The Effects of SARS-CoV-2 on Angiopoietin/Tie Axis and Vascular Endothelium (preprint)

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can cause potentially life-threatening coronavirus disease (COVID-19). COVID-19 is a multisystem disease and is associated with significant respiratory distress, systemic hyper inflammation, vasculitis and multi-organ failures. SARS-CoV-2 causes deterioration of numerous systems with increasing evidence implying that COVID-19 affects endothelium and vascular function. The endothelium is important for preserving vascular tone and homeostasis. The overactivation and dysfunction of endothelial cells are significant outcomes of severity in patients with COVID-19. The Angiopoietin 1/Tie 2 pathway plays an important role in endothelium quiescence and vessel stability. The disruption of Angiopoietins/Tie balance affects vessel contact barrier and leads to vessel leakage, and this in turn causes endothelial dysfunction. Although vascular instability through SARS-CoV-2 is associated with endothelial dysfunction, it is still not understood if the virus affects Angiopoietin/Tie axis directly or via other mechanisms such as cytokine storm and/or immune response associated with the infection. This review provides an overview of the impact SARS-CoV-2 has on endothelial function and more specifically the Angiopoietin/Tie pathway.

Risk factors for severe COVID-19 infection and the impact of COVID-19 infection on disease progression among patients with AAV (preprint)

Objective To identify risk factors for COVID-19 infection and investigate the impact of COVID-19 infection on chronic kidney disease (CKD) progression and vasculitis flare in patients with antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV).Methods This cohort study retrospectively analyzed the prevalence and severity of COVID-19 infection in 276 patients with AAV who were followed up. Logistic regression was employed to estimate the risk of COVID-19 infection as well as CKD progression and vasculitis flare upon COVID-19 infection.Results During the 6-month observation period, 213 (77.2%) of 276 patients had a diagnosis of COVID-19 infection. Of these 213 patients, 49 (23.0%) had a COVID-19-related inpatient admission, including 17 patients who died of COVID-19 infection. AAV patients with severe COVID-19 infection were more likely to be male (OR 1.921 [95% CI 1.020–3.619], P = 0.043), suffered from worse kidney function (serum creatinine [Scr], OR 1.901 [95% CI 1.345–2.687], P < 0.001), had higher C-reactive protein (CRP) (OR 1.054 [95% CI 1.010–1.101], P = 0.017) and less likely to have evidence of initial vaccination (OR 0.469 [95% CI 0.231–0.951], P = 0.036), and Scr and COVID-19 vaccination were proven to be significantly associated with severe COVID-19 infection even after multivariable adjustment. Severe COVID-19 infection was significantly associated with subsequent CKD progression (OR 7.929 [95% CI 2.030-30.961], P = 0.003) and vasculitis flare (OR 11.842 [95% CI 1.048-133.835], P = 0.046) among patients with AAV.Conclusion AAV patients who were male, and with worse kidney function were more susceptible to severe COVID-19 infection, which subsequently increased the risk of CKD progression and vasculitis flare.

Microfluidic antibody profiling after repeated SARS-CoV-2 vaccination links antibody affinity and concentration to impaired immunity and variant escape in patients on anti-CD-20 therapy (preprint)

Background: Patients with autoimmune/inflammatory conditions on anti-CD20 therapies, such as Rituximab, have suboptimal humoral responses to vaccination and are vulnerable to poorer clinical outcomes following SARS-CoV-2 infection. We aimed to examine how the fundamental parameters of antibody responses, namely affinity and concentration, shape the quality of humoral immunity after vaccination in these patients. Methods: We performed in depth antibody characterisation in sera collected four to six weeks after each of three vaccine doses to wild-type (WT) SARS-CoV-2 in Rituximab-treated primary vasculitis patients (n=14) using Luminex and pseudovirus neutralisation assays, whereas a novel microfluidic-based immunoassay was used to quantify polyclonal antibody affinity and concentration against both WT and Omicron (B.1.1.529) variants. Comparative antibody profiling was performed at equivalent time points in healthy individuals after three antigenic exposures to WT SARS-CoV-2 (one infection and two vaccinations; n=15) and in convalescent patients after WT SARS-CoV-2 infection (n=30). Results: Rituximab-treated patients had lower antibody levels and neutralisation titres against both WT and Omicron SARS-CoV-2 variants compared to healthy individuals. Neutralisation capacity was weaker against Omicron versus WT both in Rituximab-treated patients and in healthy individuals. In the Rituximab cohort, this was driven by lower antibody affinity against Omicron versus WT (median [range] KD: 21.6 [9.7-38.8] nM vs 4.6 [2.3-44.8] nM, p=0.0004). By contrast, healthy individuals with hybrid immunity produced a broader antibody response, a subset of which recognised Omicron with higher affinity than antibodies in Rituximab-treated patients (median [range] KD: 1.05 [0.45-1.84] nM vs 20.25 [13.2-38.8] nM, p=0.0002), underpinning the stronger serum neutralisation capacity against Omicron in the former group. Rituximab-treated patients had similar anti-WT antibody levels and neutralisation titres to unvaccinated convalescent individuals, despite two more exposures to SARS-CoV-2 antigen. Temporal profiling of the antibody response showed evidence of affinity maturation in healthy convalescent patients after a single SARS-CoV-2 infection which was not observed in Rituximab-treated patients, despite repeated vaccination. Discussion: Our results enrich previous observations of impaired humoral immune responses to SARS-CoV-2 in Rituximab-treated patients and highlight the significance of quantitative assessment of serum antibody affinity and concentration in monitoring anti-viral immunity, viral escape, and the evolution of the humoral response.

