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Pulmonary fibrosis and cytokine release syndrome after hyperactivation with sintilimab
Author(s) -
Hu Jing,
Li Yanxiu,
Chen Xuesong,
Luo Can,
Zuo Xiangrong
Publication year - 2020
Publication title -
journal of clinical pharmacy and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.622
H-Index - 73
eISSN - 1365-2710
pISSN - 0269-4727
DOI - 10.1111/jcpt.13217
Subject(s) - nintedanib , medicine , pulmonary fibrosis , idiopathic pulmonary fibrosis , cytokine storm , cytokine , fibrosis , methylprednisolone , cytokine release syndrome , adverse effect , pulmonary hypertension , chemotherapy , immunotherapy , gastroenterology , immunology , cancer , lung , disease , covid-19 , infectious disease (medical specialty) , chimeric antigen receptor
What is known and objective Immunotherapy‐related adverse events (irAEs) are common immunotherapy‐associated diseases. Severe pulmonary fibrosis with hypercytokinaemia has not been reported with programmed cell death 1 (PD‐1) inhibitors. We describe a case of sintilimab‐induced pulmonary fibrosis with cytokine storm induced in a 50‐year‐old patient with colon cancer refractory to second‐line systemic chemotherapy. Case summary Our patient developed hypercytokinaemia with elevated levels of interleukin (IL)‐6 and IL‐10 and pulmonary fibrosis, which differed from other irAEs. The patient benefited from a back‐titrated regimen of methylprednisolone with the initial dosage of 2 mg/kg and anti‐fibrotic effect of nintedanib and was successfully weaned from the ventilator. What is new and conclusion This is the first report that a PD‐1 inhibitor may have caused pulmonary fibrosis and a cytokine storm. This case indicates that the addition of nintedanib and glucocorticoid might possibly have potentially therapeutic effects of PD‐1 induced pulmonary fibrosis and hypercytokinaemia.