Department of Endocrinology, Carol Davila University of Medicine and Pharmacy, C.I. Parhon National Institute of Endocrinology, Bucharest, Romania;
Rom J Morphol Embryol. 2022 Jan-Mar;63(1):39-48. doi: 10.47162/RJME.63.1.03.
Cortisol is a key element in acute stress including a severe infection. However, in coronavirus-associated disease, 20% of subjects experience hypocortisolemia due to direct or immune damage of pituitary and adrenal glands. One extreme form of adrenal insufficiency is found in 2∕3 of cases with viral and post-viral adrenal infarction (AI) (with∕without adrenal hemorrhage) that is mostly associated with a severe coronavirus disease 2019 (COVID-19) infection; it requires prompt glucocorticoid intervention. Some reports are incidental findings at computed tomography (CT)∕magnetic resonance imaging (MRI) scans for non-adrenal complications like pulmonary spreading and others are seen on post-mortem analysis. This is a review of PubMed-accessible, English papers focusing on AI in addition to the infection, between March 1, 2020 and November 1, 2021. Exclusion criteria were acute adrenal insufficiency without the histopathological (HP) and∕or imaging report of adrenal enlargement, necrosis, etc., respective adrenal failure due to pituitary causes, or non-COVID-19-related adrenal events. We identified a total of 84 patients (different levels of statistical evidence), as follows: a retrospective study on 51 individuals, two post-mortem studies comprising nine, respectively 12 patients, a case series of five subjects, seven single-case reports. HP aspects include necrosis associated with ischemia, cortical lipid degeneration (+/- focal adrenalitis), and infarcts at the level of adrenal cortex, blood clot into vessels, acute fibrinoid necrosis in arterioles and capsules, as well as subendothelial vacuolization. Collateral potential contributors to adrenal damage are thrombotic events, coagulation anomalies, antiphospholipid syndrome, endothelial dysfunction, severe COVID-19 infection with multiorgan failure, etc. Clinical picture is variable from acute primary adrenal insufficiency to asymptomatic or mild evolution, even a retrospective diagnostic; it may be a part of long COVID-19 syndrome; glucocorticoid therapy for non-adrenal considerations might mask cortisol deficient status due to AI∕hemorrhage. Despite its rarity, the COVID-19-associated AI/hemorrhage represents a challenging new chapter, a condition that is essential to be recognized due to its gravity since prompt intervention with glucocorticoid replacement is lifesaving.
皮质醇是急性应激(包括严重感染)的关键因素。然而,在冠状病毒相关疾病中,由于垂体和肾上腺的直接或免疫损伤,20%的患者出现皮质醇减少症。肾上腺功能不全的一种极端形式见于 2/3 的病毒性和病毒性后肾上腺梗死(AI)(伴或不伴肾上腺出血)病例,这些病例主要与严重的 2019 年冠状病毒病(COVID-19)感染有关;需要及时进行糖皮质激素干预。一些报道是在计算机断层扫描(CT)/磁共振成像(MRI)扫描时偶然发现的,用于肺部扩散等非肾上腺并发症,还有一些是在尸检时发现的。这是对 2020 年 3 月 1 日至 2021 年 11 月 1 日期间,在 PubMed 上可获取的关于除感染外 AI 的英文文献的综述。排除标准是无肾上腺增大、坏死等组织病理学(HP)和/或影像学报告的急性肾上腺功能不全,分别由垂体原因引起的肾上腺衰竭,或与 COVID-19 无关的肾上腺事件。我们共确定了 84 名患者(不同级别的统计证据),如下所示:对 51 名个体进行的回顾性研究,对 9 名和 12 名个体分别进行的 2 项尸检研究,对 5 名个体的病例系列研究,对 7 名个体的单病例报告。HP 方面包括与缺血相关的坏死、皮质脂质变性(+/-局灶性肾上腺炎)、肾上腺皮质水平的梗死、血管内血栓形成、小动脉和包膜内急性纤维蛋白样坏死以及血管内皮下空泡化。肾上腺损伤的潜在辅助因素有血栓事件、凝血异常、抗磷脂综合征、内皮功能障碍、多器官衰竭的严重 COVID-19 感染等。临床表型从急性原发性肾上腺功能不全到无症状或轻度进展,甚至是回顾性诊断,均有所不同;它可能是长期 COVID-19 综合征的一部分;由于 AI/出血引起的皮质醇缺乏状态,非肾上腺考虑因素的糖皮质激素治疗可能会掩盖这种状态。尽管 COVID-19 相关 AI/出血较为罕见,但却是一个具有挑战性的新章节,由于其严重性,必须认识到这种情况,因为及时进行糖皮质激素替代治疗是救命的。