Long COVID is primarily a Spike protein Induced Thrombotic Vasculitis (preprint)

Long COVID describes an array of often debilitating symptoms in the aftermath of SARS-CoV-2 infection, with similar symptomatology affecting some people post-vaccination. With an estimated > 200 million Long COVID patients worldwide and cases still rising, the effects on quality of life and the economy are significant, thus warranting urgent attention to understand the pathophysiology. Herein we describe our perspective that Long COVID is a continuation of acute COVID-19 pathology, whereby coagulopathy is the main driver of disease and can cause or exacerbate other pathologies common in Long COVID, such as mast cell activation syndrome and dysautonomia. Considering the SARS-CoV-2 spike protein can independently induce fibrinaloid microclots, platelet activation, and endotheliitis, we predict that persistent spike protein will be a key mechanism driving the continued coagulopathy in Long COVID. We discuss several treatment targets to address the coagulopathy, and predict that (particularly early) treatment with combination anticoagulant and antiplatelet drugs will bring significant relief to many patients, supported by a case study. To help focus attention on such treatment targets, we propose Long COVID should be referred to as Spike protein Induced Thrombotic Vasculitis (SITV). These ideas require urgent testing, especially as the world tries to co-exist with COVID-19.

Systemic vasculitis: one year in review 2023.

Systemic vasculitides are heterogeneous disabling diseases characterised by chronic inflammation of the blood vessels potentially leading to tissue destruction and organ failure. The recent COVID-19 pandemic has had a significant impact on the epidemiology and management of patients with systemic vasculitis. In parallel, new insights have been provided on systemic vasculitis pathogenetic mechanisms, possible new therapeutic targets, and newer glucocorticoid-sparing treatments with better safety profiles. As in the previous annual reviews of this series, in this review we will provide a critical digest of the most recent literature regarding pathophysiology, clinical manifestations, diagnostic tools and treatment options in small- and large-vessel vasculitis focusing on precision medicine in vasculitis.

Successful Medical-Surgical Management of Intracardiac Thrombosis and Pulmonary Pseudoaneurysms in an Adolescent With Hughes-Stovin Syndrome.

We present an adolescent male with a single intracardiac mass and pulmonary emboli, complicated by peripheral venous thrombosis and subsequent development of pulmonary pseudoaneurysms, leading to diagnosis of Hughes-Stovin syndrome. Remission was achieved with cyclophosphamide, corticosteroids, and pseudoaneurysm resection and maintained with infliximab and methotrexate.

Managing Immunosuppression in Vasculitis Patients in Times of Coronavirus Disease 2019.

The coronavirus disease 2019 (COVID-19) pandemic has led to the emergence of multiple challenges in the care of patients with systemic rheumatic diseases. Patients with vasculitis represent a group of particular concern due to existing risk factors which include a higher burden of comorbidities and specific immunosuppressive therapies used for treatment. Vaccination and the use of other risk mitigation strategies are crucial for the care of these patients. This review provides an overview of existing evidence to contribute to the understanding and specific requirements of the treatment and management of patients with vasculitis during the time of COVID-19.

[Kawasaki disease cytokine release syndrome and Kawasaki disease shock syndrome: A case report]. / Síndrome de tormenta de citocinas y síndrome de choque por enfermedad de Kawasaki: reporte de un caso.

