Hormones and cytokines as biomarkers for immediate cure measures in severe neurosurgical patients: base for inclusion in a neuromonitoring algorithm

Introduction

In spite of dramatic recent achievements in neuroendocrine immunology and neuroprotection, an adequate treatment strategy for interrupting molecular cascade reactions in severe brain damage is not quite clear. The role of daily monitoring of the hormone and cytokine levels in these patients in the ICU is not quite understood and so far recognized.

Methods

Two hundred and eighty-two patients with severe traumatic brain injury (GCS < 8 at admission), 226 patients with aneurismal subarachnoid haemorrhage and 325 operated patients with brain tumors were studied. Prolactin (as immunomodulator), free and total thyroxine and triiodothyronine (FT4, T4, FT3 and T3), and cytokines (IL-6, sIL-2R, NT-proBNP) were assayed in blood and CSF by RIA kits and chemiluminescent analysis (Immulite 2000). The obtained data were compared with clinical, neurological and neuroimaging data.

Results

Independent of causation and gender, an abrupt serum prolactin level decrease (P < 0.001) started 2–3 days before respiratory and brain inflammatory complaints were verified by roentgenogram. Significant decreases, especially T3 and FT3 to undetected values (P < 0.05), were characterized for worsening patient conditions (brain ischemia/hypoxia and brain edema increasing, consciousness depression (r = -0.239, P < 0.000415)). Simultaneously there were marked significantly increased sIL-2R, IL-6, and NT-proBNP levels in blood and CSF in comparison with normal values (P < 0.001). The highest values were found in patients with unfavourable outcomes.

Conclusion

Serum and CSF hormone and cytokine level daily monitoring in critically ill patients with severe brain damage, ARDS, haemodynamic disturbances, sepsis and polyorgan deficit strictly reflects the patient condition (upregulation and downregulation of neuroendocrine and immune systems and its roles in neurosystemic and systemic inflammatory responses) and allows immediate prognosis of the disease process. The 'brain low T3 syndrome' earlier proposed by us for severe neurosurgical patients serves as a basis for brief thyroid hormone substitution therapy in addition to conventional therapy, taking into account the crucial role of T3 in neurogenesis in the adult brain and its important influences on endothelium and cardiodynamics.