Subakut Sklerozan Panensefalit\'li çocuklarda serum S-100B düzeyleri

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 SSPE\'li 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-100B\'nin SSPE\' de nöronal hasarda güvenilir bir belirteç olmadığını göstermektedir.

Serum S-100B levels in children with Subacute Sclerosing Panencephalitis

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.

___

  • Garg RK. Subacute sclerosing panencephalitis. J Neu- rol 2008;14(12):1439-52.
  • 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.
  • Schulpis KH, Margeli A, Akalestos A, et al. Effects of mode of delivery on maternal-neonatal plasma anti- oxidant status and on protein S-100B serum concen- trations. Scand J Clin Lab Invest 2006;66(6):733-42.
  • Gazzolo D, Abella R, Marinoni E, et al. New markers of neonatal neurology. J Maternal-Fetal Neonat Med 2009;12(1): 1-5.
  • Rothermundt M, Peters M, Prehn JH, Arolt V. S100B in brain damage and neurodegenaration. Microsc Res Tech 2003;60(5):614-32.
  • Dyken PR. Subacute sclerosing panencephalitis. Neu- rol Clin 1985;3(2):179-95.
  • Jabbour JT, Garcia JH, Lemmi H, Ragland J, Duenas DA, Sever JL. Subacute sclerosing pan encephalitis. JAMA 1969;207(12):2248-54.
  • Oztürk A, Gürses C, Baykan B, Gökyigit A, Eraksoy M. Subacute sclerosing panencephalitis: Clinical and magnetic resonance imaging evaluation of 36 pa- tients. J Child Neurol 2002;17(1):25-9.
  • 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 pan- encephalitis. AJNR Am J Neuroradiol 2009;30(2):271- 5.
  • Lins H, Wallesch CW, Wunderlich MT. Sequential analyses of neurobiochemical markers of cerebral damage in cerebrospinal fluid and serum in CNS in- fections. Acta Neurol Scand 2005;112(2):303-08.
  • Ahlemeyer B, Beier H, Semkova I, Schaper C, Kriegl- stein 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.
  • 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.
  • Giussani DA, Thakor AS, Frulio R, Gazzolo D. Acute hypoxia increases S100beta protein in association with blood flow redistribution away from peripheral cir- culations in fetal sheep. Pediatr Res 2005;58(2):179- 84.
  • 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.
  • Simonian NA, Coyle JT. Oxidative Stres in Neuro- degenerative Diseases. Ann Rev Pharmacol Toxicol 1996;36(1):83-106.
  • Michael T, Lin, M. Mitochondrial dysfunction and oxi- dative stress in neurodegenerative diseases. Nature 2006;443(3):787-95.
  • Li SW, Barger L, Liu RE, Mrak MST. S100b induction of the proinflammatory cytokine interleukin-6 in neu- rons. J Neurochem 2000;74(1):143-50.
  • 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.
  • 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 Psy- chiatry 1999;45:1508-11.
  • Chaves ML, Camozzato AL, Ferreira ED, et al. Se- rum levels of S100B and NSE proteins in Alzheimer’s disease patients. J Neuroinflammation 2010; 7(1):1-6.
  • Gazzolo D, Grutzfeld Dariusz, et al. Increased S100B in cerebrospinal fluid of infants with bacterial menin- gitis: Relationship to brain damage and routine cere- brospinal fluid findings. Clin Chem 2004;50(8):941-4.