook of Clinical Neurology, 2014
    Co-Authors: Mark J Mccabe, Mehul T Dattani
    Abstract:

    Hypothalamo-pituitary development during embryogenesis is a highly complex process involving the interaction of a network of spatiotemporally regulated signaling molecules and transcription factors. Mutations in any of the genes encoding these components can lead to congenital Hypopituitarism, which is often associated with a wide spectrum of defects affecting craniofacial/midline development. In turn, these defects can be incompatible with life, or lead to disorders encompassing holoprosencephaly (HPE) and cleft palate, and septo-optic dysplasia (SOD). In recent years, there has been increasing evidence of an overlapping genotype between this spectrum of disorders and Kallmann syndrome (KS), defined as the association of hypogonadotropic hypogonadism (HH) and anosmia. This is consistent with the known phenotypic overlap between these disorders and opens a new avenue of identifying novel genetic causes of the Hypopituitarism spectrum. This chapter reviews the genetic and molecular events leading to the successful development of the hypothalamo-pituitary axis during embryogenesis, and focuses on genes in which variations/mutations occur, leading to congenital Hypopituitarism and associated defects.

  • genetic regulation of pituitary gland development in human and mouse
    Endocrine Reviews, 2009
    Co-Authors: Daniel Kelberman, Karine Rizzoti, Robin Lovellbadge, Iain C A F Robinson, Mehul T Dattani
    Abstract:

    Normal hypothalamopituitary development is closely related to that of the forebrain and is dependent upon a complex genetic cascade of transcription factors and signaling molecules that may be either intrinsic or extrinsic to the developing Rathke’s pouch. These factors dictate organ commitment, cell differentiation, and cell proliferation within the anterior pituitary. Abnormalities in these processes are associated with congenital Hypopituitarism, a spectrum of disorders that includes syndromic disorders such as septo-optic dysplasia, combined pituitary hormone deficiencies, and isolated hormone deficiencies, of which the commonest is GH deficiency. The highly variable clinical phenotypes can now in part be explained due to research performed over the last 20 yr, based mainly on naturally occurring and transgenic animal models. Mutations in genes encoding both signaling molecules and transcription factors have been implicated in the etiology of Hypopituitarism, with or without other syndromic features, in mice and humans. To date, mutations in known genes account for a small proportion of cases of Hypopituitarism in humans. However, these mutations have led to a greater understanding of the genetic interactions that lead to normal pituitary development. This review attempts to describe the complexity of pituitary development in the rodent, with particular emphasis on those factors that, when mutated, are associated with Hypopituitarism in humans.

  • genetic forms of Hypopituitarism and their manifestation in the neonatal period
    Early Human Development, 2009
    Co-Authors: Kyriaki S Alatzoglou, Mehul T Dattani
    Abstract:

    The anterior pituitary gland is a central regulator of growth, reproduction and homeostasis. The development of the pituitary gland depends on the sequential temporal and spatial expression of transcription factors and signalling molecules. Naturally occurring and transgenic murine models have demonstrated a role for many of these molecules in the aetiology of congenital Hypopituitarism. These include the transcription factors HESX1, PROP1, POU1F1, LHX3, LHX4, PITX1, PITX2, OTX2, SOX2 and SOX3. Mutations in any of the genes involved in pituitary development may result in congenital Hypopituitarism, which manifests as the deficiency in one or more pituitary hormones. The phenotype can be highly variable and may consist of isolated Hypopituitarism, or more complex disorders such as septo-optic dysplasia (SOD) and holoprosencephaly. Neonates with congenital Hypopituitarism may present with non-specific symptoms, with or without associated developmental defects such as ocular, midline and genital abnormalities. Alternatively, they may be initially asymptomatic but at risk of developing pituitary hormone deficiencies over time. The overall incidence of mutations in known transcription factors in patients with Hypopituitarism is low, indicating that many genes remain to be identified. Their characterization will further elucidate the pathogenesis of this complex condition and will shed light on normal pituitary development.

