Symmetric cutaneous vasculitis in COVID‐19 pneumonia

Castelnovo, Laura; Capelli, F; Tamburello, A.; Faggioli, Paola; Mazzone, Antonino

doi:10.1111/jdv.16589

Cited by 47 publications

(54 citation statements)

References 4 publications

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“…typical vasculitis findings in other organ systems, including Kawasaki disease-like presentations (4,5). No evidence suggests a multisystem inflammatory syndrome or a Kawasaki diseaselike presentation, as the patient did not show any of the classic clinical physical findings.…”

Section: E275mentioning

confidence: 78%

Focal Cerebral Arteriopathy in a Pediatric Patient with COVID-19

et al. 2020

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T he neuroinvasive mechanism of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is not fully understood. SARS-CoV-2 may enter the central nervous system hematogenously, with other proposed routes, including the olfactory and trigeminal nerves, cerebral spinal fluid (CSF), and lymphatic system (1). Neurologic manifestations in pediatric patients with coronavirus disease 2019 (COV-ID-19) have uncommonly been reported. Herein, we report a presumptive case of ischemic stroke due to focal cerebral arteriopathy (FCA) associated with COVID-19. Case Presentation A previously healthy 12-year-old-boy with a new onset of generalized seizures was initially treated with diazepam. Shortly thereafter, he developed right-sided hemiparesis and dysarthria. There was no previous history of fever, cough, shortness of breath, skin rash, hemoglobinopathy, or recent trauma. No one in his family had a known history of COVID-19 infection. The diagnosis of COVID-19 was made according to the presence of SARS-CoV-2 viral nucleic acid in the nasopharyngeal swab using 2019 novel coronavirus real-time reverse-transcriptase polymerase chain reaction assay. Test results for the presence of SARS-CoV-2 viral nucleic acid in the CSF were also positive. Viral genome was extracted using a viral RNA kit (High Pure; Roche, Basel, Switzerland), with a multiplex one-step reverse-transcriptase realtime polymerase chain reaction test (Pishtaz Teb Zaman Diagnostics, Tehran, Iran) to amplify COVID-19 E, N, and ORF1ab and/or RdRp genes. A CSF bacterial culture showed no growth after 3 days, and tests for herpes simplex viruses 1 and 2 and varicella-zoster virus (QIAGEN, Hilden, Germany) were negative. The serum ferritin level was 86.7 ng/L, the C-reactive protein level was 3 mg/L, and the erythrocyte sedimentation rate was 45 mm/h. CSF analysis demonstrated 21 mg/dL of protein, 62 mg/dL of glucose, 100 red blood cells per cubic millimeter (using traumatic lumbar puncture), and no white blood cells. The CSF opening pressure was 25 mm of H 2 O. d-dimer level was not obtained. The platelet count was 285310 3 /µL, the prothrombin time was 12.1 seconds, the international normalized ratio was 0.9, and the partial thromboplastin time was 27 seconds. The antinuclear antibody level was normal.

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Section: E275mentioning

confidence: 78%

Focal Cerebral Arteriopathy in a Pediatric Patient with COVID-19

et al. 2020

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“…In our patient, we report the presence of overexpression of endothelial cells in medium-size vessels (while not in microvessels), vascular lumen obliteration by inflammatory cells with wall breakthrough, thrombosed vessels, and hemorrhagic infarction of the gallbladder. In fact, expression of endothelial cells could trigger a cytokine storm which recruits macrophages and causes inflammatory reactions, similar to those of vasculitis, and the activation of a thrombophilic status [24]. Indeed, SARS-CoV-2 infection upregulates the expression of pro-inflammatory cytokines, such as IL-6 and tumor necrosis factor-alpha (TNF-α).…”

Section: Discussionmentioning

confidence: 99%

Histopathological findings in a COVID-19 patient affected by ischemic gangrenous cholecystitis

