Table 1.

Summary of clinical studies and Main Outcomes Addressing the effect of TBI on Peripheral Metabolism

Study (year)	Subjects	Purpose	Measurements	Main results
(Silva et al., 2018) (Silva et al., 2018)	Mechanicall y-ventilated patients with severe TBI	Relationship between neuromuscular electrophysiological disorders (NED) and muscle atrophy in TBI patients.	The muscle structure (thickness and echogenicity) was assessed by B-mode ultrasound.	Mechanically-ventilated patients with TBI developed NED and muscle atrophy
(Shibahashi et al., 2017) (Shibahashi et al., 2017)	Olderpatients (age ≥ 60 years) with TBI	Evaluate skeletal muscle mass as predictive marker for TBI outcome.	Skeletal muscle mass and clinical outcomes (Glasgow scale)	Reduced skeletal muscle mass was associated with poorer outcome after TBI
(Rizoli et al., 2017) (Rizoli et al., 2017)	Patients with isolated moderate-to-severe TBI	Association between catecholamine levels post-trauma and functional outcome.	Epinephrine (Epi) and norepinephrine (NE) and clinical outcomes (Glasgow scale)	Elevated circulating catecholamines, are independently associated with functional outcome and mortality after TBI
(Czorlich et al., 2017) (Czorlich et al., 2017)	Patients with severe TBI	Evaluate the impact of body mass index (BMI) on mortality and early neurologic outcome	Patients were categorized into underweight, normal, pre-obese and obese based on BMI. Early neurologic outcome was classified using the Glasgow Outcome Scale.	The BMI ≥35 is an independent predictor of mortality and is associated with an inferior early functional neurologic outcome.
(Mossberg et al., 2017) (Mossberg et al., 2017)	Patients with isolated moderate to severe TBI	The effects of recombinant human growth hormone (rhGH) replacement on physical and cognitive functioning in TBI patients.	Peak cardiorespiratory capacity, body composition, muscle force testing and neuropsychological tests.	The rhGH replacement has a positive impact on cardiorespiratory fitness and a positive impact on perceptual fatigue in survivors of TBI with altered GH secretion.
(Rau et al., 2017) (Rau et al., 2017)	Patients with isolated moderate to severe TBI	Analyze whether hyperglycemia is associated with higher morbidity and mortality in TBI patients.	TBI patients were allocated into four groups: Stress-induced hyperglycemia (SIH), diabetic hyperglycemia (DH), diabetes normoglycemia, and non-diabetic normoglycemia (NDN)	Patients with SIH and DH had significantly higher mortality than patients with NDN. The mortality was significantly higher in patients with SIH and but not with DH.
(Lu et al., 2017) (Lu et al., 2017)	Patients with isolated moderate to severe TBI	Determine if TBI patients have a higher risk of myocardial dysfunction than the general population and to identify the risk factors of myocardial dysfunction in TBI patients.	Patients who visited ambulatory care centers or were hospitalized with a diagnosis of TBI.	Diabetes, hypertension, peptic ulcer disease, chronic liver disease and chronic renal disease were risk factors of myocardial dysfunction in TBI patients
(Hendrick et al., 2016) (Hendrick et al., 2016)	Nonhead injured trauma patients	Impact of beta-blockers on Nonhead injured trauma patients	Mortality, length stay in intensive care unit (ICU)	Beta-blockers had not effect on mortality and ICU in TBI patients
(Park et al., 2016) (Park et al., 2016)	Patients with diffuse axonal injury.	Investigate the regional cerebral metabolism related to growth hormone deficiency (GHD) after traumatic brain injury (TBI)	Patients underwent brain F-18 FDG PET study and an insulin tolerance test (ITT).	Compared with subjects with TBI but normal GH, patients with GHD after TBI showed decreased cerebral glucose metabolism.
(Giuliano et al., 2017) (Giuliano et al., 2017)	Patients with complicated mild TBI	Evaluate whether mild TBI patients with GH deficiency had developed alterations in the glycolipid profile and clinical indices of injury severity and neurological outcome.	GH deficiency was investigated by the combined test (GH releasing hormone + arginine). The glycolipid and clinical outcomes (Glasgow scale) were also evaluated.	TBI Patients had high occurrence of isolated GH deficiency, which was associated with visceral adiposity and metabolic alterations.
(Di Battista et al., 2016) (Di Battista et al., 2016)	Patients with moderate-to-severe TBI	Early dynamic profile of circulating inflammatory cytokines/chemokines and interrelationships between these mediators with catecholamines and clinical indices of injury severity and neurological outcome.	Plasma cytokine, chemokin, catecholamines. Neurological outcome was assessed using the extended Glasgow outcome scale (GOSE)	Positive association between catecholamines , cytokines and chemokine with poor outcome at 6 months after TBI.
(Ko et al., 2016) (Ko et al., 2016)	Patients with moderate-to-severe TBI	The effect of β-Adrenergic receptor blockers (BBs) on TBI-induced cascade of immune and inflammatory.	Patients who received early propranolol after TBI (Feldman et al.) were compared with those who did not (non-EPAT). Data including demographics, hospital length of stay (LOS) and mortality were collected.	Early administration of propranolol after TBI was associated with improved survival.
(Majdan et al., 2015) (Majdan et al., 2015)	Patients with severe TBI	Analyze whether BMI, height and weight of patients were related to severity, patterns and outcomes of TBI caused by low level falls.	Patients were categorized into underweight, normal, pre-obese and obese based on BMI and demographic characteristics, injury severity, patterns and outcomes were compared.	The patients in all BMI groups were of similar injury severity and neurological status. Obese and pre-obese patients required longer stay at ICU.