[Cerebral low T3 syndrome]. / Mozgovoi sindrom nizkogo T3.

The authors studied the time course of changes in the parameters of the cerebral thyronergic system (total and free triiodthyronine (T3) and thyroxin (T4), thyroxine-binding globulin (TBG), thyroid-stimulating hormone (TSH) by radioimmunoassay (Immunotech, Czechia; CIS, France), proinflammatory cytokine of TNF-alpha by enzyme immunoassay (Innogenetic, Belgium) in the blood and cerebrospinal fluid (CSF) in 59 patients (37 males and 22 females whose age ranged from 21 to 64 years) in acute subarachnoidal hemorrhage due to arterial aneurysmal rupture. On admission, the condition of 47 (79.7%) was rated as grades III-VI according to the Hunt-Hess scale, which was responsible for high mortality rates (33.89% in the assessment of outcomes according to the Glasgow outcome scale). The causes of death were ischemic and hemorrhagic insults, edema of the brain, cerebral stem wedging. Laboratory findings were analyzed in relation to the clinical condition of patients, outcomes, and the degree of secondary vasospasm assessed by Doppler transcranial study by the average blood flow velocity in the middle cerebral artery. They revealed a significant depression of thyroidal metabolism with developed the total low T3 syndrome just before surgical treatment in patients with deterioration in the early postoperative period. The significant correlations found by the authors between the decreased blood T3 and TSH levels and 1) the severity of neurological disorders; 2) the degree of vasospasm, and 3) the outcome of disease, as well as negative correlations of elevated TNF-alpha levels not only in the blood, but also in CSF with the content of CT3, CT4 and with the severity of neurological symptomatology are indicative of the development of isolated syndrome in the brain, which is characterized by specific thyroidal metabolic disorders, which the author propose to call the cerebral low T3 syndrome (by taking into account the presence of the autonomic systems of thyroidal homeostatic provision).

Thyroid hormones in comatose patients with traumatic brain injury.

The objective was to study if thyroid hormones, cortisol, prolactin and brain injury marker levels were changed in traumatic brain injury (TBI) patients with changing levels of consciousness. We estimated the above named parameters in 32 patients (27 men and 5 women aged 11-55). Admission Glasgow Coma Score was < 8. Follow-up period--30 days. The length of coma was 3 to 25 days. There were significant decreases in TSH, TBG, FT3 and F_levels (p < 0.05, for each) and a T3 increase (as compared to very low preceding values) on day 1 before emergence from coma and considerable post-coma increase in TBG, FT3, TSH and F levels (p < 0.001 each) on days 1-3 in patients with diffuse axonal injury (DAI). In patients with contusions and epidural and subdural hematomas (CH) T3 and T4 levels continued to fall until 4-6 postcoma days. TSH values significantly increased up to average normal ranges (p < 0.05) on days "-" 2 and "-" 1 before emergence from coma and remained so. Significantly lower levels of TSH, F and PRL were found in patients with CH in the mostly remote period (on days "-" 12-"-" 8) before emergence from coma in comparison with DAI patients. In blood the following correlations of examined parameters were established: between NSE and T3 (r = -0.39), NSE and FT3 (r = -0.59), TNF alpha and TBG (r = -0.64), TNF alpha and T3 (r = -0.3) and S-100 and T3 (r = -0.3) (p < 0.05, for each). The results obtained confirmed a low T3 syndrome in comatose TBI patients. We demonstrated an objective and informative interdependence: the turning-point moment of the emergence from coma was accompanied by significant changes of examined hormone levels and brain injury marker levels. The results may serve as a base for recommending monitoring FT3 and T3 levels simultaneously with that of other injury markers and adequate T3 replacement therapy in the early posttraumatic period.