Sphenoid plasmacytoma as initial presentation of multiple myeloma-case report.

Plasmacytoma is a rare plasma cell neoplasm. Whether solitary or associated with multiple myeloma (MM), it rarely involves the skull base, particularly the sphenoid bone. We present a unique case of sphenoid bone plasmacytoma secondary to MM, highlighting diagnostic and therapeutic challenges. A 56-year-old female presented with headaches, vomiting, epistaxis, and cranial nerve deficits. Cerebral imaging revealed a 65-mm tumor infiltrating the sphenoid bone and adjacent structures. Subtotal resection was performed using an endoscopic nasal approach. Histopathology revealed plasmacytoma, and diagnostic workup confirmed MM. By the end of biological exploration, relapse of the sphenoid plasmacytoma was observed, and the patient was successfully treated with radiotherapy, immunochemotherapy, and autologous stem cell transplantation. After 18-month follow-up, sustained complete remission was confirmed. Although rare, the diagnosis of plasmacytoma should be considered in cases of skull base tumors. This localization is highly predictive of MM, warranting comprehensive investigations to initiate prompt and adequate management.

Vascular complications of Behçet disease.

Behçet disease is a multi-systemic complex vasculitis with unknown etiology characterized by different clinical involvements, including mucocutaneous, ocular, vascular, articular, neurological, and gastrointestinal manifestations. Growing evidence supports that different phenotypes, characterized by clusters of co-existing involvements, can be distinguished. Namely, the vascular phenotype identifies a specific group of patients who suffer from recurrent inflammatory thrombosis and arterial involvement. Vascular disease develops in up to 40% with a definite male preponderance and is usually an early manifestation. Venous involvement is significantly more common than arterial disease, and lower extremity deep vein thrombosis is its most frequent manifestation. Arterial disease involves mostly pulmonary arteries and aorta and manifests mainly in the form of aneurysms. Glucocorticoids and immunosuppressants are the recommended first-line treatments in vasculo-Behçet. Furthermore, controlled trials are still needed to assess the role of adding anticoagulation to the treatment regimen, with an accent on new oral anticoagulants. Treatment with anti-TNF alpha agents seems promising, but the management strategies are not clear yet.

COVID-19 Associated Coagulopathy and Thrombotic Complications.

The SARS-CoV-2 virus caused a global pandemic within weeks, causing hundreds of thousands of people infected. Many patients with severe COVID-19 present with coagulation abnormalities, including increase D-dimers and fibrinogen. This coagulopathy is associated with an increased risk of death. Furthermore, a substantial proportion of patients with severe COVID-19 develop sometimes unrecognized, venous, and arterial thromboembolic complications. A better understanding of COVID-19 pathophysiology, in particular hemostatic disorders, will help to choose appropriate treatment strategies. A rigorous thrombotic risk assessment and the implementation of a suitable anticoagulation strategy are required. We review here the characteristics of COVID-19 coagulation laboratory findings in affected patients, the incidence of thromboembolic events and their specificities, and potential therapeutic interventions.

[Atherosclerosis in systemic lupus erythematosus]. / Athérosclérose au cours du lupus érythémateux systémique.

CONTEXT: Evidence from epidemiological studies demonstrates that patients with systemic lupus erythematosus (SLE) are at increased risk for the development of cardiovascular disease. Traditional cardiovascular risk factors' play an important role in this phenomenon but do not account for the entire risk in lupus patients. OBJECTIVES: The incidence and prevalence of cardiovascular events and infraclinical atherosclerosis are reviewed. Combinations of traditional risk factors with lupus-specific and treatment-related variables are detailed. RESULTS: Atherosclerosis is more prevalent and occurs prematurely in lupus patients. Relative risk of myocardial infarction is between 5 to 8 times greater that of general population, and may exceed 50 in women between 35 and 44 years old. SLE was also found as an independent risk factor for subclinical atherosclerosis, and more than one third of lupus patient show evidence of carotid plaques of coronary artery calcifications. Lupus patients have more frequent traditional risk factors compared with general population of similar age and sex. Besides the traditional risk factors, SLE specific risk factors have been identified among witch advanced age at diagnosis, current disease activity, duration of the disease and renal activity. Moreover, lipid abnormalities in patients with SLE are common and likely are one of the major causes of premature atherosclerosis in these patients; the dyslipoprotein associated increased triglycerides and depressed HDL-cholesterol with proinflammatory HDL production. Autoimmunity may have a part of responsibility, but data's in favour of this hypothesis are not strong. Other mechanisms such as vascular inflammation, oxidative stress, immune complexes and complement activation may also elicit endothelial damage and promote atherosclerosis are associated with the pathogenesis of both SLE and atherosclerosis. Steroids may have a true double-edged role with a pro-atherogenic risk regarding the exacerbation of metabolic risk factors and a "beneficial" anti-inflammatory role. It is becoming increasingly apparent that antimalarials treatment in SLE has an atheroprotective and a cardioprotective effect. The other immunosuppressive drugs may reduce progression of atherosclerosis and cardiovascular events but their precise role remains to be elucidated. Despite their role in primary prevention in target general population, for now, systematic prescription of statins does not show a great benefit in the cardiovascular risk in lupus patients. CONCLUSION: Mechanisms of atherosclerosis in SLE remain elusive. It is partially explained by the interaction of traditional cardiovascular risk factors, lupus-specific factors and therapy specially corticosteroids. Management strategies of lupus should include early all those items.