Interictal serum S100B levels in chronic neurocysticercosis and idiopathic epilepsy

Portela, Luis Valmor; Tort, Adriano Bretanha Lopes; Walz, Roger; Bianchin, Marino M.; Trevisol-Bittencourt, Paulo César; Wille, Paulo Roberto; Cardoso, Rita; Ishida, María Akíko; VonWangenheim, A.; Grisard, Edmundo C.; Steindel, Mario; Gonçalves, Carlos Alberto; Souza, Diogo O.

doi:10.1034/j.1600-0404.2003.00159.x

Cited by 27 publications

(20 citation statements)

References 22 publications

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“…These results are also in agreement with data reported by Portela et al (35) that revealed no changes in serum S100B levels in patients with epilepsy and chronic NC. However, in their series only patients (N = 20) harboring inactive forms were considered.…”

Section: Discussionsupporting

confidence: 83%

Serum and cerebrospinal fluid S100B concentrations in patients with neurocysticercosis

Lima

Walz

Tort

et al. 2006

Braz J Med Biol Res

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The clinical manifestations of neurocysticercosis (NC) are varied and depend on the number and location of cysts, as well as on the host immune response. Symptoms usually occur in NC when cysticerci enter a degenerative course associated with an inflammatory response. The expression of brain damage markers may be expected to increase during this phase. S100B is a calcium-binding protein produced and released predominantly by astrocytes that has been used as a marker of reactive gliosis and astrocytic death in many pathological conditions. The aim of the present study was to investigate the levels of S100B in patients in different phases of NC evolution. Cerebrospinal fluid and serum S100B concentrations were measured in 25 patients with NC: 14 patients with degenerative cysts (D), 8 patients with viable cysts (V) and 3 patients with inactive cysts. All NC patients, except 1, had five or less cysts. In most of them, symptoms had been present for at least 1 month before sample collection. Samples from 8 normal controls (C) were also assayed. The albumin quotient was used to estimate the blood-brain barrier permeability. There were no significant differences in serum (P = 0.5) or cerebrospinal fluid (P = 0.91) S100B levels among the V, D, and C groups. These findings suggest that parenchymal changes associated with a relatively small number of degenerating cysts probably have a negligible impact on glial tissue.

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Section: Discussionsupporting

confidence: 83%

Serum and cerebrospinal fluid S100B concentrations in patients with neurocysticercosis

Lima

Walz

Tort

et al. 2006

Braz J Med Biol Res

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“…As previously mentioned, S100B is widely used as a marker for epileptic disorders [ 31 , 32 ], and its secretion is modulated by anti-inflammatory drugs [ 35 , 36 ]. Our studies have suggested that the hippocampal and CSF S100B are altered after SE induction in the Li-pilocarpine model [ 14 ].…”

Section: Discussionmentioning

confidence: 99%

“…The S100B protein is a glial protein that is a widely used marker for brain injury conditions, including epileptic disorders [ 31 , 32 ], and indeed displays an augmented secretion during brain injury condition, working as a neurotrophic cytokine or simply as a damage-associated molecular pattern (DAMP) [ 33 ]. Moreover, S100B secretion is modulated by LPS [ 34 ] and anti-inflammatory drugs [ 35 , 36 ].…”

Section: Introductionmentioning

confidence: 99%

Effects of dexamethasone on the Li-pilocarpine model of epilepsy: protection against hippocampal inflammation and astrogliosis

