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A 60-year-old man was hospitalised with persistent fever, arm pain, dry cough and cholestasis. Diagnostic workup was remarkable for elevated inflammatory markers. Infectious diseases and autoimmune screening were negative. Imaging modalities excluded a neoplastic aetiology. Liver biopsy was negative for granulomatous or lymphomatous infiltrations. Giant cell arteritis (GCA) was suspected, but temporal artery Doppler ultrasound and biopsy were non-diagnostic. A positron emission tomography scan showed intense metabolic uptake in large vessels suggesting the diagnosis of GCA. Prednisolone was initiated with clinical and analytical improvement. At 1-year follow-up, there were no relapses and the patient remains symptom free., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2020. No commercial re-use. See rights and permissions. Published by BMJ.)

A 73-year-old man was transferred to the neurosurgery ward, with a presumptive diagnosis of cerebral abscess. The case was also discussed with the internists as internal medicine consultants. The neurosurgeons pointed out a right temporal lobe abscedated lesion on CT, but we noticed that the hypodense attenuation that usually surrounds the abscess wall (vasogenic oedema) extended to a broader, well-delimitated area, suggesting medium cerebral artery territory. The patient had left-sided hemiplegia with a confusional state and low-grade fever. Considering possible haematogenous dissemination, an echocardiography was performed, confirming mitral endocarditis. Blood cultures and aspirated pus isolated Escherichia coli. Investigating the patient's medical history, we learned he had been submitted to bladder catheterisation 7 weeks before for acute urinary retention due to benign prostatic hyperplasia, and empirically medicated for urinary tract infection. E. coli had also been isolated in a urine specimen at the time. The clinical history of the patient cancelled the pathogenesis of cerebral abscess., (2015 BMJ Publishing Group Ltd.)

Cardiogenic flash pulmonary oedema is a common and potentially fatal cause of acute respiratory distress. Although it often results from acute decompensated heart failure, abrupt-onset aortic regurgitation can sharply rise cardiac filling pressure and, consequently, pulmonary venous pressure, leading to rapid fluid accumulation in the interstitial and alveolar spaces. We report a case of a 64-year-old woman admitted to the emergency department with a flash pulmonary oedema; a careful clinical investigation subsequently revealed a rare aetiology for this 'common' presentation. After a detailed auscultation that unmasked a diastolic cardiac murmur, an acute severe aortic insufficiency was further confirmed by echocardiography, showing inflammation and thickening of the entire aorta wall. The patient was submitted to valve replacement surgery, and histological examination, to our surprise, showed features of aortitis, remarkable for the presence of giant cells. A diagnosis of idiopathic aortitis versus inaugural giant cell arteritis was proposed and treatment started with corticosteroids.