  • congenital Hypopituitarism clinical molecular and neuroradiological correlates
    Clinical Endocrinology, 2009
    Co-Authors: Ameeta Mehta, James P. G. Turton, Peter C Hindmarsh, Hiten Mehta, Isabelle Russelleggitt, David Taylor, W K Chong, Mehul T Dattani
    Abstract:

    ObjectiveRecent studies have suggested that mutations in genes encoding several hypothalamo-pituitary (H-P) transcription factors result in Hypopituitarism [isolated GH deficiency (IGHD) and combined pituitary hormone deficiency (CPHD)], which may in turn be related to the neuroanatomy revealed by magnetic resonance (MR) imaging. Although studies have focused on patients with either optic nerve hypoplasia (ONH) or isolated Hypopituitarism with normal optic nerves, few studies have compared the two groups. We aimed to relate the clinical phenotype of a large cohort (n = 170) of children with congenital Hypopituitarism including septo-optic dysplasia (SOD) attending a single centre to the neuroradiological and genetic findings.DesignClinical, biochemical, MR imaging and molecular data were analysed retrospectively in 170 patients with or 'at-risk' (with ONH) of Hypopituitarism to determine predictors of Hypopituitarism.ResultsThe presence of ONH was significantly associated with an absent septum pellucidum [odds ratio (OR) 31 center dot 5, 95% confidence intervals (CI) 7 center dot 3-136 center dot 6, P < 0 center dot 001], an abnormal corpus callosum (OR 10 center dot 5, 95% CI 3 center dot 8-28 center dot 6, P < 0 center dot 001) and stalk abnormalities (OR 2 center dot 3, 95% CI 1 center dot 2-4 center dot 2, P = 0 center dot 009). The risk of Hypopituitarism was 27 center dot 2 times greater in patients with an undescended posterior pituitary (95% CI 3 center dot 6-205 center dot 1, P < 0 center dot 001). Anterior pituitary hypoplasia (OR 3 center dot 1, 95% CI 1 center dot 3-7 center dot 0, P = 0 center dot 006) and an absent pituitary stalk (P < 0 center dot 001) were also significantly associated with Hypopituitarism. With respect to the type or severity of Hypopituitarism, CPHD was more often associated with an abnormal corpus callosum (OR 6 center dot 1, 95% CI 1 center dot 4-27 center dot 4, P = 0 center dot 008) and stalk abnormalities (OR 2 center dot 8, 95% CI 1 center dot 3-6 center dot 1, P = 0 center dot 006). Male to female ratio was significantly greater in patients with normal optic nerves (3 center dot 3:1) as compared with those with ONH (1 center dot 2:1). The prevalence of diabetes insipidus, thyrotrophin and ACTH deficiencies was significantly greater in patients with ONH as compared with 'idiopathic' Hypopituitarism. Mutations in pituitary transcription factors and genes regulating GH secretion were rare (5/170) in this cohort of patients with sporadic Hypopituitarism.ConclusionOur data suggest that individuals presenting with ONH are at high risk for neuroradiologic and endocrine abnormalities. The neuroradiologic features are predictive not only of the presence, but also of the type, of Hypopituitarism. The association of midline abnormalities with Hypopituitarism in this cohort suggests a common developmental origin for these features, the aetiology of which remains unidentified in the majority of cases.

  • Hypopituitarism oddities congenital causes
    Hormone Research in Paediatrics, 2007
    Co-Authors: Daniel Kelberman, Mehul T Dattani
    Abstract:

    Background: The last 15 years have witnessed an explosion in our knowledge of hypothalamo-pituitary development, acquired mainly from naturally-occurring and transgenic animal model

B Saller - One of the best experts on this subject based on the ideXlab platform.

  • structured assessment of Hypopituitarism after traumatic brain injury and aneurysmal subarachnoid hemorrhage in 1242 patients the german interdisciplinary database
    Journal of Neurotrauma, 2011
    Co-Authors: Harald Schneider, Anna Kopczak, M Schneider, Ilonka Kreitschmannandermahr, Ulrich Tuschy, Henri Wallaschofski, Steffen Fleck, Michael Faust, C Renner, B Saller
    Abstract:

    Abstract Clinical studies have demonstrated that traumatic brain injury (TBI) and aneurysmal subarachnoid hemorrhage (SAH) are frequent causes of long-term disturbances of hypothalamo-pituitary function. This study aimed to assess the prevalence and associated factors of post-traumatic Hypopituitarism in a large national registry of patients with TBI and SAH. Data were collected from 14 centers in Germany and Austria treating patients for TBI or SAH and performing endocrine assessments. Data were collected using a structured, internet-based study sheet, obtaining information on clinical, radiological, and hormonal parameters. A total of 1242 patients (825 TBI, age 43.5±19.7 years; 417 SAH, age 49.7±11.8 years) were included. We studied the prevalence of Hypopituitarism reported based on different definitions of laboratory values and stimulation tests. Stimulation tests for the corticotropic and somatotropic axes were performed in 26% and 22% of the patients, respectively. The prevalence of Hypopituitarism...

