Circulating irisin and chemerin levels as predictors of seizure control in children with idiopathic epilepsy

Abstract

Irisin and chemerin peptides expression are triggered by hypoxia and involved in activation of inflammatory cascades in various organs including the brain; however, their role in epilepsy is not fully illustrated. This study aims to explore the predictive role of irisin and chemerin for seizure control in children with idiopathic epilepsy. This cross-sectional comparative study included 50 children with idiopathic epilepsy; 25 of them had controlled seizures over the previous 6 months and 30 age- and sex-matched healthy children as controls. Epilepsy characteristics, seizure severity Chalfont score, and response to medications were assessed in relation to serum irisin and chemerin levels. In comparison to healthy controls, serum chemerin and irisin levels were significantly higher in children with idiopathic epilepsy especially those with uncontrolled seizures. Serum chemerin and irisin levels had significant positive correlation with seizure severity Chalfont score and the duration of epilepsy. Elevated Chalfont score (OR 3.19), serum chemerin (OR 2.01), and irisin (OR 2.03) are predictors of uncontrolled seizures. Circulating chemerin and irisin have 80% and 76% sensitivity and 88% and 92% specificity at cutoff point > 191.38 ng/ml and > 151.2 ng/ml respectively for prediction of uncontrolled seizures in children with idiopathic epilepsy. Elevated circulating level of irisin and chemerin may predict poor seizure control in children with idiopathic epilepsy suggesting the role of hypoxia-triggered neuroinflammation in the pathogenesis of childhood idiopathic epilepsy.

Relationship of Circulating Irisin with Body Composition, Physical Activity, and Cardiovascular and Metabolic Disorders in the Pediatric Population

“…Irisin was also studied in Egyptian children with epilepsy. Children with idiopathic epilepsy presented higher irisin levels compared with controls [46]. Plasma irisin showed a positive correlation with the severity of seizures and the duration of the disease, probably playing a role as a predictor of uncontrolled seizures.…”

Evaluation of serum ghrelin, nesfatin-1, irisin, and vasoactive intestinal peptide levels in temporal lobe epilepsy patients with and without drug resistance: a cross-sectional study

“…In summary, in previous studies, significant alterations were reported in ghrelin [15][16][17][18] , irisin 20 , FNDC5/irisin 18 , and nesfatin-1 16,18 levels. Despite this, there is also lack of evidence of whether these four neuropeptide levels are altered with drug resistant temporal lobe epilepsy (DRTLE) or not.…”

“…In a previous study, it was found that chronic antiepileptic drug treatment (valproate) decreased the PTZ-induced increase in serum and brain irisin levels in PTZ-kindling in rats 18 . Significantly increased serum levels of irisin were reported in children with idiopathic epilepsy 20 . These controversial results may have been associated with different factors; the present study conducted on adults and the subjects had therefore received longer antiepileptic drug therapy.…”

“…In addition, FNDC5, the precursor of irisin, is present in the brain 19 . Significant alterations in serum levels of irisin 20 and FNDC5/ irisin 18 have been reported. Nesfatin-1 is a recently identified neuropeptide, produced in different areas of the brain 21 .…”

Irisin Is Correlated with Blood Pressure in Obstructive Sleep Apnea Patients

“…Meanwhile, it could be discovered in our results that SpO 2 nadir was related to AHI and irisin, which means that SpO 2 nadir may be regarded as intermediate pathway to connect AHI and irisin. It is reported that irisin expression is triggered by hypoxia-induced sympathetic activation and involved in activation of inflammatory cascades in various organs [ 40 – 42 ]. Also, some previous studies showed that irisin functioned as a protective factor by upregulating the cellular antioxidants, sustaining mitochondrial membrane potential, and reversing ATP production to counter the free radical damage induced by hypoxia [ 43 – 45 ].…”