Abstrakt
Methyl alcohol intoxication is a global problem with high mortality and long-term visual sequelae and severe brain damage in survivors. The role of neuroinflammation in the mechanisms of methyl alcohol-induced toxic brain damage has not been well studied.
We measured the acute concentrations and dynamics of lipoxins LxA4 and LxB4 and the interleukins IL-4, IL-5, IL-9, IL-10, and IL-13 in the serum of patients treated with methyl alcohol poisoning and the follow-up concentrations in survivors two years after discharge from the hospital. A series of acute measurements was performed in 28 hospitalized patients (mean age 54.2 +/- 5.2 years, mean observation time 88 +/- 20 h) and the follow-up measurements were performed in 36 subjects who survived poisoning (including 12/28 survivors from the acute group).
Visual evoked potentials (VEP) and magnetic resonance imaging of the brain (MRI) were performed to detect long-term visual and brain sequelae of intoxication. The acute concentrations of inflammatory mediators were higher than the follow-up concentrations: LxA4, 62.0 +/- 6.0 vs. 30.0 +/- 5.0 pg/mL; LxB4, 64.0 +/- 7.0 vs. 34.0 +/- 4.0 pg/mL; IL-4, 29.0 +/- 4.0 vs. 15.0 +/- 1.0 pg/mL; IL-5, 30.0 +/- 4.0 vs. 13.0 +/- 1.0 pg/mL; IL-9, 30.0 +/- 4.0 vs. 13.0 +/- 1.0 pg/mL; IL-10, 38.0 +/- 5.0 vs. 16.0 +/- 1.0 pg/mL; IL-13, 35.0 +/- 4.0 vs. 14.0 +/- 1.0 pg/mL (all p < 0.001).
The patients with higher follow-up IL-5 concentration had prolonged latency P1 (r=0.413; p=0.033) and lower amplitude N1P1 (r=-0.498; p=0.010) of VEP. The higher follow-up IL-10 concentration was associated with MRI signs of brain necrotic damage (r=0.533; p=0.001) and brain hemorrhage (r=0.396; p=0.020).
Our findings suggest that neuroinflammation plays an important role in the mechanisms of toxic brain damage in acute methyl alcohol intoxication.