Department of Morphology, Surgery and Experimental Medicine, Institute of Obstetrics and Gynaecology, University of Ferrara, 44121, Ferrara, Italy.
Department of Women Health, Infancy and Adolescence, AUSL Ravenna, 48121, Ravenna, Italy.
Acta Neurol Belg. 2020 Apr;120(2):277-288. doi: 10.1007/s13760-020-01308-3. Epub 2020 Feb 28.
Hypoxic-ischemic encephalopathy, also referred as HIE, is a type of brain injury or damage that is caused by a lack of oxygen to the brain during neonatal period. The incidence is approximately 1.5 cases per 1000 live births in developed countries. In low and middle-income countries, the incidence is much higher (10‒20 per 1000 live births). The treatment for neonatal HIE is hypothermia that is only partially effective (not more than 50% of the neonates treated achieve an improved outcome). HIE pathophysiology involves oxidative stress, mitochondrial energy production failure, glutaminergic excitotoxicity, and apoptosis. So, in the last years, many studies have focused on peptides that act somewhere in the pathway activated by severe anoxic injury leading to HIE. This review describes the pathophysiology of perinatal HIE and the mechanisms that could be the target of innovative HIE treatments.
缺氧缺血性脑病,也称为 HIE,是一种在新生儿期由于大脑缺氧引起的脑损伤或损害。在发达国家,其发病率约为每 1000 例活产儿中有 1.5 例。在低收入和中等收入国家,发病率更高(每 1000 例活产儿中有 10-20 例)。新生儿 HIE 的治疗方法是低温治疗,但仅部分有效(接受治疗的新生儿中,不超过 50%的新生儿获得改善的结果)。HIE 的病理生理学涉及氧化应激、线粒体能量产生衰竭、谷氨酰胺兴奋性毒性和细胞凋亡。因此,在过去几年中,许多研究都集中在某些肽上,这些肽在导致 HIE 的严重缺氧损伤所激活的途径中发挥作用。这篇综述描述了围产期 HIE 的病理生理学,以及可能成为创新 HIE 治疗目标的机制。