et al. 2020

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Background: Since its first documentation, a novel coronavirus (SARS-CoV-2) infection has emerged worldwide, with the consequent declaration of a pandemic disease (COVID-19). Severe forms of acute respiratory failure can develop. In addition, SARS-CoV-2 may affect organs other than the lung, such as the liver, with frequent onset of late cholestasis. We here report the histological findings of a COVID-19 patient, affected by a tardive complication of acute ischemic and gangrenous cholecystitis with a perforated and relaxed gallbladder needing urgent surgery. Case presentation: A 59-year-old Caucasian male, affected by acute respiratory failure secondary to SARS-CoV-2 infection was admitted to our intensive care unit (ICU). Due to the severity of the disease, invasive mechanical ventilation was instituted and SARS-CoV-2 treatment (azithromycin 250 mg once-daily and hydroxychloroquine 200 mg trice-daily) started. Enoxaparin 8000 IU twice-daily was also administered subcutaneously. At day 8 of ICU admission, the clinical condition improved and patient was extubated. At day 32, patient revealed abdominal pain without signs of peritonism at examination, with increased inflammatory and cholestasis indexes at blood tests. At a first abdominal CT scan, perihepatic effusion and a relaxed gallbladder with dense content were detected. The surgeon decided to wait and see the evolution of clinical conditions. The day after, conditions further worsened and a laparotomic cholecystectomy was performed. A relaxed and perforated ischemic gangrenous gallbladder, with a local tissue inflammation and perihepatic fluid, was intraoperatively met. The gallbladder and a sample of omentum, adherent to the gallbladder, were also sent for histological examination. Hematoxylin-eosin-stained slides display inflammatory infiltration and endoluminal obliteration of vessels, with wall breakthrough, hemorrhagic infarction, and nerve hypertrophy of the gallbladder. The mucosa of the gallbladder appears also atrophic. Omentum vessels also appear largely thrombosed. Immunohistochemistry demonstrates an endothelial overexpression of medium-size vessels (anti-CD31), while not in micro-vessels, with a remarkable activity of macrophages (anti-CD68) and T helper lymphocytes (anti-CD4)

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“…The possibility of progressively evolving fibrosis would be supported by our findings from histopathology and electron microscopy, where we observed organization and pseudo-honeycombing as well as interstitial fibroblast activation with collagen deposition. Another parallel between CTDs and COVID-19 are the vasculitis-like changes, vascular dysfunction or microangiopathies that have been described in a subset of patients ( 29 – 31 ). While thromboembolic complications occurred in only two patients in our cohort (both ANA-positive), it would be of great interest to screen patients with more widespread vascular or cutaneous involvement for the presence of ANA.…”

Section: Discussionmentioning

confidence: 99%

Clinical, Serological, and Histopathological Similarities Between Severe COVID-19 and Acute Exacerbation of Connective Tissue Disease-Associated Interstitial Lung Disease (CTD-ILD)

et al. 2020

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Background and Objectives Understanding the pathophysiology of respiratory failure in coronavirus disease 2019 (COVID-19) is indispensable for development of therapeutic strategies. Since we observed similarities between COVID-19 and interstitial lung disease in connective tissue disease (CTD-ILD), we investigated features of autoimmunity in SARS-CoV-2-associated respiratory failure. Methods We prospectively enrolled 22 patients with RT-PCR-confirmed SARS-CoV-2 infection and 10 patients with non-COVID-19-associated pneumonia. Full laboratory testing was performed including autoantibody (AAB; ANA/ENA) screening using indirect immunofluorescence and immunoblot. Fifteen COVID-19 patients underwent high-resolution computed tomography. Transbronchial biopsies/autopsy tissue samples for histopathology and ultrastructural analyses were obtained from 4/3 cases, respectively. Results Thirteen (59.1%) patients developed acute respiratory distress syndrome (ARDS), and five patients (22.7%) died from the disease. ANA titers ≥1:320 and/or positive ENA immunoblots were detected in 11/13 (84.6%) COVID-19 patients with ARDS, in 1/9 (11.1%) COVID-19 patients without ARDS (p = 0.002) and in 4/10 (40%) patients with non-COVID-19-associated pneumonias (p = 0.039). Detection of AABs was significantly associated with a need for intensive care treatment (83.3 vs. 10%; p = 0.002) and occurrence of severe complications (75 vs. 20%, p = 0.03). Radiological and histopathological findings were highly heterogeneous including patterns reminiscent of exacerbating CTD-ILD, while ultrastructural analyses revealed interstitial thickening, fibroblast activation, and deposition of collagen fibrils. Conclusions We are the first to report overlapping clinical, serological, and imaging features between severe COVID-19 and acute exacerbation of CTD-ILD. Our findings indicate that autoimmune mechanisms determine both clinical course and long-term sequelae after SARS-CoV-2 infection, and the presence of autoantibodies might predict adverse clinical course in COVID-19 patients.

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Symmetric cutaneous vasculitis in COVID‐19 pneumonia

Abstract: Figure 1 Purpuric rash of a leg with surrounding partially infiltrated rash areas. Figure 2 Purpuric rash of a knee.

Cited by 47 publications

References 4 publications

Focal Cerebral Arteriopathy in a Pediatric Patient with COVID-19

Focal Cerebral Arteriopathy in a Pediatric Patient with COVID-19

Histopathological findings in a COVID-19 patient affected by ischemic gangrenous cholecystitis

Clinical, Serological, and Histopathological Similarities Between Severe COVID-19 and Acute Exacerbation of Connective Tissue Disease-Associated Interstitial Lung Disease (CTD-ILD)

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