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Involvement of NLRP 3 inflammasome in rituximab‐induced interstitial lung disease: a case report
Author(s) -
Kong H.,
Wang Y.,
Zeng X.,
Zhu Q.,
Xie W.,
Dai S.
Publication year - 2014
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.12198
Subject(s) - inflammasome , rituximab , interstitial lung disease , medicine , lung disease , lung , immunology , inflammation , antibody
Summary What is known and objective Rituximab is a chimeric anti‐ CD 20 IgG1 monoclonal antibody for the treatment of various forms of lymphoma and haematological autoimmune diseases. Interstitial lung disease is a rare but lethal pulmonary toxicity of rituximab. Nod‐like receptor pyrin domain‐containing protein 3 ( NLRP 3) inflammasome is a molecular platform activated upon signs of cellular ‘danger’ to trigger the maturation of pro‐inflammatory cytokines. We report the first case of rituximab‐induced interstitial lung disease (R‐ ILD ) with NLRP 3 inflammasome activation in the lung. Case summary A 30‐year‐old male patient diagnosed with idiopathic thrombocytopenic purpura ( ITP ) was treated with four cycles of rituximab in one month. Three weeks after last rituximab administration, he developed progressive dyspnoea associated with respiratory failure, which was diagnosed as R‐ ILD . The patient showed a good response to steroid treatment, and lung biopsy was performed 5 days after the treatment. Immunohistopathological studies of lung specimens showed high expressions of inflammasome components NLRP 3, apoptosis‐associated speck‐like protein containing a caspase recruitment domain ( ASC ) and caspase‐1 in lung interstitium with a heavy infiltration of CD 19‐positive cells. The levels of inflammasome‐related cytokines IL ‐1β and IL ‐18 in the serum were declined during the therapy. What is new and conclusions This is the first report confirmed the role of NLRP 3 inflammasome in pulmonary toxicity of rituximab. Inhibited activation of NLRP 3 inflammasome in lung by steroid treatment could reverse R‐ ILD and block subsequent lung fibrosis. This result could open a new sight into the pathogenesis and provide a new target for the treatment of R‐ ILD .