Eisenhut Michael
Luton and Dunstable University Hospital NHS Foundation Trust, Lewsey Road, Luton LU40DZ, UK.
Int J Otolaryngol. 2019 Nov 6;2019:4367240. doi: 10.1155/2019/4367240. eCollection 2019.
Sensorineural hearing loss is mainly acquired and affects an estimated 1.3 billion humans worldwide. It is related to aging, noise, infection, ototoxic drugs, and genetic defects. It is essential to identify reversible and preventable causes to be able to reduce the burden of this disease. Inflammation is involved in most causes and leads to tissue injury through vasospasm-associated ischemia. Vasospasm is reversible. This review summarized evidence linking inflammation-induced vasospasm to several forms of acquired sensorineural hearing loss. The link between vasospasm and sensorineural hearing loss is directly evident in subarachnoid haemorrhage, which involves the release of vasoconstriction-inducing cytokines like interleukin-1, endothelin-1, and tumour necrosis factor. These proinflammatory cytokines can also be released in response to infection, autoimmune disease, and acute or chronically increased inflammation in the ageing organism as in presbyacusis or in noise-induced cochlear injury. Evidence of vasospasm and hearing loss has also been discovered in bacterial meningitis and brain injury. Resolution of inflammation-induced vasospasm has been associated with improvement of hearing in autoimmune diseases involving overproduction of interleukin-1 from inflammasomes. There is mainly indirect evidence for vasospasm-associated sensorineural hearing loss in most forms of systemic or injury- or infection-induced local vascular inflammation. This opens up avenues in prevention and treatment of vascular and systemic inflammation as well as vasospasm itself as a way to prevent and treat most forms of acquired sensorineural hearing loss. Future research needs to investigate interventions antagonising vasospasm and vasospasm-inducing proinflammatory cytokines and their production in randomised controlled trials of prevention and treatment of acquired sensorineural hearing loss. Prime candidates for interventions are hereby inflammasome inhibitors and vasospasm-reducing drugs like nitric oxide donors, rho-kinase inhibitors, and magnesium which have the potential to reduce sensorineural hearing loss in meningitis, exposure to noise, brain injury, arteriosclerosis, and advanced age-related and autoimmune disease-related inflammation.
感音神经性听力损失主要是后天获得性的,全球估计有13亿人受其影响。它与衰老、噪音、感染、耳毒性药物和基因缺陷有关。识别可逆和可预防的病因对于减轻这种疾病的负担至关重要。炎症参与了大多数病因,并通过与血管痉挛相关的缺血导致组织损伤。血管痉挛是可逆的。本综述总结了将炎症诱导的血管痉挛与几种后天性感音神经性听力损失形式联系起来的证据。血管痉挛与感音神经性听力损失之间的联系在蛛网膜下腔出血中直接可见,蛛网膜下腔出血涉及如白细胞介素-1、内皮素-1和肿瘤坏死因子等诱导血管收缩的细胞因子的释放。这些促炎细胞因子也可因感染、自身免疫性疾病以及衰老机体中急性或慢性炎症增加(如在老年性耳聋或噪声性耳蜗损伤中)而释放。在细菌性脑膜炎和脑损伤中也发现了血管痉挛和听力损失的证据。在涉及炎性小体过度产生白细胞介素-1的自身免疫性疾病中,炎症诱导的血管痉挛的缓解与听力改善有关。在大多数全身性或损伤性或感染性局部血管炎症形式中,血管痉挛相关的感音神经性听力损失主要是间接证据。这为预防和治疗血管性和全身性炎症以及血管痉挛本身开辟了途径,作为预防和治疗大多数后天性感音神经性听力损失形式的一种方法。未来的研究需要在后天性感音神经性听力损失的预防和治疗随机对照试验中研究拮抗血管痉挛和血管痉挛诱导的促炎细胞因子及其产生的干预措施。干预的主要候选药物是炎性小体抑制剂和降低血管痉挛的药物,如一氧化氮供体、 Rho激酶抑制剂和镁,它们有可能减少脑膜炎、噪声暴露、脑损伤、动脉硬化以及与年龄相关和自身免疫性疾病相关的晚期炎症中的感音神经性听力损失。