Abdürrahim KOCYİĞİT, Hakim ÇELİK, Akın İŞCAN, Alpay ÇAKMAK, İbrahim HOCANLI, Mustafa ÇALIK

Serum S-100B levels in children with subacute sclerosing panencephalitis

Amaç: S-100B santral sinir sisteminde yaygın olarak bulunan, kan beyin bariyeri yıkımında ve nöronal hasarda periferik belirteç olarak kullanılan bir proteindir. Bu çalışmanın amacı, Subakut sklerozan panensefalitli hastalarda S-100B düzeylerini araştırmaktır. Gereç ve yöntem: Çalışmada, SSPE li 40 hasta ile 40 sağlıklı kontrol grubu alındı. Serum S-100B protein konsantrasyonları elektrokemiluminesan immunoassay (ECLIA) yöntemi ile üretici standartlarına göre ölçüldü. Bulgular: Ortalama S-100B seviyeleri SSPEli hasta grubunda 0.095 ± 0.017 μg/L, kontrol grubunda ise 0.097 ± 0.019 μg/L bulundu. Aralarında istatistiksel olarak anlamlı farklılık bulunmadı (p>0.05). Hasta grubu beyin atrofisinin varlığına göre iki altgruba ayrıldı. S-100B seviyeleri beyin atrofisi olan grupta 0.096±0.018 μg/L, atrofisi olmayan grupta ise 0.094±0.014 μg/L idi. Bu farklılık istatistiksel olarak anlamlı değildi (p>0.05). Sonuç: Bizim sonuçlarımız, S-100Bnin SSPE de nöronal hasarda güvenilir bir belirteç olmadığını göstermektedir.

Subakut sklerozan panensefalit li çocuklarda serum S-100B düzeyleri

Objectives: S-100B a protein prevalent in the central nervous system is a peripheral biomarker for blood-brain barrier disruption and neuronal damage. The objective of the study was to investigate the S-100B levels in patients with subacute sclerosing panencephalitis. Materials and methods: A group of 40 patients with SSPE and 40 healthy controls were recruited. Serum S-100B protein concentrations were measured using a commercially available electrochemiluminescence immunoassay (ECLIA) kit, as supplied and according to the manufacturer s standards. Results: Median S-100B levels were 0.095 ± 0.017 μg/L in patients with SSPE and 0.097±0.019 μg/L in the control group. This difference was not statistically significant (p>0.05). The patient group was further subdivided into two subgroups according to the presence or absence of brain atrophy. The S-100B levels were 0.096 ± 0.018 μg/L in the subgroup with atrophy and 0.094±0.014 μg/L in the subgroup without atrophy. This difference was also not statistically significant (p>0.05). Conclusions: Our results suggest that serum S-100B is not a reliable marker for neuronal damage in SSPE.

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1. Garg RK. Subacute sclerosing panencephalitis. J Neurol 2008;14(12):1439-52.
2. Geyer C, Ulrich A, Grafe G, stach B, Till H. Diagnostic value of S 100B and neuron- specific enolase in mild pediatric traumatic brain injury. J neurosurg Pediatr 2009;4(2):339-44.
3. Schulpis KH, Margeli A, Akalestos A, et al. Effects of mode of delivery on maternal-neonatal plasma antioxidant status and on protein S-100B serum concentrations. Scand J Clin Lab Invest 2006;66(6):733-42.
4. Gazzolo D, Abella R, Marinoni E, et al. New markers of neonatal neurology. J Maternal-Fetal Neonat Med 2009;12(1): 1-5.
5. Rothermundt M, Peters M, Prehn JH, Arolt V. S100B in brain damage and neurodegenaration. Microsc Res Tech 2003;60(5):614-32.
6. Dyken PR. Subacute sclerosing panencephalitis. Neurol Clin 1985;3(2):179-95.
7. Jabbour JT, Garcia JH, Lemmi H, Ragland J, Duenas DA, Sever JL. Subacute sclerosing pan encephalitis. JAMA 1969;207(12):2248-54.
8. Oztürk A, Gürses C, Baykan B, Gökyigit A, Eraksoy M. Subacute sclerosing panencephalitis: Clinical and magnetic resonance imaging evaluation of 36 patients. J Child Neurol 2002;17(1):25-9.
9. Aydin K, Okur O, Tatli B, Sarwar SG, Ozturk C, Dilber C. Reduced gray matter volume in the frontotemporal cortex of patients with early subacute sclerosing panencephalitis. AJNR Am J Neuroradiol 2009;30(2):271- 5.
10. Lins H, Wallesch CW, Wunderlich MT. Sequential analyses of neurobiochemical markers of cerebral damage in cerebrospinal fluid and serum in CNS infections. Acta Neurol Scand 2005;112(2):303-08.
11. Ahlemeyer B, Beier H, Semkova I, Schaper C, Krieglstein J. S-100beta protects cultured neurons against glutamate- and staurosporine-induced damage and is involved in the antiapoptotic action of the 5 HT(1A)- receptor agonist, Bay x 3702. Brain Res 2000;858(1): 121-8.
12. Van Eldik LJ, Wainwright MS. The Janus face of glial derived S100B: beneficial and detrimental functions in the brain. Restor Neurol Neurosci 2003;21(3-4):97- 108.
13. Giussani DA, Thakor AS, Frulio R, Gazzolo D. Acute hypoxia increases S100beta protein in association with blood flow redistribution away from peripheral circulations in fetal sheep. Pediatr Res 2005;58(2):179- 84.
14. Oses JP, Leke R, Portela LV, et al. Biochemical brain markers and purinergic parameters in rat CSF after seizure induced by pentylenetetrazol. Brain Res Bull 2004; 64(2): 237-42.
15. Simonian NA, Coyle JT. Oxidative Stres in Neurodegenerative Diseases. Ann Rev Pharmacol Toxicol 1996;36(1):83-106.
16. Michael T, Lin, M. Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases. Nature 2006;443(3):787-95.
17. Li SW, Barger L, Liu RE, Mrak MST. S100b induction of the proinflammatory cytokine interleukin-6 in neurons. J Neurochem 2000;74(1):143-50.
18. Yuksel D, Yilmaz D, Uyar NY, Senbil N, Gurer Y, Anlar B. Tau proteins in the cerebrospinal fluid of patients with subacute sclerosing panencephalitis. Brain Dev 2010;32(3): 467-71.
19. Wiesmann M, Wandinger KP, Missler U, Eckhoff D, Rothermundt M, Arolt V, et al. Elevated plasma levels of S-100b protein in schizophrenic patients. Biol Psychiatry 1999;45:1508-11.
20. Chaves ML, Camozzato AL, Ferreira ED, et al. Serum levels of S100B and NSE proteins in Alzheimers disease patients. J Neuroinflammation 2010; 7(1):1-6.
21. Gazzolo D, Grutzfeld Dariusz, et al. Increased S100B in cerebrospinal fluid of infants with bacterial meningitis: Relationship to brain damage and routine cerebrospinal fluid findings. Clin Chem 2004;50(8):941-4.