GH deficiency after traumatic brain injury: improvement in quality of life with GH therapy: analysis of the KIMS database

Gardner, Clarissa; Mattsson, Anders; Daousi, Christina; Korbonits, Márta; Kołtowska-Häggström, Maria; Cuthbertson, Daniel J.

doi:10.1530/eje-14-0654

Cited by 55 publications

(31 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In a third study [18], the Pfizer International Metabolic Database was retrospectively reviewed, and patients with GH deficiency caused by TBI ( n = 564) and non-functioning pituitary adenoma ( n = 3773) were compared with regard to clinical characteristics at baseline and after 1 year of GH replacement therapy. QoL was examined after up to 8 years.…”

Section: Pharmacological Agents With Demonstrated Neuroprotective Ementioning

confidence: 99%

Pharmacologic Neuroprotection for Functional Outcomes After Traumatic Brain Injury: A Systematic Review of the Clinical Literature

et al. 2016

View full text Add to dashboard Cite

Introduction Traumatic brain injury (TBI) is a major cause of death and disability worldwide. The deleterious effects of secondary brain injury may be attenuated by early pharmacological therapy in the emergency room and intensive care unit (ICU). Current medical management of acute TBI is primarily supportive, aimed at reducing intracranial pressure (ICP) and optimizing cerebral perfusion. There are no pharmacological therapies to date that have been unequivocally demonstrated to improve neurological outcomes after TBI. Objectives The purpose of this systematic review was to evaluate the recent clinical studies from January 2013 through November 2015 that investigated neuroprotective functional outcomes of pharmacological agents after TBI. Methods The following databases were searched for relevant studies: MEDLINE (OvidSP January Week 1, 2013–November Week 2 2015), Embase (OvidSP 2013 January 1–2015 November 24), and the unindexed material in PubMed (National Library of Medicine/National Institutes of Health [NLM/NIH]). This systematic review included only full-length clinical studies and case series that included at least five patients and were published in the English language. Only studies that examined functional clinical outcomes were included. Results Twenty-five of 527 studies met our inclusion criteria, which investigated 15 independent pharmacological therapies. Eight of these therapies demonstrated possible neuroprotective properties and improved functional outcomes, of which five were investigated with randomized clinical trials: statins, N-acetyl cysteine (NAC), Enzogenol, Cerebrolysin, and nitric oxide synthase inhibitor (VAS203). Three pharmacological agents did not demonstrate neuroprotective effects, and four agents had mixed results. Conclusions While there is currently no single pharmacological therapy that will unequivocally improve clinical outcomes after TBI, several agents have demonstrated promising clinical benefits for specific TBI patients and should be investigated further.

show abstract

Section: Pharmacological Agents With Demonstrated Neuroprotective Ementioning

confidence: 99%

Pharmacologic Neuroprotection for Functional Outcomes After Traumatic Brain Injury: A Systematic Review of the Clinical Literature

et al. 2016

View full text Add to dashboard Cite

show abstract

“…In recent years, there has been an increasing amount of strong evidence that suggests that patients with TBI are at considerable risk of dysfunction of the hypothalamic-pituitary axis, and this risk is associated with morbidity and possibly mortality 6–9 . Furthermore, clinical trials have demonstrated that treatment with replacement hormones is convenient and physiologically relevant 9, 10 . According to one report, the incidence of hypothalamic-pituitary dysfunction induced by TBI is 5.4% to 90% 6 .…”

Section: Introductionmentioning

confidence: 99%

“…Although many clinical trials have focused on dysfunction of the hypothalamic-pituitary axis caused by TBI 10, 19–21 , few studies have paid close attention to neuroendocrine and physiopathological alterations of the hypothalamic-pituitary axis induced by TBI in the acute phase. It is interesting to explore the neuroendocrine changes and apoptosis of brain cells in the hypothalamic-pituitary axis that are caused by intracranial hypertension.…”

Section: Introductionmentioning

confidence: 99%

Assessment of the role of intracranial hypertension and stress on hippocampal cell apoptosis and hypothalamic-pituitary dysfunction after TBI