  • predictors of anterior pituitary insufficiency after traumatic brain injury
    Clinical Endocrinology, 2007
    Co-Authors: M Schneider, H J Schneider, Alexander Yassouridis, B Saller, F Von Rosen, G K Stalla
    Abstract:

    BACKGROUND Several studies have reported a high prevalence of Hypopituitarism after traumatic brain injury (TBI). Risk stratification is a prerequisite for cost-effective hormonal screening of these patients. However, it is still unclear which risk factors predispose patients to develop anterior Hypopituitarism after TBI. OBJECTIVE To assess clinical and radiological risk factors for post-traumatic Hypopituitarism. PATIENTS AND METHODS Seventy-eight consecutive patients (52 men, 26 women; mean age 36.0 years, range 18-65 years) with mild, moderate or severe TBI were studied. Endocrine and clinical parameters were assessed 3 and 12 months after TBI. RESULTS We found diffuse axonal injury, basal skull fracture and older age to be major risk factors of post-traumatic Hypopituitarism. CONCLUSIONS We have defined specific risk factors for the development of post-traumatic Hypopituitarism that are consistent with pathophysiological considerations. These findings might help to identify at-risk patients.

Gianluca Aimaretti - One of the best experts on this subject based on the ideXlab platform.

  • manifesto for the current understanding and management of traumatic brain injury induced Hypopituitarism
    Journal of Endocrinological Investigation, 2011
    Co-Authors: Fatih Tanriverdi, Gianluca Aimaretti, Alberto M Pereira, A Agha, Felipe F Casanueva, Fahrettin Kelestimur, M Klose, Brent E Masel, Vesna Popovic, H J Schneider
    Abstract:

    Traumatic brain injury (TBI)-induced Hypopituitarism remains a relevant medical problem, because it may affect a significant proportion of the population. In the last decade important studies have been published investigating pituitary dysfunction after TBI. Recently, a group of experts gathered and revisited the topic of TBI-induced Hypopituitarism. During the 2-day meeting, the main issues of this topic were presented and discussed, and current understanding and management of TBI-induced Hypopituitarism are summarized here.

  • pituitary imaging abnormalities in patients with and without Hypopituitarism after traumatic brain injury
    Journal of Endocrinological Investigation, 2007
    Co-Authors: H J Schneider, M Schneider, G K Stalla, Philipp G Samann, Chiara Giulia Croce, G Corneli, C Sievers, Ezio Ghigo, Gianluca Aimaretti
    Abstract:

    Recent evidence suggests that patients with traumatic brain injury (TBI) are at substantial risk of Hypopituitarism. The pathomechanisms, however, are not completely understood yet. Little is known about the association of morphological changes in the sella region with pituitary function in TBI. In this study, we assessed morphological abnormalities of the sella region in patients with TBI and their relation to endocrine function. We studied magnetic resonance (MR) or computed tomography (CT) scans of 22 patients with TBI [17 men, 5 women, age (mean+/-SD) 43.5+/-10.6 yr, time after trauma 17.4 +/-15.0 yr]. Of these, 15 patients had some degree of Hypopituitarism. We found abnormalities of the sella region in 80% of the patients with Hypopituitarism and 29% of those without Hypopituitarism (Fisher's exact test, p=0.032). The most common abnormality was loss of volume or empty sella, followed by native signal inhomogeneities, perfusion deficit, and lack of neurohypophyseal signal. Our results indicate that pituitary imaging abnormalities are more common in TBI patients with Hypopituitarism than those without. Both immediate trauma-induced pathology as necrosis and hemorrhage as well as multifactorial mid- to long-term changes may underlie these abnormalities.

  • residual pituitary function after brain injury induced Hypopituitarism a prospective 12 month study
    The Journal of Clinical Endocrinology and Metabolism, 2005
    Co-Authors: Gianluca Aimaretti, Maria Rosaria Ambrosio, Carolina Di Somma, M Gasperi, Salvatore Cannavo, Carla Scaroni, Alessandra Fusco, Patrizia Del Monte, Ernesto De Menis, Marco Faustinifustini
    Abstract:

    Context: Traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH) are conditions at high risk for the development of Hypopituitarism. Objective: The objective of the study was to clarify whether pituitary deficiencies and normal pituitary function recorded at 3 months would improve or worsen at 12 months after the brain injury. Design and Patients: Pituitary function was tested at 3 and 12 months in patients who had TBI (n = 70) or SAH (n = 32). Results: In TBI, the 3-month evaluation had shown Hypopituitarism (H) in 32.8%. PanHypopituitarism (PH), multiple (MH), and isolated (IH) Hypopituitarism had been demonstrated in 5.7, 5.7, and 21.4%, respectively. The retesting demonstrated some degree of H in 22.7%. PH, MH, and IH were present in 5.7, 4.2, and 12.8%, respectively. PH was always confirmed at 12 months, whereas MH and IH were confirmed in 25% only. In 5.5% of TBI with no deficit at 3 months, IH was recorded at retesting. In 13.3% of TBI with IH at 3 months, MH was demonstrated at 12-month ret...

