Alteration in brain natriuretic peptide (BNP) plasma concentration following severe traumatic brain injury
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Background. Brain natriuretic peptide (BNP) is a potent natriuretic and vasodilator factor which, by its systemic effects, can decrease cerebral blood flow (CBF). In aneurysmal subarchnoid hemorrhage (aSAH), BNP plasma concentrations were found to be associated with hyponatremia and were progressively elevated in patients who eventually developed delayed ischemic deficit secondary to vasospasm. The purpose of the present study was to evaluate trends in BNP plasma concentrations during the acute phase following severe (traumatic brain injury) TBI.
Methods. BNP plasma concentration was evaluated in 30 patients with severe isolated head injury (GCS < 8 on admission) in four time periods after the injury (period 1: days 1–2; period 2: days 4–5; period 3: days 7–8; period 4: days 10–11). All patients were monitored for ICP during the first week after the injury.
Findings. The initial BNP plasma concentrations (42 ± 36.9 pg/ml) were 7.3 fold (p < 0.01) higher in TBI patients as compared to the control group (5.78 ± 1.90 pg/ml). BNP plasma concentrations were progressively elevated through days 7–8 after the injury in patients with diffused SAH as compared to patients with mild or no SAH (p < 0.001) and in patients with elevated ICP as compared to patients without elevated ICP (p < 0.001). Furthermore, trends in BNP plasma concentrations were significantly and positively associated with poor outcome.
Interpretation. BNP plasma concentrations are elevated shortly after head injury and are continuously elevated during the acute phase in patients with more extensive SAH and in those with elevated ICP, and correlate with poor outcomes. Further studies should be undertaken to evaluate the role of BNP in TBI pathophysiology.
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