Session: MON 142-166-Hypothalamus-Pituitary Development & Biology
Poster Board MON-151
In our study we attempted to find out CSF and plasma markers that would enable us to understand the pathogenesis, prediction and targeted treatment of NPH.
In patients with CSF disorders, hypercortisolemia was found repeatedly. Cortisol is formed from cortisone through the activity of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD 1). Among its glucocorticoid activity it competes for mineralocorticoid receptors in the brain and may directly influence osmotic gradient. Through cytokine composition, cortisol influences also immune mechanisms, which may be counter-regulated by 7-hydroxylated metabolites of DHEA, interconverted also with 11β-HSD 1. The levels of homocysteine, an independent risk factor for dementia development, were also investigated.
In our patients (n=10; NPH, 65-80 years), the medians of selected parameters in CSF before shunt insertion were as follows: cortisol, 21.35 nmol/L; cortisone, 9.26 nmol/L; DHEA, 0.22 nmol/L; DHEAs, 1.00 nmol/L; 7-α-OH-DHEA, 1.33 pmol/L; 7-β-OH-DHEA, 0.96 pmol/L; 7-oxo-DHEA, 1.19 pmol/L; 16-α-OH-DHEA, 3.10 pmol/L and homocysteine, 1.03 µmol/L. To determine the results of NPH improvement, cortisol/cortisone ratio was calculated - this ratio significantly decreased after one month from shunt insertion (p= 0.016) and remains stable after half year. After one month period, an increasing trend of 7-oxo-DHEA and decreasing trend of homocysteine were observed. Patients are followed up and their status is currently monitored.
Our results should highlight the laboratory changes which in future would help the physician in an objective evaluation of the disease stage. An early and accurate diagnosis of NPH would be helpful in its therapeutic strategy, which would suppress or attenuate progression of the disease.
Acknowledgement: Project was supported by IGA MZCR NT/12349-4 and NT/13369-4 of Czech Ministry of Health.
Nothing to Disclose: LS, MB, MM, JK, RH
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