LAUSR

Dear Editor in Chief, The coronavirus disease-19 (COVID-19) pandemic is still ongoing with serious implications affecting daily lives and social gatherings, posing a significant mental health burden on society. The characterization of neuropsychological manifestations in COVID-19 is complex as it encompasses psychosocial factors, virus-related injury mechanisms, and neurological immune-mediated damage. Severe acute respiratory syndrome coronavirus-2 (SARSCoV-2) has shown intrinsic neurotropism and may cause direct damage to the central nervous system (CNS) during acute infection and post-infective neurological complications. The virus binds to the angiotensin-converting enzyme 2 receptor on the surface of neurovascular cells (i.e., endothelial cells, pericytes, and glial cells), whose dysfunction may result in a wide range of neurological manifestations. Endothelial activation facilitates both venous and arterial thrombotic events, hence the increased risk of ischemic or hemorrhagic stroke. Blood–brain barrier (BBB) impairment determines the loss of immune-privilege leading to inflammatory CNS events [1]. The cytokine storm triggered by the most severe cases of SARS-CoV-2 infection may also induce a neurovascular unit and BBB dysfunction, thus causing indirect CNS damage [2]. Acute cerebrovascular disease has been reported in about 2.8% of COVID-19 patients with an overall estimate of venous and arterial thromboembolic complications between 5 and 15% in some series. Multiple cases of CNS demyelinating diseases have been described in patients with SARS-CoV-2 infection and acute transverse myelitis appeared to be an unexpectedly frequent neurological postinfective complication as well. Acute encephalopathies and encephalitis, presenting with mild to moderate confusion or overt delirium, have been reported in up to 31.8% of hospitalized COVID-19 patients with neurological symptoms. Other manifestations include seizures, cranial nerve abnormalities, and impairment of taste, smell, and vision [3]. Posterior reversible encephalopathy syndrome (PRES) has been reported as a rare occurrence, predominantly in patients with comorbidities and severe infections [4]. We present the case of a young female who was diagnosed with systemic lupus erythematosus (SLE) and active renal disease in September 2020. She was hospitalized and successfully treated with cyclophosphamide and steroid pulses after undergoing a renal biopsy, which revealed class IV lupus nephritis. She later developed proximal deep venous thrombosis of the axillary and subclavian veins from a peripherally inserted central catheter. Laboratory exams revealed a low positive titer of anti-cardiolipin and anti-β2glycoprotein-I IgG antibodies which may have contributed to a thrombotic diathesis. After initiating low molecular weight heparin, the patient became oligo-anuric and developed an expanding perirenal hematoma, treated by angiographic embolization, in the previously biopsied kidney. For developing renal insufficiency, she underwent continuous veno-venous hyperfiltration followed by hemodialysis until renal function recovery and spontaneous diuresis resumption. Laboratory exams also indicated a progressive improvement of SLE-related serological abnormalities (C3 0.21→0.84 g/L [0.9–1.8]; C4 0.05→0.15 g/L [0.09–0.36]; anti-dsDNA 2560.0→25.9 IU/mL]). During the recovery phase a surveillance nasopharyngeal swab resulted positive for SARS-CoV-2 and, even in absence of any overt respiratory symptom, laboratory tests revealed a biochemical profile consistent with the viral infection, characterized by increased levels of ferritin (1745 μg/L [10–120 μg/L]), C-reactive * Roberta Ramonda [email protected]