Brown tumor of lumber spint in patient with chronic renal failure

Brown tumors are erosive bone lesions caused by increased osteoclastic activity. They usually occur in the severe forms of secondary  hyperparathyroidism, as in patients with hemodialysis-dependent chronic renal disease. Involvement of the lumbar spine with this tumor causing neural compression is extremely rare. We report a 49-year-old man, who had been on haemodialysis for CRF for over 15 years, presented with leg weakness and back pain over the thoracolumbar junction. There were no motor or sensory disturbances. Spinal MRI revealed osteolytic lesions of the ribs and lumbar vertebrae L1. The clinical and radiological abnormalities resolved after parathyroidectomy and spine surgery

Cavernome intramedullaire: a propos d’un cas

Le cavernome intramédullaire, malformation vasculaire rare, représente environ 5 à 12 % des malformations vasculaires spinales et 3 % des malformations vasculaires intra-durales. Il peut être longtemps asymptomatique ou se manifester par une altération brutale ou progressive des fonctions médullaires. Le diagnostic repose sur l’imagerie par résonance magnétique (IRM) médullaire et l’anatomopathologie. La chirurgie représente l’essentiel de la prise en charge, néanmoins elle n’est pas dénudée de complications. Nous rapportons un cas de cavernome intramédullaire chez une patiente de 24 ans, admise dans un tableau de compression médullaire dorsale lente avec une paraparésie évoluant depuis 2 ans. L’IRM médullaire a objectivé une lésion intramédullaire en regard deT7-T8. La patiente a bénéficié d’une exérèse totale de la tumeur et l’histologie a confirmé le cavernome intramédullaire. L’évolution a été marquée par une aggravation partielle du déficit moteur. A travers cette observation, les auteurs discutent les aspects cliniques, radiologiques ainsi que la prise en charge de cette pathologie rare.Mots clés: Cavernome, intramédullaire, malformation vasculair

SARS-CoV-2 Infects Endothelial Cells In Vivo and In Vitro

SARS-CoV-2 infection can cause fatal inflammatory lung pathology, including thrombosis and increased pulmonary vascular permeability leading to edema and hemorrhage. In addition to the lung, cytokine storm-induced inflammatory cascade also affects other organs. SARS-CoV-2 infection-related vascular inflammation is characterized by endotheliopathy in the lung and other organs. Whether SARS-CoV-2 causes endotheliopathy by directly infecting endothelial cells is not known and is the focus of the present study. We observed 1) the co-localization of SARS-CoV-2 with the endothelial cell marker CD31 in the lungs of SARS-CoV-2-infected mice expressing hACE2 in the lung by intranasal delivery of adenovirus 5-hACE2 (Ad5-hACE2 mice) and non-human primates at both the protein and RNA levels, and 2) SARS-CoV-2 proteins in endothelial cells by immunogold labeling and electron microscopic analysis. We also detected the co-localization of SARS-CoV-2 with CD31 in autopsied lung tissue obtained from patients who died from severe COVID-19. Comparative analysis of RNA sequencing data of the lungs of infected Ad5-hACE2 and Ad5-empty (control) mice revealed upregulated KRAS signaling pathway, a well-known pathway for cellular activation and dysfunction. Further, we showed that SARS-CoV-2 directly infects mature mouse aortic endothelial cells (AoECs) that were activated by performing an aortic sprouting assay prior to exposure to SARS-CoV-2. This was demonstrated by co-localization of SARS-CoV-2 and CD34 by immunostaining and detection of viral particles in electron microscopic studies. Moreover, the activated AoECs became positive for ACE-2 but not quiescent AoECs. Together, our results indicate that in addition to pneumocytes, SARS-CoV-2 also directly infects mature vascular endothelial cells in vivo and ex vivo, which may contribute to cardiovascular complications in SARS-CoV-2 infection, including multipleorgan failure