Measurement of serum melatonin in intensive care unit patients: changes in traumatic brain injury, trauma, and medical conditions

Marc A Seifman, Keith Gomes, Phuong N Nguyen, Michael Bailey, Jeffrey V Rosenfeld, David J Cooper, Maria Cristina Morganti-Kossmann, Marc A Seifman, Keith Gomes, Phuong N Nguyen, Michael Bailey, Jeffrey V Rosenfeld, David J Cooper, Maria Cristina Morganti-Kossmann

Abstract

Melatonin is an endogenous hormone mainly produced by the pineal gland whose dysfunction leads to abnormal sleeping patterns. Changes in melatonin have been reported in acute traumatic brain injury (TBI); however, the impact of environmental conditions typical of the intensive care unit (ICU) has not been assessed. The aim of this study was to compare daily melatonin production in three patient populations treated at the ICU to differentiate the role of TBI versus ICU conditions. Forty-five patients were recruited and divided into severe TBI, trauma without TBI, medical conditions without trauma, and compared to healthy volunteers. Serum melatonin levels were measured at four daily intervals at 0400 h, 1000 h, 1600 h, and 2200 h for 7 days post-ICU admission by commercial enzyme linked immunosorbent assay. The geometric mean concentrations (95% confidence intervals) of melatonin in these groups showed no difference being 8.3 (6.3-11.0), 9.3 (7.0-12.3), and 8.9 (6.6-11.9) pg/mL, respectively, in TBI, trauma, and intensive care cohorts. All of these patient groups demonstrated decreased melatonin concentrations when compared to control patients. This study suggests that TBI as well as ICU conditions, may have a role in the dysfunction of melatonin. Monitoring and possibly substituting melatonin acutely in these settings may assist in ameliorating long-term sleep dysfunction in all of these groups, and possibly contribute to reducing secondary brain injury in severe TBI.

Keywords: TBI; circadian; intensive care unit; melatonin; trauma.

Figures

Figure 1
Figure 1
Temporal profile of geometric mean serum melatonin concentrations in TBI patients, with peaks at 2200 h on Day 1 and 0400 h on Day 8, and nadir at 1000 h on Day 4.
Figure 2
Figure 2
Temporal profile of geometric mean serum melatonin concentrations in trauma patients without TBI, with peaks at 0400 h on Days 2, 3, 4, 5, and 7, and nadir at 1600 h on Day 5.
Figure 3
Figure 3
Temporal profile of geometric mean serum melatonin concentrations in ICU patients, with peaks at varying times on the initial 3 days, then peaks at 0400 h on days 4–7.
Figure 4
Figure 4
Temporal profile of mean serum melatonin concentrations in controls, with a diurnal variation displaying maximum values at night, and minimum values during the day (p < 0.0001). The geometric mean concentrations for the control patients are significantly higher than those of the other patient groups.
Figure 5
Figure 5
Comparison graph of time point effect. Night-time timepoints (0400 h and 2200 h) were significantly elevated compared to daytime time points, and 0400 h significantly higher than 2200 h.
Figure 6
Figure 6
Comparison graph of day effect. Day 1 values were significantly elevated when compared with days 2–6.

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Source: PubMed

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