Cytokine levels in febrile seizure patients: A systematic review and meta-analysis

Kwon, Aram; Kwak, Byung Ok; Kim, Kyungmin; Ha, Jongseok; Kim, Soojin; Bae, Sun Hwan; Son, Jae Sung; Lee, Ran

doi:10.1016/j.seizure.2018.04.023

Cited by 53 publications

(60 citation statements)

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“…Although the mechanisms of febrile seizure are still under debate, the immune activity may overlap with the counter regulating hormonal activity and proinflammatory status described in stress hyperglycemia [1,4,5,72,73]. In febrile seizures, the role of inflammatory cytokines in the pathogenic cascade of febrile seizures has been supported by several studies [55][56][57][58]. Figure A2.…”

Section: Discussionmentioning

confidence: 98%

“…During acute severe illness, the role of proinflammatory cytokines in inducing stress hyperglycemia is complex. The role of inflammatory cytokines in the pathogenic cascade of febrile seizures is supported by several studies and could provide the common pathways with stress hyperglycemia [55][56][57][58]. Proinflammatory cytokines like Insulin resistance is mainly characterized by reduced insulin-mediated glucose uptake secondary to defects in postreceptor insulin signaling and altered glucose transporter.…”

Section: Conflicts Of Interestmentioning

confidence: 98%

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Stress Hyperglycemia as Predictive Factor of Recurrence in Children with Febrile Seizures

2020

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Stress hyperglycemia and hyperlactatemia are commonly referred to as markers of stress severity and poor outcome in children with severe acute illness or febrile seizures. Our prospective study aimed to explore the risk factors for stress hyperglycemia and the predictive value of stress hyperglycemia for febrile seizure recurrence. We evaluated as risk factors for blood glucose level, serum lactate, acid–base status, and the clinical parameters relevant to the severity of the infectious context or to febrile seizure event: fever degree, fever duration, seizure type and aspect, seizure duration, and recurrence. Among 166 febrile seizures events in 128 children, the prevalence of stress hyperglycemia (blood glucose >140 mg/dl) was 16.9%. The comparison of the stress versus non-stress hyperglycemia groups revealed lower pH (median (interquartile range): 7.46 (7.37, 7.53) vs. 7.48 (7.42, 7.53), p = 0.049), higher lactate levels (30.50 mg/dl (15, 36) vs. 19.50 mg/dl (15, 27), p = 0.000), slightly lower HCO3 (20.15 (20.20, 21.45) vs. 21.35 (20, 22.40), p = 0.020) in the stress hyperglycemia group. Multiple logistic regression analysis showed that prolonged febrile seizures (>15 min), recurrent febrile seizure (>1 seizure), focal seizure type, body temperature ≥39.5 °C and higher lactate values were significantly associated with stress hyperglycemia. These findings suggest a particular acute stress reaction in febrile seizures, with stress hyperglycemia playing an important role, particularly in patients with a recurrent seizure pattern. A more complex future approach linking pathogenic mechanisms and genetic traits would be advised and could provide further clues regarding recurrence pattern and individualized treatment.

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Section: Discussionmentioning

confidence: 98%

Section: Conflicts Of Interestmentioning

confidence: 98%

Stress Hyperglycemia as Predictive Factor of Recurrence in Children with Febrile Seizures

2020

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“…Febrile seizure (FS) is the most common form of childhood seizure occurring in 2-5% of children younger than 6 years (Kwon et al 2018). Though HMGB1 has not been directly implicated in the pathogenesis of FS, elevated levels of serum HMGB1 along with cytokines (IL-1b, IL-6, IL-10, interferon-c, and TNF-a) have been reported in patients (Choi et al 2011).…”

Section: Mechanistic Insights Of Hmgb1 In Epileptogenesis: Insights Fmentioning

confidence: 99%

High mobility group box 1 (HMGB1) as a novel frontier in epileptogenesis: from pathogenesis to therapeutic approaches

Paudel

Semple

Jones

et al. 2019

Journal of Neurochemistry

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Epilepsy is a serious neurological condition exhibiting complex pathology and deserving of more serious attention. More than 30% of people with epilepsy are not responsive to more than 20 anti‐epileptic drugs currently available, reflecting an unmet clinical need for novel therapeutic strategies. Not much is known about the pathogenesis of epilepsy, but evidence indicates that neuroinflammation might contribute to the onset and progression of epilepsy following acquired brain insults. However, the molecular mechanisms underlying these pathophysiological processes are yet to be fully understood. The emerging research suggests that high‐mobility group box protein 1 (HMGB1), a DNA‐binding protein that is both actively secreted by inflammatory cells and released by necrotic cells, might contribute to the pathogenesis of epilepsy. HMGB1 as an initiator and amplifier of neuroinflammation, and its activation is implicated in the propagation of seizures in animal models. The current review will highlight the potential role of HMGB1 in the pathogenesis of epilepsy, and implications of HMGB1‐targeted therapies against epilepsy. HMGB1 in this context is an emerging concept deserving further exploration. Increased understanding of HMGB1 in seizures and epilepsy will pave the way in designing novel and innovative therapeutic strategies that could modify the disease course or prevent its development.

