The neuro-inflammation and excitotoxicity in perinatal brain injury: The emerging role of brain mast cells

Perinatal brain injury is a serious neurodevelopmental problem that can be occurred in preterm and term newborn infants. It is well established that neuro-inflammation is implicated in the pathophysiology of perinatal brain injury. The excitotoxicity is considered as a common molecular mechanism of perinatal brain injury. These insults are capable of leading to neuro-inflammation, but however neuro-inflammation is also able to induce the excitotoxicity in the developing brain. Thus, neuro-inflammation is both a cause and a consequence of excitotoxicity resulting in the brain damages during perinatal period. Excessive glutamate accumulation in the synaptic cleft in the brain is a prominent mechanism in the excitotoxicity while vasoactive and pro-inflammatory mediators such as histamine, prostaglandins, interleukin 1 (IL-1) β and tumor necrosis factor (TNF)-α released from brain-resident immune cells play a major role in neuro-inflammation that lead to the brain damages. Although the role of brain-resident microglial cells has been well documented in these neuro-inflammation processes, evidence for the role of brain mast cells (BMCs) has recently begun to emerge. Growing evidence indicates that brain mast cells are first responders of inflammatory insults in the developing brain and their activation is involved in induced brain injury. We have recently demonstrated that ibotenate-induced excitotoxicity leads to the activation of brain mast cells in a model of ibotenate-induced brain injury in newborn rats. Thus, in this review we point out the current knowledge on the bidirectional role of brain mast cells in neuro-inflammation and excitotoxicity underlying perinatal brain injury

Effect of COVID-19 pandemic on children undergone percutaneous endoscopic gastrostomy due to neurologic diseases

Aim: To investigate the effects of SAR-CoV-2 infection on nutritional status in patients who underwent percutaneous endoscopic gastrostomy (PEG) for neurological disorders. Methods: The clinical and laboratory follow-up data of the patients who underwent PEG in our clinic between 2002 and 2018 were evaluated before and during the pandemic. The results were analyzed statistically. Results: Twenty patients were included. They were 70.9±64.4 months old at the time of PEG, 97.9±67.8 months before the pandemic, and 105.5±60.8 months during the pandemic (p=0.048). Weight for age at the time of PEG increased from 10.7±4.6 kg to 15.6±7.2 kg before the pandemic. Hemoglobin was 12.3±1.4 g/dl at the time of PEG, 13.5±1.6 g/dl before the pandemic (p=0.045). Vitamin D was 24.1±8.9 ng/ml at the time of PEG and increased to 45.7±9.7 ng/ml during the pandemic (p=0.018). The annual number of visits before the pandemic was 9.8±5.7 and decreased to 2±1.7 during the pandemic (p=0.003). Twelve (%60) of the patients developed PEG complications, 6(30%) had their PEG replaced. Those who had developed PEG complications had low levels of albumin (3.3±0.4 vs 4±0.4 g/dl, p=0.022) and vitamin B12 (578±199 vs 1299±533 pg/ml, p=0.007). Conclusions: Even if PEG is applied late, it provides a partial improvement in patients, but the COVID-19 pandemic reversed these benefits and caused an increase in PEG complications. In order for the patient to get the maximum benefit from PEG, close follow-up is essential