Letter to the editor of clinical endocrinology: Assessment of adrenal function in patients who survive COVID-19.
Letter to the editor of clinical endocrinology: Assessment of adrenal function in patients who survive COVID-19.
复制标题
致临床内分泌学编辑的信：评估 COVID-19 存活患者的肾上腺功能。
DOI：
10.1111/cen.14816
复制
发表时间：
2023
影响因子：
3.2
通讯作者：
Clarke SA
中科院分区：
文献类型：
--
作者：
Clarke SA
人们普遍认为，COVID-19的影响超出了呼吸系统。此外，仅在英国，估计就有130万人患有长期COVID（感染后症状持续超过12周），1一项研究发现，57%的COVID-19患者在感染后6个月内至少出现一种长期COVID症状。2因此，目前的努力集中在了解急性COVID-19后持续症状的病理生理学，以期为新疗法的开发提供信息。Kanczkowski及其同事3最近发表的一篇文章试图确定COVID-19患者中是否存在肾上腺损伤的组织学证据。考虑到ACE 2受体和跨膜丝氨酸蛋白酶2（TMPRSS;细胞进入的允许蛋白）已在肾上腺微血管和肾上腺皮质本身中被鉴定，这一点特别相关，4为SARS-CoV-2获得细胞进入并导致肾上腺皮质功能障碍的能力提供了生物学上的可接受性。使用40名死于COVID-19的患者的尸检样本，作者观察到肾上腺周围脂肪组织和肾上腺实质内的小血管炎和血管周围淋巴浆细胞浸润，但没有观察到肾上腺皮质细胞的广泛降解。此外，他们使用单克隆抗体在45%的肾上腺组织的肾上腺皮质细胞中鉴定了SARS-CoV-2刺突蛋白，并使用多重逆转录定量聚合酶链反应（RT-qPCR）证实了SARS-CoV-2在COVID-19患者的30个肾上腺组织中的15个中表达。这些数据证实了肾上腺内存在SARS-CoV-2，因此提出了COVID-19患者肾上腺功能减退的问题。事实上，有几例病例报告显示，急性COVID-19患者存在肾上腺功能不全。通常，在无已知基础肾上腺病变的患者中观察到肾上腺出血。5-7还报告了继发于肾上腺梗死的肾上腺功能不全，尽管这主要发生在基础抗磷脂综合征患者中，使患者易于发生血栓形成事件。八、九
It is widely recognised that the effects of COVID‐19 extend beyond the respiratory system. Moreover, there are an estimated 1.3 million people living with long COVID (symptoms persisting beyond 12 weeks after infection) in the United Kingdom alone, 1 with one study finding that 57% of patients with COVID‐19 experienced at least one symptom of long COVID in the 6 months following infection. 2 Current endeavours are therefore focused on understanding the pathophysiology of persistent symptoms after acute COVID‐19, with a view to informing the development of novel therapeutics. A recent article by Kanczkowski and colleagues 3 sought to determine whether there was any histological evidence of adrenal damage present in patients with COVID‐19. This is particularly pertinent given that both ACE2 receptors and transmembrane serine protease 2 (TMPRSS; the permissive protein for cellular entry) have been identified in the adrenal microvasculature and the adrenal cortex itself, 4 providing biological plausibility for the ability of SARS‐CoV‐2 to both gain cellular access and cause adrenocortical dysfunction. Using autopsy samples from 40 patients who had died from COVID‐19, the authors observed small vessel vasculitis and perivascular lymphoplasmacellular infiltration within the periadrenal fat tissue and adrenal parenchyma, but did not observe extensive degradation of adrenocortical cells. Additionally, using a monoclonal antibody, they identified the SARS‐CoV‐2 spike protein in adrenocortical cells of 45% of adrenal gland tissues, and using multiplex reverse‐transcription quantitative polymerase chain reaction (RT‐qPCR) confirmed SARS‐CoV‐2 expression in 15 out of 30 adrenal gland tissues of patients with COVID‐19. These data confirm the presence of SARS‐CoV‐2 within the adrenal glands and hence raise the question of hypoadrenalism in patients with COVID‐19.Indeed, several case reports exist of adrenal insufficiency in patients diagnosed with acute COVID‐19. Typically, adrenal haemorrhage was observed in patients with no known underlying adrenal lesions. 5–7 Adrenal insufficiency secondary to adrenal infarct has also been reported, although this predominantly occurred in patients with underlying antiphospholipid syndrome, predisposing patients to thrombotic events. 8, 9