BACKGROUND: Kawasaki disease is a vasculitis of small and medium vessels, with a high prevalence throughout the world. In addition to coronary aneurysms, this vasculitis can lead to a number of systemic complications, including Kawasaki disease shock syndrome and Kawasaki disease cytokine storm syndrome. CASE REPORT: : Case report: A 12-year-old male patient, who began his condition with heartburn, sudden fever of 40 ºC and jaundice, for which he was prescribed treatment with antipyretics and bismuth subsalicylate, without satisfactory reaction. Gastroalimentary content was added three times, and centripetal maculopapular dermatosis. After 12 hospital stays, he was evaluated by personnel from the Pediatric Immunology service, who reported data on hemodynamic instability due to persistent tachycardia for hours, immediate capillary refill, intense pulse, oliguria of 0.3 mL/kg/h of partial urinary output with condensed urine; the systolic blood pressure figures were below the 50% percentile, and there was polypnea and limit saturation in 93%. In the paraclinical studies, the rapid decrease in platelet count (from 297,000 to 59,000 in 24 hours), as well as a neutrophil-lymphocyte index of 12, drew attention. The concentrations of NS1 size, IgM and IgG for dengue and PCR for SARS virus were determined. -CoV-2, which were negative. The definitive diagnosis of Kawasaki disease was established with Kawasaki disease shock syndrome. The evolution of the patient was satisfactory, with a decrease in fever after the administration of gamma globulin on the tenth day of hospitalization, and a new protocol with prednisone (50 mg/day) was started, when the cytokine storm syndrome due to illness was integrated. Kawasaki syndrome simultaneous with pre-existing disorders, that is, Kawasaki disease and Kawasaki disease shock syndrome due to thrombocytopenia, hepatosplenomegaly, fever, lymphadenopathy; in addition, ferritin of 605 mg/dL and transaminasemia. The control echocardiogram did not show coronary abnormalities and hospital discharge was granted 48 hours after starting treatment with the corticosteroid, with a 14-day follow-up plan. CONCLUSIONS: Kawasaki disease is an autoimmune vasculitis that can worsen with simultaneous syndromes associated with high mortality. It is important to know this type of alterations and their differences to properly discern and implement effective and timely treatment.

INTRODUCCIÓN: La enfermedad de Kawasaki es una vasculitis de pequeños y medianos vasos, con elevada prevalencia en todo el mundo. Además de los aneurismas coronarios, esta vasculitis puede generar diversas complicaciones sistémicas, como el síndrome de choque por enfermedad de Kawasaki y el síndrome de tormenta de citocinas por enfermedad de Kawasaki. REPORTE DE CASO: Paciente masculino de 12 años de edad, que inició su padecimiento con pirosis, fiebre súbita de 40 ºC e ictericia, por lo que se le prescribió tratamiento con antipiréticos y subsalicilato de bismuto, sin reacción satisfactoria. Se agregó vómito de contenido gastroalimentario en tres ocasiones y dermatosis maculopapular centrípeta. Después de 12 horas de estancia intrahospitalaria fue valorado por personal del servicio de Inmunología Pediátrica, quienes informaron datos de inestabilidad hemodinámica por taquicardia persistente, llenado capilar inmediato, pulso intenso, oliguria de 0.3 mL/kg/h de gasto urinario parcial con orina condensada; las cifras de tensión arterial sistólica se encontraban debajo del percentil 50%, y había polipnea y saturación limítrofe en 93%. En los estudios paraclínicos llamó la atención el rápido descenso del conteo plaquetario (de 297,000 a 59,000 en 24 horas), así como el índice neutrófilo-linfocito de 12. Se determinaron las concentraciones de antígeno NS1, IgM e IgG para dengue y PCR para virus SARS-CoV-2, que resultaron negativas. Se estableció el diagnóstico definitivo de enfermedad de Kawasaki con síndrome de choque por enfermedad de Kawasaki. La evolución del paciente fue satisfactoria, con disminución de la fiebre luego de la administración de gammaglobulina en el décimo día de hospitalización, y se inició un nuevo protocolo con prednisona (50 mg/día), al integrarse el síndrome de tormenta de citocinas por enfermedad de Kawasaki simultáneo con las alteraciones preexistentes, es decir: enfermedad de Kawasaki y síndrome de choque por enfermedad de Kawasaki por trombocitopenia, hepatoesplenomegalia, fiebre, adenopatías; además, ferritina de 605 mg/dL y transaminasemia. El ecocardiograma de control no mostró modificaciones coronarias y se otorgó el alta hospitalaria después de 48 horas de iniciar el tratamiento con el corticosteroide, con plan de seguimiento en 14 días. CONCLUSIONES: La enfermedad de Kawasaki es una vasculitis autoinmunitaria que puede agravarse con síndromes simultáneos asociados y generar elevada mortalidad. Es importante conocer este tipo de alteraciones y sus diferencias para discernir de forma adecuada e implementar el tratamiento eficaz y oportuno.

