Following brain trauma, copeptin, a stable peptide derived from the AVP precusor, does not reflect osmoregulation but correlates with injury severity (original) (raw)
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Arquivos de Neuro-Psiquiatria, 2007
BACKGROUND: Disorders of water and sodium balance are frequently seen in patients with severe brain injury (SBI), and may worsen their prognosis. PURPOSE: To evaluate vasopressin (AVP) serum levels and sodium and water balance disorders during the first week post-injury in patients with SBI. METHOD: Thirty-six adult patients with SBI (admission Glasgow Coma Scale score < 8) and an estimated time of injury < 72 hours were prospectively studied. Clinical and laboratory data were recorded and AVP was measured in venous blood samples collected on the 1st, 2nd, 3rd and 5th days following inclusion. RESULTS: AVP serum levels remained within the normal range in SBI patients (either traumatic or non-traumatic), although tended to be greater in non-survivor than in survivor patients (p=0.025 at 3rd day). In-hospital mortality was 43% (15/36), and serum sodium and plasma osmolality variabilities were greater in non-survivor than in survivor patients during the observation period (p<0...
Biomarkers in Medicine, 2018
Aim: To investigate the copeptin prognostic role in mild head trauma. Methods: We enrolled 105 adult patients who entered the emergency room because of recent mild head trauma; we evaluated: clinical picture, imaging and laboratory data (including copeptin). Results: Copeptin resulted higher in mild head trauma patients compared with controls: 29.89 pmol/l versus 7.05 pmol/l (p = 0.0008). Copeptin failed in identifying patients with or without brain lesions detected by CT scan, and patients with or without adverse events during the 30 days follow-up. Conclusion: We confirmed that mild head trauma patients have a significantly higher copeptin plasma levels compared with controls. Nevertheless, we did not observe a significant role for copeptin in traumatic brain injury patients regarding brain damage and outcome.
Endocrine consequences of traumatic brain injury. Literature review
Romanian Journal of Legal Medicine, 2016
Traumatic brain injury (TBI) is associated with increased mortality and morbidity, as well as high rates of longterm disability in survivors. TBI-related deficiencies of both anterior pituitary (posttraumatic hypopituitarism, PTHP) and posterior pituitary (diabetes insipidus PTDI or syndrome of inappropriate antidiuretic secretion, SIADH) are much more frequent than previously known and associated with an unfavourable outcome. The pathophysiology of pituitary dysfunction after TBI is not entirely clear. The traumatic event can induce skull base fractures, hemorrhages or infarction affecting the hypothalamic and pituitary region with consequent endocrine dysfunction. In addition, metabolic and vascular brain changes, frequent in a critically ill patient also aggravate the neuroendocrine dysfunction. In the first days after trauma, the deficiency of adrenocorticotropic hormone and PTDI or SIADH are the main concern because if undiagnosed and untreated are associated with severe dyselectrolitemia and hypotension with increased mortality rate. Posterior pituitary dysfunction occurs in the first days after injury; SIADH usually resolves completely, PTDI can persist in a minority of cases. In contrast, PTHP can occur after a long time interval after TBI. Some degree of PTHP is present in 30-40% of TBI survivors. Early recognition and endocrinological treatment are essential to optimize the outcome of the intensive care management and of the rehabilitation process.
Brain Injury, 2007
Primary objective: There are only limited data regarding pituitary functions in the acute phase of traumatic brain injury (TBI) and previous studies have been conducted in only small cohorts of subjects. Therefore we have investigated the pituitary functions in the early acute phase, within 24 hours of trauma, in 104 patients with TBI. Additionally, the relationships between basal pituitary hormones, severity of the trauma and mortality due to trauma were also investigated. Methods and procedures: One hundred and four TBI patients were included in the study consecutively. All patients underwent basal hormonal evaluation within the first 24 hours of admission. Twenty of 104 patients died during the acute phase. Main outcomes: Prolactin levels were negatively correlated with the Glasgow coma scale (GCS), cortisol levels were positively correlated with the GCS and cortisol levels were positively correlated with ACTH levels. Additionally there was a significant positive correlation between the total testosterone levels and the GCS in males. Logistic regression analysis revealed that mortality after TBI was unrelated to basal pituitary hormone levels. However age and GCS were significantly related to the mortality. The percentages of pituitary hormone deficiencies were as follows: 3.8% had TSH deficiency, 40.0% had gonadotrophin deficiency, 8.8% had ACTH deficiency and 20.0% had GH deficiency. Conclusions: Present data clearly demonstrate that pituitary function is disturbed in TBI and the most frequently deficient pituitary hormones were gonadotrophins in the early acute phase of TBI. Basal hormone levels including cortisol, prolactin and total testosterone were related to the severity of the trauma. However there was no relation between basal hormones and mortality due to TBI. Age and GCS were significantly related to mortality.
