老年人患SARS-CoV-2肺炎风险增加的背景审查

G. Losonczy
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摘要

在2019冠状病毒病大流行期间,老年人(>65岁)的发病率和死亡率特别高。这篇综述总结了一些重要的生理和临床方面的背景下增加的风险。呼吸道的清除可以防御吸入的颗粒,包括病毒。一些相关研究表明,老年人小气道和大气道的清除速度较慢。咳嗽峰值流量(咳嗽时呼气气流的速度,或咳嗽功率)是反映呼吸系统防御能力的另一个重要参数。同样,年龄的增长也会导致吸气和呼气肌无力,因此,咳嗽峰值流量较低。除了老年人的这些非特异性防御能力减弱外,研究还发现,老年小鼠对SARS-CoV-2病毒的特异性免疫反应几乎被阻断,前列腺素D2 (PGD2)合成的增强在这一现象中发挥了作用。PGD2的特异性拮抗剂保护老年动物免于死亡。在老年COVID-19患者中,CD8 T淋巴细胞计数低和血浆白细胞介素6 (IL-6)浓度高的患者比例更高。在COVID-19中,细胞免疫缺陷和明显炎症反应的结合已被确定为死亡的一个重要危险因素。
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Review of the background to increased risks of SARS-CoV-2 pneumonia among elderly people
Morbidity and mortality rates during the COVID-19 pandemic have been particularly high among elderly people (>65 years). This review summarises some of the important physiological and clinical aspects in the background of augmented risk. Airway clearance provides defence against inhaled particles, including viruses. Some relevant studies have indicated that clearance from the small and large airways is slower in elderly people. Cough peak flow (the speed of expiratory airflow during coughing, or cough power) is another important parameter that reflects the defence capacity of the respiratory system. Age has likewise been shown to induce inspiratory and expiratory muscle weakness and, as a consequence, a low cough peak flow. In addition to the weakening of these non-specific defences in elderly people, the specific immune response against the SARS-CoV-2 virus has been found to be nearly blocked in aged mice, and the augmented synthesis of prostaglandin D2 (PGD2) was found to play a role in this phenomenon. Aged animals were protected from death by a specific antagonist of PGD2. Among aged people suffering from COVID-19, there were disproportionally more patients with low CD8 T lymphocyte counts and high plasma concentrations of interleukin 6 (IL-6). This combination of deficient cellular immunity and overt inflammatory response in COVID-19 has been identified as a significant risk factor of mortality.
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34 weeks
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