Frail Silk: Is the Hughes-Stovin Syndrome a Behçet Syndrome Subtype with Aneurysm-Involved Gene Variants?

Hughes-Stovin syndrome is a rare disease characterized by thrombophlebitis and multiple pulmonary and/or bronchial aneurysms. The etiology and pathogenesis of HSS are incompletely known. The current consensus is that vasculitis underlies the pathogenic process, and pulmonary thrombosis follows arterial wall inflammation. As such, Hughes-Stovin syndrome may belong to the vascular cluster with lung involvement of Behçet syndrome, although oral aphtae, arthritis, and uveitis are rarely found. Behçet syndrome is a multifactorial polygenic disease with genetic, epigenetic, environmental, and mostly immunological contributors. The different Behçet syndrome phenotypes are presumably based upon different genetic determinants involving more than one pathogenic pathway. Hughes-Stovin syndrome may have common pathways with fibromuscular dysplasias and other diseases evolving with vascular aneurysms. We describe a Hughes-Stovin syndrome case fulfilling the Behçet syndrome criteria. A MYLK variant of unknown significance was detected, along with other heterozygous mutations in genes that may impact angiogenesis pathways. We discuss the possible involvement of these genetic findings, as well as other potential common determinants of Behçet/Hughes-Stovin syndrome and aneurysms in vascular Behçet syndrome. Recent advances in diagnostic techniques, including genetic testing, could help diagnose a specific Behçet syndrome subtype and other associated conditions to personalize the disease management.

[Skin and SARS-CoV-2 in pediatrics]. / Piel y SARS-CoV-2 en pediatría.

The clinical presentation, disease course, and outcome of SARS-CoV-2 infection in pediatrics differ from the presentation in adults. In a review by Hoang et al., the prevalence of dermatological manifestations was estimated in 0.25% of a total of 2,445 children with confirmed COVID-19. Similarly, the prevalence of skin manifestations was reported in 3% of 100 children in the Parri's study. A systematic review by Shah et al. analyzed 13 studies with 149 children who met eligibility criteria. The acral erythematous maculopapular lesion was the most common, as well as erythema multiforme, varicella rash, and presentations similar to Kawasaki disease. The duration of the skin lesion was one to two weeks in 43%. Skin biopsy of 18 cases complete superficial and deep perivascular and paracrine lymphocytic infiltrate and lymphocytic vasculitis were reported. RT-PCR was positive in 13.8 % of the cases. The serological markers of herpes simplex virus and parvovirus B19 analyzed were negative, except for Mycoplasma pneumoniae in two of 20 cases. The pathophysiological mechanism of skin lesions secondary to SARS-CoV-2 infection has not yet been explained; likely to be a combination of one or more complex mechanisms, direct skin damages induced by the virus, vasculitis-like reactions either indirect or secondary injuries as a consequence of a systemic inflammatory reaction. Publications from years 2019 to 2021 are reviewed in PubMed as the main search source, using key words.

La presentación clínica, curso de la enfermedad y resultado de la infección por SARS-CoV-2 en pediatría difieren de los observados en adultos. En una revisión de Hoang et al. se estimó que la prevalencia de las manifestaciones dermatológicas fue de 0.25 % de un total de 2445 niños con COVID-19 confirmada. Según Parri, se documentó 3 % en 100 niños. En la revisión sistemática de Shah et al.se analizaron 13 estudios que incluyeron 149 niños que cumplieron con los criterios de elegibilidad. La lesión maculopapular eritematosa acral fue la más común, también el eritema multiforme, el exantema de la varicela y las presentaciones similares a enfermedad de Kawasaki. La duración de las lesiones cutáneas fue de una a dos semanas en 43 %. La biopsia de piel de 18 casos reveló infiltrado linfocítico perivascular, infiltrado paracrino superficial y profundo y vasculitis linfocítica. La RT-PCR fue positiva en 13.8 %. Los marcadores serológicos analizados de virus de herpes simple y parvovirus B19 fueron negativos, y fueron positivos para Mycoplasma pneumoniae en dos de 20 casos. El mecanismo fisiopatológico de las lesiones en piel secundarias a infección por SARS-CoV-2 aún no se ha podido explicar; es probable que se trate de la combinación de uno o más mecanismos complejos, daños cutáneos directos inducidos por el virus, reacciones vasculíticas o lesiones indirectas o secundarias como consecuencia de una reacción inflamatoria sistemática. Se revisaron las publicaciones de 2019 a 2021 en PubMed como fuente principal de búsqueda, para lo cual se utilizaron palabras clave.

