key: cord-0900991-mqgzpjea authors: Uslu, Sadettin title: Effectiveness of Tocilizumab in a COVID-19 Patient with Cytokine Release Syndrome date: 2020-05-22 journal: Eur J Case Rep Intern Med DOI: 10.12890/2020_001731 sha: 608dcbf80aa5fd2284dec8e83c52904cd8091f6f doc_id: 900991 cord_uid: mqgzpjea Cytokine release syndrome (CRS) is a systemic inflammatory response that can be triggered by many factors such as infections. CRS in patients with coronavirus disease 2019 (COVID-19) is life-threatening and can occur very rapidly after COVID-19 diagnosis. Tocilizumab (TCZ), an interleukin-6 (IL-6) inhibitor, may ameliorate the CRS associated with severe COVID-19 and thus improve clinical outcomes. We present a case of life-threatening CRS caused by COVID-19 infection successfully treated with TCZ. LEARNING POINTS: Cytokine release syndrome (CRS) is a systemic inflammatory response that can be triggered by COVID-19. CRS can be life-threatening in severe COVID-19. Tocilizumab may have a role in treating severe COVID-19 patients with CRS. INTRODUCTION SARS-CoV-2 causes a mild to moderate illness characterized by fever and respiratory symptoms, with or without evidence of pneumonia. However, up to 10% of patients with COVID-19 may develop severe pneumonia with hypoxia, cytokine release syndrome (CRS) and multiorgan failure [1] . Tocilizumab (TCZ) is a humanized monoclonal inhibitor of the proinflammatory cytokine interleukin-6 (IL-6) and is licensed for use in the clinical management of CRS [2] . Peer-reviewed data on the clinical use of TCZ in severe COVID-19 are very limited. We describe a case of CRS caused by severe COVID-19 infection with a favourable response to TCZ therapy. A 41-year-old woman with a history of hypertension, presented with fever, productive cough and general fatigue. She denied any recent travel but had a history of contact with sick people. In the emergency department she was tachypnoeic (respiratory rate of 22 breaths/min), tachycardiac (130 bpm), febrile (39°C) and hypoxic (oxygen saturation (SpO 2 ) of 88% on room air). Physical examination of the lungs revealed bilateral crackles and wheeze. The white cell count was normal and the absolute lymphocyte count was low (0.61-103/µl), while the erythrocyte sedimentation rate (77; range, 0-20 mm/h) and C-reactive protein levels (110; range, 0-5 mg/l) were increased. D-dimer was 1657 ng/ml and procalcitonin was normal. Assays for influenza viruses and a respiratory syncytial virus were all negative. A nasopharyngeal swab was positive for SARS-CoV-2 on RT-PCR assay. Computed tomography (CT) at the time of admission revealed bilateral ground-glass After 3 days of hospitalization the patient's clinical condition deteriorated (respiratory rate of 26 breaths/min and SpO 2 decreased to 78%) and she required intensive care unit (ICU) admission. A chest x-ray at the time of ICU admission revealed hazy bilateral lobe opacity (Fig. 2a) . The patient was intubated and diagnosed with CRS. She was given a single intravenous (IV) dose of 400 mg TCZ and IV methylprednisone 60 mg daily for 3 days. Ventilatory support requirements reduced day-by-day. C-reactive protein, ferritin and D-dimer levels dropped from 310 mg/l, 3500 ng/dl and 2123 ng/ml on the day of ICU admission to 13.2 mg/l, 300 ng/dl and 320 ng/ml after 3 days, respectively. A chest x-ray showed that the lesions significantly improved within 3 days of TCZ administration (Fig. 2b) . The patient was successfully extubated 5 days after treatment with TCZ. No adverse events were described. On day 10, a clear improvement in the patient's general condition was observed, with an SpO 2 of 97% without any need for supplemental oxygen (Fig. 3) . Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China FDA approval summary: tocilizumab for treatment of chimeric antigen receptor T cell-induced severe or lifethreatening cytokine release syndrome COVID-19: consider cytokine storm syndromes and immunosuppression Can we use interleukin-6 (IL-6) blockade for coronavirus disease 2019 (COVID-19)-induced cytokine release syndrome (CRS)? Figure 3. Laboratory and SpO2 data