Immunosuppressants/CAR T-cell therapies
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Immunosuppressants/CAR T-cell therapies COVID-19 infection: 2 case reports
In a retrospective study conducted on patients hospitalised in Tongji Hospital, Wuhan, China, a man in his 30s [exact age not stated] developed COVID-19 infection following treatment with an unspecified CAR-T cell therapies, fludarabine and cyclophosphamide for refractory multiple myeloma (MM), and a 53-year-old man developed COVID-19 infection while receiving immunosuppressive treatment with ciclosporin [routes and duration of treatments to reactions onsets not stated]. Patient 1: A man in his early 30s, who had a history of refractory MM for more than 2 years, enrolled in a clinical trial and received fully humanized, anti- B-cell maturation antigen (BCMA), chimeric antigen receptor (CAR) T-cell therapy in October 2019. Additionally, he was started on lympho-depleting chemotherapy with fludarabine 25 mg/m2 and cyclophosphamide 20 mg/kg for consecutive 3 days. He received the sequential infusion of anti-BCMA CAR T-cells with a total dosage of 0.5×106 cells/kg of CAR Tcells. After 30 days, a complete remission was observed. He was maintained on CAR T-cells and a continued remission was noted. He was free from any symptoms without an evidence of other pathogenic infections. On 26 January 2020 (day-1), he presented to the clinic with a fever and dry cough. On day-5, his SARS-CoV- 2 nucleic acid test was found to be positive for COVID-19 infection. Immediately, he was hospitalised in an isolation. On admission, he received oxygen therapy with nasal cannula and oxygen saturation was maintained from 96-99% during this therapy. Additionally, he was started on arbidol 200mg (umifenovir) thrice daily, lopinavir/ritonavir 500mg twice daily and moxifloxacin 400mg once a day; however, his symptoms were found to be aggravated. Chest CT revealed bilateral pulmonary infiltration with consolidation. Based on these findings, he was diagnosed with severe pneumonia. His plasma cytokine profile showed elevated interleukin (IL)-2R, IL-6, tumour necrosis factor α (TNF-α) and ferritin. Based on these findings, he was diagnosed with cytokine release syndrome and cytokine storm. Peripheral blood examinantion showed an absence of B-lymphocytes and elevated cytotoxic T-cells. He received IV immune globulin [IVIG] 20g for 3 days and then once weekly. On day-18, chest CT showed prominent progression of the pulmonary infiltration along with consolidation. Based on this observation, a diagnosis of acute respiratory distress syndrome (ARDS) was made. Then he developed shortness of breath and hypoxaemia and was transferred to ICU. He was started on a high-flow oxygen therapy with methylprednisolone. Prophylactic treatment with cefoperazone/sulbactam, voriconazole and teicoplanin was initiated to prevent secondary infection. At this stage, he was unable to maintain blood oxygen saturation levels. Therefore, he received biphasic positive airway pressure ventilation and denied for mechanical ventilation. The elevated cytokines became improved with methylprednisolone exc
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