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“… 1 A meta-analysis suggested the involvement of various pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukins (ILs) in the development of and maintenance of epileptic seizures in patients with major depressive disorders. 7 Additionally, evidence suggested the vital role of neuroinflammatory markers, including Cyclooxygenase-2 (COX-2) in the pathophysiology of epilepsy. 8 The other researchers reported manifestation implicated in experimental and human epilepsy includes impairment in membrane-bound inorganic phosphate ion channels such as Na + K + ATPase, voltage- and receptor-gated ion channels impairment, impaired GABA (gamma-Aminobutyric acid), glutamatergic and cholinergic transmission.…”

Section: Introductionmentioning

confidence: 99%

“… 8 The other researchers reported manifestation implicated in experimental and human epilepsy includes impairment in membrane-bound inorganic phosphate ion channels such as Na + K + ATPase, voltage- and receptor-gated ion channels impairment, impaired GABA (gamma-Aminobutyric acid), glutamatergic and cholinergic transmission. 1 , 7 Furthermore, the researcher has well established the link between elevated c-fos expression and voltage-gated ion channels modulated convulsions. 9 Moreover, the susceptibility of neuronal tissue toward ROS (reactive oxygen species) indicated the major contribution of oxidative stress in an array of neurodegenerative disorders, including Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, and epilepsy.…”

Section: Introductionmentioning

confidence: 99%

Phyllathin From Phyllanthus Amarus Ameliorates Epileptic Convulsion and Kindling Associated Post-Ictal Depression in Mice via Inhibition of NF-κB/TLR-4 Pathway

Zhang

Hua

et al. 2020

Dose-Response

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Background: Epilepsy is a chronic, complex, unprovoked, and recurrent disorder of the nervous system that affected several people worldwide. Phyllanthus amarus (PA) has been documented to have neuroprotective potential. Aim: To evaluate the potential of standardized extract of PA and its possible mechanism of action against the Pentylenetetrazol (PTZ)-induced convulsion and kindling associated post-ictal depression in experimental mice. Materials and Methods: Phyllathin was isolated from methanolic extract of PA and well-characterized using HPTLC, ESI-MS/MS, and LC/MS. Phyllathin containing a standardized extract of PA (50, 100, and 200 mg/kg) was administered in convulsed and kindled mice, followed by an assessment of various parameters. Results: The spectral analysis confirmed the molecular formula and weight of phyllanthin as C24H34O6 and 418.2342 Da. PA (100 and 200 mg/kg) significantly ameliorated PTZ-induced ( p < 0.05) duration, onset of tonic-clonic convulsion, and mortality in mice. It also significantly attenuated ( p < 0.05) PTZ-induced kindling in mice. Alteration in brain GABA, dopamine, and glutamate, Na+K+ATPase, Ca+2-ATPase activities, and oxido-nitrosative stress in kindled mice was significantly restored ( p < 0.05) by PA treatment. It also significantly ( p < 0.05) down-regulated brain mRNA expressions of NF-κB, TNF-α, IL-1β, COX-2, and TLR-4. Histological aberrations induced by PTZ in the brain of a kindled rat was significantly ( p < 0.05) ameliorated by PA. Conclusion: Phyllanthin containing a standardized extract of PA exerts its antiepileptic potential via balancing excitatory (glutamate) and inhibitory (GABA) brain monoamines, voltage-gated ion channels (Na+K+/Ca+2-ATPase) and inhibition of NF-κB/TLR-4 pathway to ameliorate neuroinflammation (TNF-α, IL-1β, and COX-2) in experimental mice.

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Cytokine levels in febrile seizure patients: A systematic review and meta-analysis

Abstract: The results of this meta-analysis suggest that CSF IL-1β level and serum IL-6 level are associated with an increased risk of FSs in children. Based on these results, it is expected that a therapeutic agent for specific cytokines could be developed in the future to prevent FS.

Cited by 53 publications

References 33 publications

Stress Hyperglycemia as Predictive Factor of Recurrence in Children with Febrile Seizures

Stress Hyperglycemia as Predictive Factor of Recurrence in Children with Febrile Seizures

High mobility group box 1 (HMGB1) as a novel frontier in epileptogenesis: from pathogenesis to therapeutic approaches

Phyllathin From Phyllanthus Amarus Ameliorates Epileptic Convulsion and Kindling Associated Post-Ictal Depression in Mice via Inhibition of NF-κB/TLR-4 Pathway

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