Ophthalmology, Wolverhampton Eye Infirmary, Wolverhampton, UK
Ophthalmology, Wolverhampton Eye Infirmary, Wolverhampton, UK.
BMJ Case Rep. 2021 Sep 20;14(9):e242702. doi: 10.1136/bcr-2021-242702.
We describe a patient who developed acute bilateral corneal decompensation following COVID-19 pneumonia and prolonged intensive care unit ventilation. SARS-CoV-2 uses human ACE2 as the receptor for entry with subsequent downregulation of ACE2. ACE2 receptors are found in human ocular surface cells including cornea. Mouse models of ACE2 deficiency result in corneal haze, oedema and ocular surface inflammation due to upregulation of the inflammatory cascades. We therefore hypothesise that the cause of this patient's corneal decompensation was viral endotheliitis due to direct infection by the SARS-CoV-2 virus.
我们描述了一例患者，其在 COVID-19 肺炎和长时间重症监护病房通气后出现急性双侧角膜失代偿。SARS-CoV-2 使用人类 ACE2 作为进入受体，随后 ACE2 下调。ACE2 受体存在于人类眼表细胞中，包括角膜。由于炎症级联的上调，ACE2 缺乏的小鼠模型导致角膜混浊、水肿和眼表炎症。因此，我们假设该患者角膜失代偿的原因是 SARS-CoV-2 病毒的直接感染导致的病毒性血管内皮炎。
