Tumor necrosis factor α release is a major biological event associated with rituximab treatment

Bienvenu, Jacques; Chvetzoff, Roland; Salles, Gilles; Balter, Cécile; Tilly, Hervé; Herbrecht, Raoul; Morel, P; Léderlin, P.; Solal‐Céligny, Philippe; Audhuy, B.; Berthou, Christian; Gabarre, Jean; Casasnovas, Olivier; Marit, Gérald; Sebban, Catherine

doi:10.1038/sj.thj.6200133

Cited by 94 publications

(50 citation statements)

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“…Complement activation and cytokine secretion, in particular, seems to be the causative factors in side effects associated with infusion reactions [14]. Studies have found complement (C3b/c and C4b/c) and cytokine (TNF-a, IL6, and IL8) levels to be elevated after rituximab infusion [2,[14][15][16]. In particular, TNF-a has been postulated as the main component in the pathogenesis of ILD because of its proinflammatory effects by inducing chemokines, inflammatory mediators, and angiogenic factors [17].…”

Section: Discussionmentioning

confidence: 99%

“…It is now considered part of the standard therapy for CD201 NHL and has been used for autoimmune disorders such as idiopathic thrombocytopenic purpura, systemic lupus erythematous, and autoimmune hemolytic anemia [1]. The most common side effects are infusion related and include fever, chills, and rigors [2]. Respiratory complications can include cough, rhinitis, brochospasm, dyspnea, and sinusitis.…”

Section: Introductionmentioning

confidence: 99%

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Rituximab‐induced interstitial lung disease

2007

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The aim of this study is to characterize rituximab‐induced interstitial lung disease (R‐ILD). The information on all reported cases of R‐ILD was reviewed. This analysis focused on patient characteristics, underlying disease, rituximab dosing schedule, and R‐ILD characteristic‐like symptoms, diagnosis, treatment, and outcomes. Sixteen cases of R‐ILD, including our two cases, have been reported in the literature. Commonalities include older age, clinical presentation, computerized tomography findings, pulmonary function tests, and biopsy findings. Therapy included corticosteroids and broad spectrum antibiotics. Prognosis has been variable. Patients who worsen despite corticosteroids have a poor outcome. The pathogenesis of R‐ILD is largely unknown. Potential explanations for R‐ILD may include the induction and release of cytotoxic substances. R‐ILD is a rare but potentially fatal pulmonary toxicity due to rituximab. R‐ILD should be considered in patients who present with dyspnea, fever, and cough, and there is no clear evidence of infection. Prompt diagnosis and treatment with corticosteroids is essential. Am. J. Hematol. 82:916–919, 2007. © 2007 Wiley‐Liss, Inc.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Rituximab‐induced interstitial lung disease

2007

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“…However, CDC seems to be the most important mechanism of cell lysis in chronic lymphocytic leukemia (CLL) patients (Kennedy et al, 2004). CDC is probably involved in the cytokine-release syndrome and its toxicity (Bienvenu et al, 2001).…”

Section: Mechanisms Of Action Of Rituximabmentioning

confidence: 99%

Rituximab therapy in malignant lymphoma

2007

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“…Mechanisms leading to late-onset ILD remain unclear. A potential explanation may be the induction and release of cytokines following rituximab binding to CD20 + cells [2,4]. Because the patient was treated concomitantly with cytotoxic drugs, we recognise that it is difficult to completely rule out cytotoxic FIGURE 1 Chest computed tomography scan revealing diffused micronodules over bilateral lung field.…”

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confidence: 99%

Rituximab-induced pneumonitis mimicking miliary tuberculosis

Yao¹,

Liao²,

Tu³

et al. 2013

European Respiratory Review

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Rituximab, a chimeric anti-CD20 monoclonal antibody, is commonly being used in combination with chemotherapy regimens in the standard treatment of B-cell non-Hodgkin lymphoma (NHL) [1]. Rituximab is considered to be a relatively safe drug but recently, severe and fatal interstitial lung disease (ILD) was noted with an occurrence rate of 0.01-0.03% [2]. Computed tomography (CT) patterns of rituximabinduced ILD include focal (54%) or diffused (9%) alveolar patterns and macronodules (3%), or groundglass patterns (34%) [2]. In this regard, we report a patient with NHL in whom ILD developed after six cycles of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) therapy with diffused micronodules mimicking miliary tuberculosis (TB). R-CHOP was discontinued and the patient gradually recovered.This 54-year-old housewife, who initially presented with abdominal fullness due to intra-abdominal lymphadenopathy, was diagnosed with diffused large B-cell lymphoma. She was treated with R-CHOP three times a week. Several days after the sixth cycle of treatment she reported dyspnoea, fever and cough. Physical examination was unremarkable. Pulse oximetry and analysis of arterial blood gases confirmed the presence of hypoxaemia. A chest radiography and CT scan ( fig. 1) showed bilateral diffuse micronodules. Bone marrow biopsy revealed no granuloma or malignancy, and acid-fast stains and culture for mycobacteria were negative. The patient underwent bronchoscopy with bronchoalveolar lavage and transbronchial biopsies. Culture for bacteria, fungi and mycobacteria were all negative. PCR did not detect any Pneumocystis jiroveci DNA. The transbronchial biopsy revealed interstitial fibrosis and type II pneumocyte hyperplasia ( fig. 2). No granuloma or malignancy was observed. We prescribed supportive treatment without specific medications (including steroids) and her symptoms improved. 4 months later, CT of the chest also revealed marked improvement and she was asymptomatic.The common differential diagnosis of randomly distributed micronodules on CT patterns includes miliary TB, miliary fungus and haematogenous metastasis [3]. Because the patient lived in a TB-endemic region and was in an immunocompromised state, we took miliary TB as the first consideration. The final diagnosis of rituximab-induced ILD was mainly made based on the lack of pathological or microbial infection evidence and the dramatic improvement in the patient's condition after the discontinuation of R-CHOP.The time to onset of rituximab-induced ILD is usually classified as early (day 1), delayed (days 7-21) or late (.30 days). Mechanisms leading to late-onset ILD remain unclear. A potential explanation may be the induction and release of cytokines following rituximab binding to CD20 + cells [2,4]. Because the patient was treated concomitantly with cytotoxic drugs, we recognise that it is difficult to completely rule out cytotoxic FIGURE 1 Chest computed tomography scan revealing diffused micronodules over bilateral lung field. LETTER 587 drug-i...

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Tumor necrosis factor α release is a major biological event associated with rituximab treatment

Abstract: This analysis demonstrates that rituximab infusion was rapidly followed by activation of complement, B-lymphocyte cytolysis, and TNF-alpha release.

Cited by 94 publications

References 12 publications

Rituximab‐induced interstitial lung disease

Rituximab‐induced interstitial lung disease

Rituximab therapy in malignant lymphoma

Rituximab-induced pneumonitis mimicking miliary tuberculosis

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