  • Hypopituitarism following traumatic brain injury
    Growth Hormone & Igf Research, 2005
    Co-Authors: Vera Popovic, Gianluca Aimaretti, Felipe F Casanueva, Ezio Ghigo
    Abstract:

    Recent studies have demonstrated that Hypopituitarism, and in particular growth hormone (GH) deficiency, is common among survivors of traumatic brain injury (TBI) tested several months or years following head trauma. In addition, it has been shown that post-traumatic neuroendocrine abnormalities occur early and with high frequency. These findings may have significant implications for the recovery and rehabilitation of patients with TBI. Although data emerging after 2000 demonstrate the relevance of the problem, in general there is a lack of awareness in the medical community about the incidence and clinical repercussions of the pathology. Most, but not all, head trauma associated with Hypopituitarism is the result of motor accidents. The subjects at risk are those who have suffered moderate-to severe head trauma although mild intensity trauma may precede Hypopituitarism also. Particular attention should be paid to this problem in children and adolescents. Onset of pituitary deficits can evolve over years following injury. For the assessment of the GH-IGF axis in TBI patients, plasma IGF-I concentrations, plus dynamic GH testing is indicated. Some degree of Hypopituitarism is found in 35-40% of TBI patients. Among multiple pituitary deficits, the most common ones were GHD and gonadotrophin deficiency. In most series 10-15% presented with severe GHD and 15% with partial GHD after stimulating GH secretion confirming that the most common isolated deficit is GHD. Psychometric evaluation together with neurocognitive testing shows variability of disability and the possibility that untreated TBI induced Hypopituitarism contributes to the chronic neurobehavioral problems seen in many head-injured patients warrants consideration. Preliminary data, from small pilot, open-label studies show that subjects treated with GH experience significant improvements in concentration, memory, depression, anxiety and fatigue. In conclusion, pituitary failure can occur even in minor head injuries and is poorly recognized.

  • traumatic brain injury and subarachnoid haemorrhage are conditions at high risk for Hypopituitarism screening study at 3 months after the brain injury
    Clinical Endocrinology, 2004
    Co-Authors: Gianluca Aimaretti, Maria Rosaria Ambrosio, Carolina Di Somma, M Gasperi, Salvatore Cannavo, Carla Scaroni, Alessandra Fusco, Laura De Marinis, Salvatore Benvenga, Ettore Degli Uberti
    Abstract:

    Summary objective  Acquired Hypopituitarism in adults is obviously suspected in patients with primary hypothalamic–pituitary diseases, particularly after neurosurgery and/or radiotherapy. That brain injuries (BI) can cause Hypopituitarism is commonly stated and has been recently emphasized but the management of BI patients does not routinely include neuroendocrine evaluations. aim  To clarify the occurrence of Hypopituitarism in patients after traumatic brain injury (TBI) or subarachnoid haemorrhage (SAH) 3 months after the BI. subjects and methods  The occurrence of Hypopituitarism in conscious patients after traumatic brain injury [TBI, n = 100, 31 women, 69 men; age 37·1 ± 1·8 years; body mass index (BMI) 23·7 ± 0·4 kg/m2; Glasgow Coma Scale (GCS) 3–15] or subarachnoid haemorrhage [SAH, n = 40, 14 men, 26 wpmen, 51·0 ± 2·0 years; 25·0 ± 0·6 kg/m2; Fisher's scale 1–4] was studied in a multicentre study 3 months after the BI. All patients underwent wide basal hormonal evaluation; the GH/IGF-I axis was evaluated by GHRH + arginine test and IGF-I measurement. results  In TBI patients, some degree of Hypopituitarism was shown in 35%. Total, multiple and isolated deficits were present in 4, 6 and 25%, respectively. Diabetes insipidus was present in 4%. Secondary adrenal, thyroid and gonadal deficit was present in 8, 5 and 17%, respectively. Severe GH deficiency (GHD) was the most frequent pituitary defect (25%). In SAH patients, some degree of Hypopituitarism was shown in 37·5%. Despite no total Hypopituitarism, multiple and isolated deficits were present in 10 and 27·5%, respectively. Diabetes insipidus was present in 7·5%. Secondary adrenal, thyroid and gonadal deficit was present in 2·5, 7·5 and 12·5%, respectively. Severe GHD was the most frequent defect (25%). conclusions  TBI and SAH are conditions associated with high risk of acquired Hypopituitarism. The pituitary defect is often multiple and severe GHD is the most frequent defect. Thus neuroendocrine evaluations are always mandatory in patients after brain injuries.