Background In this study, we aimed to evaluate the effects of tocilizumab in adult patients admitted to hospital with COVID-19 with both hypoxia and systemic inflammation. Methods This randomised, controlled, open-label, platform trial (Randomised Evaluation of COVID-19 Therapy [RECOVERY]), is assessing several possible treatments in patients hospitalised with COVID-19 in the UK. Those trial participants with hypoxia (oxygen saturation <92% on air or requiring oxygen therapy) and evidence of systemic inflammation (C-reactive protein ≥75 mg/L) were eligible for random assignment in a 1:1 ratio to usual standard of care alone versus usual standard of care plus tocilizumab at a dose of 400 mg–800 mg (depending on weight) given intravenously. A second dose could be given 12–24 h later if the patient's condition had not improved. The primary outcome was 28-day mortality, assessed in the intention-to-treat population. The trial is registered with ISRCTN (50189673) and ClinicalTrials.gov ( NCT04381936 ). Findings Between April 23, 2020, and Jan 24, 2021, 4116 adults of 21 550 patients enrolled into the RECOVERY trial were included in the assessment of tocilizumab, including 3385 (82%) patients receiving systemic corticosteroids. Overall, 621 (31%) of the 2022 patients allocated tocilizumab and 729 (35%) of the 2094 patients allocated to usual care died within 28 days (rate ratio 0·85; 95% CI 0·76–0·94; p=0·0028). Consistent results were seen in all prespecified subgroups of patients, including those receiving systemic corticosteroids. Patients allocated to tocilizumab were more likely to be discharged from hospital within 28 days (57% vs 50%; rate ratio 1·22; 1·12–1·33; p<0·0001). Among those not receiving invasive mechanical ventilation at baseline, patients allocated tocilizumab were less likely to reach the composite endpoint of invasive mechanical ventilation or death (35% vs 42%; risk ratio 0·84; 95% CI 0·77–0·92; p<0·0001). Interpretation In hospitalised COVID-19 patients with hypoxia and systemic inflammation, tocilizumab improved survival and other clinical outcomes. These benefits were seen regardless of the amount of respiratory support and were additional to the benefits of systemic corticosteroids. Funding UK Research and Innovation (Medical Research Council) and National Institute of Health Research.

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A 40-year-old man developed acute brainstem dysfunction 3 days after hospital admission with symptoms of the novel SARS-CoV-2 infection (COVID-19). Magnetic resonance imaging showed changes in keeping with inflammation of the brainstem and the upper cervical cord, leading to a diagnosis of rhombencephalitis. No other cause explained the patient's abnormal neurological findings. He was managed conservatively with rapid spontaneous improvement in some of his neurological signs and was discharged home with continued neurology follow up.A 40-year-old never-smoker with minimum alcohol intake, originally from Nigeria and now settled in the UK with his family after moving here 7 years ago, attended the emergency department reporting a 10-day history of persistent fever and progressive dyspnoea on exertion while self-isolating at home during the COVID-19 crisis. He was on long-term treatment with ramipril and amlodipine for hypertension and on dorzolamide (a carbonic anhydrase inhibitor) with timolol maleate eye drops for closed angle glaucoma. He reported malaise, a new cough with yellow sputum and diarrhoea (non-bloody) over 3 days. There was no recent foreign travel or family history of medical conditions but he shared the concern that his wife was currently pregnant.On presentation, temperature was 38.4°C, heart rate regular at 86 beats/minute, blood pressure 129/83 mmHg; oxygen saturation 93% on room air as he was tachypnoeic at 32 breaths/minute. On auscultation, heart sounds were normal but there were bi-basal ABSTRACT Authors: A ST4 Respiratory Medicine, The Shrewsbury and Telford Hospital NHS Trust, Telford, UK; B clinical fellow, The Shrewsbury and Telford Hospital NHS Trust, Telford, UK; C consultant neurologist, The Shrewsbury and Telford Hospital NHS Trust, Telford, UK; D consultant respiratory physician, The Shrewsbury and Telford Hospital NHS Trust, Telford, UKcrackles. There was no gross focal neurological deficit. Initial 12-lead electrocardiography showed sinus tachycardia and chest X-ray showed a right lower zone consolidation. Arterial blood gas on room air revealed hypoxia (PaO 2 8.77 kPa) with pH 7.432, PaCO 2 4.21 kPa, HCO 3-20.6 mmol/L, base excess 2.6 mmol/L, lactate 0.98 mmol/L. Haemoglobin was 139 g/L, white cell count 7.0 × 10 9 /L (lymphocytes 1.2 × 10 9 /L) and C-reactive protein (CRP) marginally raised at 50 mg/L, and similar slight increases were seen in serum gamma glutamyl transferase (GGT) 107 U/L (range 0-75) and alanine aminotransferase (ALT) 88 U/L (range 0-45), with other liver tests and urinary electrolytes within the normal ranges.

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