Serum melatonin levels in survivor and non-survivor patients with traumatic brain injury

Abstract

BackgroundCirculating levels of melatonin in patients with traumatic brain injury (TBI) have been determined in a little number of studies with small sample size (highest sample size of 37 patients) and only were reported the comparison of serum melatonin levels between TBI patients and healthy controls. As to we know, the possible association between circulating levels of melatonin levels and mortality of patients with TBI have not been explored; thus, the objective of our current study was to determine whether this association actually exists.MethodsThis multicenter study included 118 severe TBI (Glasgow Coma Scale <9) patients. We measured serum levels of melatonin, malondialdehyde (to assess lipid peroxidation) and total antioxidant capacity (TAC) at day 1 of severe TBI. We used mortality at 30 days as endpoint.ResultsWe found that non-survivor (n = 33) compared to survivor (n = 85) TBI patients showed higher circulating levels of melatonin (p < 0.001), TAC (p < 0.001) and MDA (p < 0.001). We found that serum melatonin levels predicted 30-day mortality (Odds ratio = 1.334; 95% confidence interval = 1.094–1.627; p = 0.004), after to control for GCS, CT findings and age. We found a correlation between serum levels of melatonin levels and serum levels of TAC (rho = 0.37; p < 0.001) and serum levels of MDA (rho = 0.24; p = 0.008).ConclusionsAs to we know, our study is the largest series providing circulating melatonin levels in patients with severe TBI. The main findings were that non-survivors had higher serum melatonin levels than survivors, and the association between serum levels of melatonin levels and mortality, peroxidation state and antioxidant state.

Higher Serum Melatonin Levels during the First Week of Malignant Middle Cerebral Artery Infarction in Non-Surviving Patients

“…However, we found higher serum melatonin levels in non-surviving than in surviving patients, and a positive association between serum levels of melatonin and malondialdehyde. Similar findings have been found by our team in patients with severe traumatic brain injury [10] or spontaneous intracerebral hemorrhage [11]. We believe that those high serum melatonin levels in non-surviving patients could represent a response to the great neuroinflammation (not assessed in our study) and oxidation states (assessed in our study by serum malondialdehyde concentrations).…”

“…Our team found lower serum melatonin levels at the time of admission of cerebral infarction in surviving patients than in non-surviving patients [9]. In addition, our team also found higher serum melatonin levels in non-surviving than in surviving patients at admission of traumatic brain injury (TBI) [10] and of spontaneous intracerebral hemorrhage (ICH) [11]. We believe that our findings in patients with cerebral infarction, TBI, and ICH showing higher melatonin levels in non-surviving than in surviving patients could be due to the efforts of patients to reduce the great neuroinflammation and oxidation states.…”

Clinical significance of detecting serum melatonin and SBDPs in brain injury in preterm infants

“…Studies have shown that endogenous melatonin is massively produced in the cerebrospinal fluid of adults with head injury and the serum of diseases children with severe traumatic brain injury, 5,21 indicating that melatonin has antioxidant and neuroprotective effects. Studies targeting the models of brain injury 3,4,22,23 have shown that melatonin can reduce neuronal death by stabilizing the endothelial permeability. Recently, it has also been confirmed that melatonin can remove damaged mitochondria by activating the mitochondrial autophagocytes, 24e26 thereby inhibiting inflammation induced by brain injury.…”

The role of human and microbial metabolites of triptophane in severe diseases and critical ill (review)

“…Изучение метаболомного профиля сыворотки при черепно-мозговой травме позволило выявить снижение концентрации индол-3-пропановой кислоты в сыворотке крови [42], в то время как содержание другого индольного производного серотонина, а именно мелатонина, повышалось в крови после черепно-мозговой травмы у детей, что, возможно, связано с ответом на окислительный стресс или воспаление, вызванного травмой [43]. Уровень мелатонина в крови впоследствии умерших пациентов с тяжелой черепно-мозговой травмой был выше, чем у выживших, и найдена корреляция его с уровнями малонового диальдегида (показателя перекисного окисления липидов) и общей антиоксидантной активности, отражающая тяжесть повреждения головного мозга [44]. Ранее также была обнаружена связь повышенных концентраций мелатонина в крови с показателем смертности у септических пациентов [45].…”