背景:迄今为止,关于与COVID-19相关的皮肤疾病的临床-组织病理学相关性的研究很少。
方法:病例1是一个90岁的老人,从鼻咽拭子检测出SARS-CoV-2阳性。两天后,他住院,11天后转移到重症监护病房。胸部CT显示双侧磨玻璃影。就在那一天,躯干出现红斑丘疹,肩膀和脖子,几天后变得紫癜。组织学评估显示患有紫癜性慢性浅表性皮炎。浅层和乳头状真皮出现水肿,血管周围淋巴粒细胞浸润和红细胞外渗。在上皮内水平,检测到海绵状和粒细胞浸润。小动脉,毛细血管和毛细血管后小静脉显示内皮肿胀并出现扩张。患者接受了羟氯喹治疗,阿奇霉素,洛匹那韦-利托那韦和托珠单抗。遗憾的是,由于严重的肺损伤,他死了.案件2是一个85岁的老人,入住重症监护病房,他被插管的地方。两天前,他从鼻咽拭子中检测出SARS-CoV-2阳性。胸部RX显示双侧非典型肺炎。七天后,涉及躯干的皮肤发红,上肢,颈部和面部发育,配置亚红皮病。组织学评估显示乳头和浅表网状真皮水肿,和浅层真皮中的血管周围淋巴细胞浸润。患者接受了羟氯喹治疗,阿奇霉素,洛匹那韦-利托那韦和托珠单抗。红皮病及呼吸道症状逐渐好转直至愈合。
结论:病例1中检测到的内皮肿胀可能是SARS-CoV-2诱导的内皮功能障碍的形态学表达。我们假设皮肤损伤可能是由内皮功能障碍引起的,由SARS-CoV-2感染内皮细胞或免疫系统激活引起。内皮完整性的破坏可以增强微血管通透性,炎症细胞和细胞因子的外渗,皮肤损伤。病例2发展为与COVID-19相关的亚红皮病,并在组织学水平检测到非特异性慢性皮炎。我们推测紫癜性皮疹可能代表更严重的凝血病的皮肤体征,如血管异常在组织学上突出显示的那样,而副红皮病可能是病毒血源性传播的表达,诱导非特异性慢性皮炎。
BACKGROUND: To date, very few studies on clinical-histopathological correlations of cutaneous disorders associated with COVID-19 have been conducted.
METHODS: The Case 1 was a 90-year-old man, who tested positive for SARS-CoV-2 from a nasopharyngeal swab. Two days later, he was hospitalized and after eleven days transferred to Intensive Care Unit. A chest CT showed bilateral ground-glass opacities. Just that day, an erythematous maculo-papular rash appeared on trunk, shoulders and neck, becoming purpuric after few days. Histological evaluations revealed a chronic superficial dermatitis with purpuric aspects. The superficial and papillary dermis appeared edematous, with a perivascular lympho-granulocytic infiltrate and erythrocytic extravasation. At intraepithelial level, spongiosis and a granulocyte infiltrate were detected. Arterioles, capillaries and post-capillary venules showed endothelial swelling and appeared ectatic. The patient was treated with hydroxychloroquine, azithromycin, lopinavir-ritonavir and tocilizumab. Regrettably, due to severe lung impairment, he died. The Case 2 was a 85-year-old man, admitted to Intensive Care Unit, where he was intubated. He had tested positive for SARS-CoV-2 from a nasopharyngeal swab two days before. A chest RX showed bilateral atypical pneumonia. After seven days, a cutaneous reddening involving trunk, upper limbs, neck and face developed, configuring a sub-erythroderma. Histological evaluations displayed edema in the papillary and superficial reticular dermis, and a perivascular lymphocytic infiltrate in the superficial dermis. The patient was treated with hydroxychloroquine, azithromycin, lopinavir-ritonavir and tocilizumab. Sub-erythroderma as well as respiratory symptoms gradually improved until healing.
CONCLUSIONS: The endothelial swelling detected in the Case 1 could be a morphological expression of SARS-CoV-2-induced endothelial dysfunction. We hypothesize that cutaneous damage could be initiated by endothelial dysfunction, caused by SARS-CoV-2 infection of endothelial cells or induced by immune system activation. The disruption of endothelial integrity could enhance microvascular permeability, extravasation of inflammatory cells and cytokines, with cutaneous injury. The Case 2 developed a sub-erythroderma associated with COVID-19, and a non-specific chronic dermatitis was detected at histological level. We speculate that a purpuric rash could represent the cutaneous sign of a more severe coagulopathy, as highlighted histologically by vascular abnormalities, while a sub-erythroderma could be expression of viral hematogenous spreading, inducing a non-specific chronic dermatitis.