A CASE OF KAWASAKI DISEASE IN AN EIGHT-YEAR-OLD BOY.

Kawasaki disease is an acute systemic disease characterized by the predominant lesions of middle and small arteries, alongside destructive and proliferative vasculitis development. The aetiology is currently being discussed. Infectious factors are mostly preferred, in addition, autoimmune mechanisms and genetic heredity are considered. The diagnosis of Kawasaki disease is established by clinical signs; laboratory changes are usually taken into account as are ancillary criteria. The article discusses the clinical case of Kawasaki disease in an 8-year-old boy. Given the variety and inconsistency of the clinical symptoms (the child had four of the five mandatory criteria together with prolonged fever), there was a late diagnosis, namely on day 10 of the disease. Due to the high risk of cardiovascular complications in the differential diagnosis of children with fever lasting more than 3 days should be considered Kawasaki disease, followed by mandatory heart echocardiography during the first 10 days of the disease, especially if the fever is accompanied by the increase of acute phase reactants. When treating children with chronic fever without a specific source, the doctor should be wary of Kawasaki disease, as it can clinically simulate acute respiratory viral disease, the onset of diffuse connective tissue disease, and infectious endocarditis, and can have common features and require differential diagnostics with coronavirus associated multisystem inflammatory syndrome.

Hypocomplementemic urticarial vasculitis case with hemophagocytic lymphohistiocytosis following SARS-CoV-2 mRNA vaccination.

A 61-year-old man with no previous record of autoimmune disease developed fever, polyarthralgia, purpura, and urticaria-like rash 2 weeks after the first dose of the Moderna mRNA-1273 vaccine, and symptoms deteriorated following the second dose. He presented reduced erythrocyte and platelet counts, hyperferritinemia, high sIL-2R levels, and severe hypocomplementemia. We diagnosed hypocomplementemic urticarial vasculitis (HUVS), and his symptoms as well as laboratory findings improved following treatment with mPSL 1000 mg/day for 3 days and PSL 40 mg/day. Twelve weeks following treatment initiation, the patient relapsed with fever, sore throat, pancytopenia, and hyperferritinemia when the PSL dose was reduced to 12.5 mg/day. Bone marrow biopsy and MRI presented fatty marrow and hemophagocytosis. The patient's blood cells started recovering using ATG + CsA + EPAG therapy for hemophagocytic lymphohistiocytosis (HLH). This is the first case report of HUVS and HLH following SARS-CoV-2 mRNA vaccination. It is presumed that SARS-CoV-2 mRNA vaccine can induce the excessive production of certain types of cytokines, such as TNF-α, IL-1, IL-4, IL-5, IL-6, and IL-17 as a consequence of IL-6 Amplification (IL-6 Amp). SARS-CoV-2 mRNA-vaccines can cause disruption of immune homeostasis in healthy individuals. An extremely rare disease of HUVS complicated by HLH can be developed as a consequence.

Single cell RNA-seq resolution revealed CCR1+/SELL+/XAF+ CD14 monocytes mediated vascular endothelial cell injuries in Kawasaki disease and COVID-19.