Neuroendocrine dysfunction in the acute phase of traumatic brain injury
Clinical Endocrinology, 2004
BACKGROUND Pituitary hormone abnormalities have been reported in up to 50% of survivors of traumatic brain injury ( TBI) who were investigated several months or longer following the event. The frequency of pituitary dysfunction in the early post-TBI period is unknown. AIM To evaluate the prevalence of anterior and posterior pituitary dysfunction in the early phase following TBI. SUBJECTS Fifty consecutive patients admitted to the neurosurgical unit with severe or moderate TBI [initial Glasgow Coma Scale (GCS) score 3 -13], and 31 matched healthy control volunteers were studied. METHODS The glucagon stimulation test (GST) was performed at a median of 12 days (range 7-20) following TBI. Baseline thyroid function, PRL, IGF-1, gonadotrophins, testosterone or oestradiol, plasma sodium, plasma and urine osmolalities or the standard observed water deprivation test were performed. The control subjects underwent the GST for GH and cortisol responses; other parameters were compared to locally derived reference ranges. RESULTS Control data indicated that peak serum GH of > 5 ng / ml and cortisol > 450 nmol/l following glucagon stimulation should be taken as normal. Nine TBI patients (18%) had GH response < 5 ng/ml (12 mU/l). Eight patients (16%) had peak cortisol responses < 450 nmol/l. Compared to controls, basal cortisol values were significantly lower in patients with subnormal cortisol responses to glucagon and significantly higher in patients with normal cortisol responses ( P < 0·05). GH and cortisol deficiencies were unrelated to patient age, BMI, initial GCS or IGF-1 values ( P > 0·05). Forty patients (80%) had gonadotrophin deficiency, with low sex steroid concentrations, which was unrelated to the presence of hyperprolactinaemia. In males there was a positive correlation between serum testosterone concentration and GCS ( r = 0·32, P = 0·04). One patient had TSH deficiency. Hyperprolactinaemia was present in 26 patients (52%) and serum PRL levels correlated negatively with the GCS score ( r = − − − − 0·36, P = 0·011). Thirteen patients (26%) had cranial diabetes insipidus (DI) and seven (14%) had syndrome of inappropriate ADH secretion. CONCLUSION Our data show that post-traumatic neuroendocrine abnormalities occur early and with high frequency, which may have significant implications for recovery and rehabilitation of TBI patients.
The prognostic value of plasma Δ-copeptin levels in patients with isolated traumatic brain injury
European Journal of Trauma and Emergency Surgery, 2013
Purpose Traumatic brain injury (TBI) is one of the most common causes of death among trauma patients. Earlier prediction of possible poor neurological outcomes, even upon admission to the emergency department, may help to guide treatment. The aim of this prospective study was to assess the predictive value of plasma copeptin levels for early morbidity and mortality in patients with isolated TBI. Methods This prospective study comprised 53 patients who were admitted to the emergency department with isolated TBI. Forty-two of these patients (group I) survived at least 1 month after the TBI; the other 11 (group II) did not. Plasma levels of copeptin were measured in these TBI patients at admission and 6 h after trauma, and were compared with those of healthy volunteers (group III). Results At admission, the copeptin levels of the TBI patients (groups I and II combined) were not statistically significantly different from those of the control group (III). The copeptin levels 6 h after trauma were also not statistically significantly different from those at admission. D-Copeptin levels (the difference between the copeptin level at the 6th hour after trauma and that at admission) were higher in the patients who died within a month of the TBI. Further, D-copeptin levels were higher in patients who showed no improvement in the modified Rankin score when compared with patients with an improved modified Rankin score. The best cutoff point for D-copeptin was 0.51 ng/ml for predicting mortality and 0.23 ng/ml for predicting improvement in the modified Rankin score. Conclusions Plasma D-copeptin levels may help physicians predict the prognoses of patients suffering from traumatic brain injury.
The Hypothalamo-Pituitary-Adrenal Axis Response to Experimental Traumatic Brain Injury
Journal of Neurotrauma, 2001
Alterations in the hypothalamo-pituitary-adrenal (HPA) axis following traumatic brain injury have not been documented in detail. We used fluid percussion injury (FPI) to evaluate the early changes in components of the HPA axis following experimental traumatic brain injury. Wistar rats were sacrificed at 2 or 4 h following sham or FPI surgery. In situ hybridization histochemistry was used to determine the expression of mRNAs of corticotrophin releasing hormone (CRH) and arginine vasopressin (AVP) in the hypothalamus and pro-opiomelanocortin (POMC) in the pituitary. A group of animals undergoing no surgery were used as control. Repeated blood sampling from an indwelling catheter demonstrated that plasma corticosterone (CORT) levels peaked 30 min following surgery in sham and FPI animals but there was no significant difference in CORT concentration between these groups at any time. Pituitary POMC expression was increased following sham and FPI surgery (compared with control non-operated animals) but with no significant difference between the two groups undergoing surgery. Hypothalamic CRH mRNA expression was significantly higher in animals undergoing FPI compared with sham surgery. Hypothalamic AVP mRNA expression was not significantly increased when compared with control nonoperated animals. These data indicate that the anaesthesia and/or surgery associated with FPI or sham surgery induces a generalised activation of the HPA axis. The selective increase in CRH mRNA in animals undergoing FPI may be due to specific effects of traumatic brain injury rather than a general stress response and may suggest an additional neurotransmitter role for CRH following head injury. The absence of an AVP response suggests that the effects of FPI may be mediated through the CRH-alone-containing subpopulation of neurons.
Posterior pituitary dysfunction after traumatic brain injury
Journal of Clinical …, 2004
Disorders of water balance are well recognized after traumatic brain injury (TBI), but there are no reliable data on their true prevalence in post-TBI patients. We aimed to evaluate the prevalence of posterior pituitary dysfunction in a large cohort of survivors of TBI.
Endocrine Dysfunction After Traumatic Brain Injury: An Ignored Clinical Syndrome?
Neurocritical Care
Traumatic brain injury (TBI) incurs substantial health and economic burden, as it is the leading reason for death and disability globally. Endocrine abnormalities are no longer considered a rare complication of TBI. The reported prevalence is variable across studies, depending on the time frame of injury, time and type of testing, and variability in hormonal values considered normal across different studies. The present review reports evidence on the endocrine dysfunction that can occur after TBI. Several aspects, including the pathophysiological mechanisms, clinical consequences/challenges (in the acute and chronic phases), screening and diagnostic workup, principles of therapeutic management, and insights on future directions/research agenda, are presented. The management of hypopituitarism following TBI involves hormonal replacement therapy. It is essential for health care providers to be aware of this complication because at times, symptoms may be subtle and may be mistaken to b...