Vizuete

Hansen

Negri

et al. 2018

J Neuroinflammation

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BackgroundTemporal lobe epilepsy (TLE) is the most common form of partial epilepsy and is accompanied, in one third of cases, by resistance to antiepileptic drugs (AED). Most AED target neuronal activity modulated by ionic channels, and the steroid sensitivity of these channels has supported the use of corticosteroids as adjunctives to AED. Assuming the importance of astrocytes in neuronal activity, we investigated inflammatory and astroglial markers in the hippocampus, a key structure affected in TLE and in the Li-pilocarpine model of epilepsy.MethodsInitially, hippocampal slices were obtained from sham rats and rats subjected to the Li-pilocarpine model of epilepsy, at 1, 14, and 56 days after status epilepticus (SE), which correspond to the acute, silent, and chronic phases. Dexamethasone was added to the incubation medium to evaluate the secretion of S100B, an astrocyte-derived protein widely used as a marker of brain injury. In the second set of experiments, we evaluated the in vivo effect of dexamethasone, administrated at 2 days after SE, on hippocampal inflammatory (COX-1/2, PGE2, and cytokines) and astroglial parameters: GFAP, S100B, glutamine synthetase (GS) and water (AQP-4), and K+ (Kir 4.1) channels.ResultsBasal S100B secretion and S100B secretion in high-K+ medium did not differ at 1, 14, and 56 days for the hippocampal slices from epileptic rats, in contrast to sham animal slices, where high-K+ medium decreased S100B secretion. Dexamethasone addition to the incubation medium per se induced a decrease in S100B secretion in sham and epileptic rats (1 and 56 days after SE induction). Following in vivo dexamethasone administration, inflammatory improvements were observed, astrogliosis was prevented (based on GFAP and S100B content), and astroglial dysfunction was partially abrogated (based on Kir 4.1 protein and GSH content). The GS decrease was not prevented by dexamethasone, and AQP-4 was not altered in this epileptic model.ConclusionsChanges in astroglial parameters emphasize the importance of these cells for understanding alterations and mechanisms of epileptic disorders in this model. In vivo dexamethasone administration prevented most of the parameters analyzed, reinforcing the importance of anti-inflammatory steroid therapy in the Li-pilocarpine model and possibly in other epileptic conditions in which neuroinflammation is present.Electronic supplementary materialThe online version of this article (10.1186/s12974-018-1109-5) contains supplementary material, which is available to authorized users.

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“…Serum neurotropic protein S100B, secreted and synthesized by oligodendrocyte and astroglia, is a sensitive indicator of brain injury [43]. Pathological changes, such as proliferation of gliocytes, damage of blood brain barrier, demyelinating of central nerves, and neuron injury that take place in the brain after epileptic seizure, lead to increased S100B protein [44,45]. In the current study, we showed that levetiracetam treatment lowered S100B protein levels in patients with refractory epilepsy (P \ 0.05).…”

Section: Discussionmentioning

confidence: 45%

The Effects of Levetiracetam on Cerebrospinal Fluid and Plasma NPY and GAL, and on the Components of Stress Response System, hs-CRP, and S100B Protein in Serum of Patients with Refractory Epilepsy

Chen

Tan

et al. 2015

Cell Biochem Biophys

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Our objective is to explore the effects of levetiracetam on the levels of neuropeptides, serum activity and concentrations of oxidative stress and inflammatory response proteins, and levels of brain injury marker in patients with refractory epilepsy. Seventy-two patients with refractory epilepsy received levetiracetam treatment. Neuropeptides galanin (GAL) and neuropeptide Y (NPY) in plasma and cerebrospinal fluid (CSF) were detected using double-antibody sandwich immunoassay and radioimmunoassay, respectively. Enzyme-linked immunosorbent assay was used to detect serum activity of paraoxonase (PON1) and serum concentrations of oxidized low-density lipoprotein (ox-LDL) and S100B. Arylesterase (ARE) activity was measured by colorimetric assay, and immune scatter turbidimetry was used to detect a high-sensitivity C-reactive protein (hs-CRP). After treatment, NPY and GAL in plasma and CSF of the patients were significantly decreased as compared to concentrations before treatment (P < 0.05). Levetiracetam reduced serum activities of PON1 and ARE (P < 0.05) and led to markedly increased serum levels of ox-LDL (P < 0.05). Serum concentrations of hs-CRP and S100B protein were significantly lower after levetiracetam administrations than before treatment (P < 0.05). Levetiracetam treatment had a clear beneficial effect on the overall quality of life (QOL) scores of the patients, as indicated by significantly improved cognitive functioning, behavior problems, emotional conditioning, physical condition, social functioning, self-assessed life quality score, self-assessed health score, and the total QOL score (P < 0.05). Levetiracetam can improve life quality of patients with refractory epilepsy, decrease NPY and GAL in plasma and cerebrospinal fluid, serum PON1 and ARE activities, and serum levels of ox-LDL, hs-CRP, and S100B. Levetiracetam therefore may be considered a drug of choice for treating refractory epilepsy.

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Interictal serum S100B levels in chronic neurocysticercosis and idiopathic epilepsy

Abstract: Serum S100B is normal in patients with focal epilepsy related or not to chronic NCC.

Cited by 27 publications

References 22 publications

Serum and cerebrospinal fluid S100B concentrations in patients with neurocysticercosis

Serum and cerebrospinal fluid S100B concentrations in patients with neurocysticercosis

Effects of dexamethasone on the Li-pilocarpine model of epilepsy: protection against hippocampal inflammation and astrogliosis

The Effects of Levetiracetam on Cerebrospinal Fluid and Plasma NPY and GAL, and on the Components of Stress Response System, hs-CRP, and S100B Protein in Serum of Patients with Refractory Epilepsy

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