INTRODUCTION: The COVID-19 pandemic provide the opportunities to explore the numerous similarities in clinical symptoms with Kawasaki disease (KD), including severe vasculitis. Despite this, the underlying mechanisms of vascular injury in both KD and COVID-19 remain elusive. To identify these mechanisms, this study employs single-cell RNA sequencing to explore the molecular mechanisms of immune responses in vasculitis, and validate the results through in vitro experiments. METHOD: The single-cell RNA sequencing (scRNA-seq) analysis of peripheral blood mononuclear cells (PBMCs) was carried out to investigate the molecular mechanisms of immune responses in vasculitis in KD and COVID-19. The analysis was performed on PBMCs from six children diagnosed with complete KD, three age-matched KD healthy controls (KHC), six COVID-19 patients (COV), three influenza patients (FLU), and four healthy controls (CHC). The results from the scRNA-seq analysis were validated through flow cytometry and immunofluorescence experiments on additional human samples. Subsequently, monocyte adhesion assays, immunofluorescence, and quantitative polymerase chain reaction (qPCR) were used to analyze the damages to endothelial cells post-interaction with monocytes in HUVEC and THP1 cultures. RESULTS: The scRNA-seq analysis revealed the potential cellular types involved and the alterations in genetic transcriptions in the inflammatory responses. The findings indicated that while the immune cell compositions had been altered in KD and COV patients, and the ratio of CD14+ monocytes were both elevated in KD and COV. While the CD14+ monocytes share a large scale of same differentiated expressed geens between KD and COV. The differential activation of CD14 and CD16 monocytes was found to respond to both endothelial and epithelial dysfunctions. Furthermore, SELL+/CCR1+/XAF1+ CD14 monocytes were seen to enhance the adhesion and damage to endothelial cells. The results also showed that different types of B cells were involved in both KD and COV, while only the activation of T cells was recorded in KD. CONCLUSION: In conclusion, our study demonstrated the role of the innate immune response in the regulation of endothelial dysfunction in both KD and COVID-19. Additionally, our findings indicate that the adaptive immunity activation differs between KD and COVID-19. Our results demonstrate that monocytes in COVID-19 exhibit adhesion to both endothelial cells and alveolar epithelial cells, thus providing insight into the mechanisms and shared phenotypes between KD and COVID-19.

Successful Treatment of Post-COVID-19 Severe ANCA-Associated Vasculitis: Case Report (preprint)

Background The SARS-CoV-2 pandemic has become the most serious health problem of today globally. Kidney involvement in patients with coronavirus disease 2019 (COVID-19) is common and associated with high mortality. Although acute tubular necrosis due to hemodynamic instability is the most common cause, other complex and destructive processes related to cytokine storm and activation of innate and adaptive immunity have also been reported.Case presentation: Herein, we present successful treatment of proteinase-3 anti-neutrophil cytoplasmic antibodies (PR3-ANCA)-associated vasculitis case presenting with severe pulmonary-renal syndrome as a rare and fatal complication of COVID-19 infection.Conclusions AAV is a serious disease and prompt treatment is one of the most important factors in patient survival.

An innovative hybrid training method for ultrasound in giant cell arteritis, polymyalgia rheumatica and large vessel vasculitis (preprint)

To circumvent the lack of hands-on ultrasound training resulting from inability to conduct face-to-face workshops during the COVID-19 pandemic, especially as local expertise was not available, we developed a novel hybrid method combining virtual and physical training. The objective was to achieve appropriate expertise in ultrasound for the safe and accurate diagnosis of giant cell arteritis, polymyalgia rheumatica, and large vessel vasculitis. To evaluate the effectiveness of training, competency assessment was conducted using the hybrid platform.

Spontaneous dissection of the superior mesenteric artery related to COVID-19.

Background: Spontaneous peripheral dissections are rare, and in a substantial number of cases, the underlying aetiology remains unclear. Patients and methods: We report the case of a 63-year-old male patient with a recent asymptomatic SARS-CoV-2 infection who presented with sudden-onset intermittent abdominal pain. Imaging studies revealed a dissection of the superior mesenteric artery (SMA) and large-vessel vasculitis involving the SMA as well as the carotid, subclavian, axillary and femoropopliteal arteries. In the absence of other predisposing factors, we supposed an association with prior COVID-19 and performed a systematic review of the literature to search for similar cases with arterial dissection related to acute or recent SARS-CoV-2 infection. Results: We identified 25 cases, including ours: 13 males and 12 females, with a median age of 48 years. In 22/25 patients, arterial dissection occurred within 4 weeks after the diagnosis of COVID-19 and involved the cerebral (11/25; 44%), coronary (10/25; 40%), splanchnic (3/25; 12%) and renal (2/25; 8%) arteries. Conclusions: Although initially known for its respiratory manifestations, it has become evident that SARS-CoV-2 not only infects pneumocytes but also enters the vascular endothelium, leading to endothelial dysfunction and hypercoagulability and - as shown in our case - large-vessel vasculitis, which may predispose patients to intramural haemorrhage and arterial dissection.