Tan

Yang

et al. 2017

Sci Rep

View full text Add to dashboard Cite

In recent years, hypopituitarism caused by traumatic brain injury (TBI) has been explored in many clinical studies; however, few studies have focused on intracranial hypertension and stress caused by TBI. In this study, an intracranial hypertension model, with epidural hematoma as the cause, was used to explore the physiopathological and neuroendocrine changes in the hypothalamic–pituitary axis and hippocampus. The results demonstrated that intracranial hypertension increased the apoptosis rate, caspase-3 levels and proliferating cell nuclear antigen (PCNA) in the hippocampus, hypothalamus, pituitary gland and showed a consistent rate of apoptosis within each group. The apoptosis rates of hippocampus, hypothalamus and pituitary gland were further increased when intracranial pressure (ICP) at 24 hour (h) were still increased. The change rates of apoptosis in hypothalamus and pituitary gland were significantly higher than hippocampus. Moreover, the stress caused by surgery may be a crucial factor in apoptosis. To confirm stress leads to apoptosis in the hypothalamus and pituitary gland, we used rabbits to establish a standard stress model. The results confirmed that stress leads to apoptosis of neuroendocrine cells in the hypothalamus and pituitary gland, moreover, the higher the stress intensity, the higher the apoptosis rate in the hypothalamus and pituitary gland.

show abstract

“…35 Initial screening for GH (and ACTH) deficiency was performed using the glucagon stimulation test with peak GH cutoff <5lg/l. 35 The diagnosis of GHD was then confirmed using the GHRH-arginine test, with age-and BMI-adjusted cutoffs, 21 and/or insulin tolerance test (peak GH <3lg/l), in all patients. Serum GH was assayed using the Immulite 2000 assay.…”

Section: Endocrine Assessmentmentioning

confidence: 99%

“…29,32,33 Following TBI, GH replacement also improves cognition, psychological function, and quality of life (QoL) in patients with GHD. [34][35][36][37][38] This could be produced through an effect on WM tract recovery, and changes in the levels of IGF-I might mediate this effect. However, the effects of GHD/IGF-I status on WM recovery following TBI are unknown.…”

mentioning

confidence: 99%

Serum insulin‐like growth factor‐I levels are associated with improved white matter recovery after traumatic brain injury

Feeney

Sharp

Hellyer

et al. 2017

Annals of Neurology

View full text Add to dashboard Cite

ObjectiveTraumatic brain injury (TBI) is a common disabling condition with limited treatment options. Diffusion tensor imaging measures recovery of axonal injury in white matter (WM) tracts after TBI. Growth hormone deficiency (GHD) after TBI may impair axonal and neuropsychological recovery, and serum insulin‐like growth factor‐I (IGF‐I) may mediate this effect. We conducted a longitudinal study to determine the effects of baseline serum IGF‐I concentrations on WM tract and neuropsychological recovery after TBI.MethodsThirty‐nine adults after TBI (84.6% male, median age = 30.5 years, 87.2% moderate–severe, median time since TBI = 16.3 months, n = 4 with GHD) were scanned twice, 13.3 months (range = 12.1–14.9) apart, and 35 healthy controls were scanned once. Symptom and quality of life questionnaires and cognitive assessments were completed at both visits (n = 33). Our main outcome measure was fractional anisotropy (FA), a measure of WM tract integrity, in a priori regions of interest: splenium of corpus callosum (SPCC) and posterior limb of internal capsule (PLIC).ResultsAt baseline, FA was reduced in many WM tracts including SPCC and PLIC following TBI compared to controls, indicating axonal injury, with longitudinal increases indicating axonal recovery. There was a significantly greater increase in SPCC FA over time in patients with serum IGF‐I above versus below the median for age. Only the higher IGF‐I group had significant improvements in immediate verbal memory recall over time.InterpretationWM recovery and memory improvements after TBI were greater in patients with higher serum IGF‐I at baseline. These findings suggest that the growth hormone/IGF‐I system may be a potential therapeutic target following TBI. Ann Neurol 2017;82:30–43

show abstract

GH deficiency after traumatic brain injury: improvement in quality of life with GH therapy: analysis of the KIMS database

Cited by 55 publications

References 46 publications

Pharmacologic Neuroprotection for Functional Outcomes After Traumatic Brain Injury: A Systematic Review of the Clinical Literature

Pharmacologic Neuroprotection for Functional Outcomes After Traumatic Brain Injury: A Systematic Review of the Clinical Literature

Assessment of the role of intracranial hypertension and stress on hippocampal cell apoptosis and hypothalamic-pituitary dysfunction after TBI

Serum insulin‐like growth factor‐I levels are associated with improved white matter recovery after traumatic brain injury

Contact Info

Product

Resources

About