Neuroinflammation markers and methyl alcohol induced toxic brain damage.

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 ±â€¯5.2 years, mean observation time 88 ±â€¯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 ±â€¯6.0 vs. 30.0 ±â€¯5.0 pg/mL; LxB4, 64.0 ±â€¯7.0 vs. 34.0 ±â€¯4.0 pg/mL; IL-4, 29.0 ±â€¯4.0 vs. 15.0 ±â€¯1.0 pg/mL; IL-5, 30.0 ±â€¯4.0 vs. 13.0 ±â€¯1.0 pg/mL; IL-9, 30.0 ±â€¯4.0 vs. 13.0 ±â€¯1.0 pg/mL; IL-10, 38.0 ±â€¯5.0 vs. 16.0 ±â€¯1.0 pg/mL; IL-13, 35.0 ±â€¯4.0 vs. 14.0 ±â€¯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.

Reference values of cardio-ankle vascular index in a random sample of a white population.

OBJECTIVES: Cardio-ankle vascular index (CAVI), a parameter of arterial stiffness, has been increasingly used for cardiovascular risk estimation. Currently used CAVI reference values are derived from the Japanese population. It is not clear whether the same reference values can be used in the white population. The aim of the present study was to describe cardiovascular risk factors influencing CAVI and to establish CAVI reference values. METHODS: A total of 2160 individuals randomly selected from the Brno city population aged 25-65 years were examined. Of these, 1347 patients were free from cardiovascular disease, nondiabetic and untreated by antihypertensive or lipid-lowering drugs, forming the reference value population. CAVI was measured using the VaSera VS-1000 device (Fukuda Denshi, Tokyo, Japan). RESULTS: At each blood pressure (BP) level, there was a quadratic association between CAVI and age, except for a linear association in the optimal BP group. Although there was no association between BP and CAVI in younger patients, there was a linear association between CAVI and BP after 40 years of age. Reference values by age and sex were established. In each age group, except for the male 60-65-year group, reference values in our population were lower than in the Japanese one with the difference ranging from -0.29 to 0.21 for men, and from -0.38 to -0.03 for women. CONCLUSION: This is the first study providing CAVI reference values in a random sample of the white population. Our results suggest that the currently used values slightly overestimate CAVI in younger white, possibly underestimating cardiovascular risk.

Threshold for diagnosing hypertension by automated office blood pressure using random sample population data.

OBJECTIVE: Manual office blood pressure (BP) is still recommended for diagnosing hypertension. However, its predictive value is decreased by errors in measurement technique and the white-coat effect. The errors can be eliminated by automated office BP (AOBP) measurement taking multiple readings with the participant resting quietly alone. Therefore, use of AOBP in clinical practice requires a threshold value for hypertension diagnosis. The aim of the present study was to determine an AOBP threshold corresponding to the 140/90 mmHg manual office BP using data from a large random population sample. METHODS: In 2145 participants (mean age 47.3 ±â€Š11.3 years) randomly selected from a Brno population aged 25-64 years, BP was measured using manual mercury and automated office sphygmomanometers. RESULTS: Manual SBP (mean difference 6.39 ±â€Š9.76 mmHg) and DBP (mean difference 2.50 ±â€Š6.54 mmHg) were higher than the automated BP. According to polynomial regression, automated systole of 131.06 (95% confidence interval 130.43-131.70) and diastole of 85.43 (95% confidence interval 85.03-85.82) corresponded to the manual BP of 140/90 mmHg. Using this cut-off, the white-coat hypertension was present in 24% of participants with elevated manual BP, whereas 10% had masked hypertension and 11% masked uncontrolled hypertension. In individuals with masked uncontrolled hypertension, only AOBP was associated with the urinary albumin-creatinine ratio, whereas there was no association with manual BP. CONCLUSION: AOBP of 131/85 mmHg corresponds to the manual BP of 140/90 mmHg. This value may be used as a threshold for diagnosing hypertension using AOBP. However, outcome-driven studies are required to confirm this threshold.