Eosinophilic granulomatosis with polyangiitis (Churg-Strauss) induced by immune checkpoint inhibitors

Roger, Anissa; Groh, Matthieu; Lorillon, Gwenaël; Pendu, C. Le; Maillet, Jérémy; Arangalage, Dimitri; Tazi, Abdellatif; Lebbe, Célèste; Baroudjian, Barouyr; Delyon, Julie

doi:10.1136/annrheumdis-2018-213857

Cited by 33 publications

(21 citation statements)

References 10 publications

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“…Increased AEC, serum IL-6, Il-10 and IgE levels were associated with corticosteroid-refractory adverse events and with grade 3 or greater cutaneous AEs, but the direct accountability of eosinophils was not assessed in these exceptional cases. 24 Even if some severe cutaneous AEs like drug reaction with eosinophilia and systemic symptoms (DRESS) require high-dose corticosteroids, 25,26 multiple recent reports of Eo-irAEs like eosinophilic fasciitis [27][28][29][30] or eosinophilic granulomatosis with polyangiitis 31 suggest that topical or low-dose oral corticosteroids, with or without CSsparing treatments, can give excellent results. Taking account these data, and given that in our work (i) Eo-ir and Eo-irAEs accounted for half of all ICI discontinuations and (ii) no deaths were directly attributable to eosinophil-organ damage, we suggest that the initiation of corticosteroids and the maintenance of the ICI might be an effective therapeutic strategy in patients with moderate-to-severe eosinophilia and whose cancer is under control.…”

Section: Discussionmentioning

confidence: 99%

Moderate-to-severe eosinophilia induced by treatment with immune checkpoint inhibitors: 37 cases from a national reference center for hypereosinophilic syndromes and the French pharmacovigilance database

et al. 2020

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A better understanding of immune-related adverse events is essential for the early detection and appropriate management of these phenomena. We conducted an observational study of cases recorded at the French reference center for hypereosinophilic syndromes and in the French national pharmacovigilance database. Thirty-seven reports of eosinophilia induced by treatment with immune checkpoint inhibitors (ICIs) were included. The median [range] time to the absolute eosinophil count (AEC) peak was 15 [4─139] weeks. The median AEC was 2.7 [0.8─90.9] G/L. Eosinophil-related manifestations were reported in 21 of the 37 cases (57%). If administered, corticosteroids were always effective (n = 10 out of 10). Partial or complete remission of eosinophilia was obtained in some patients not treated with corticosteroids, after discontinuation (n = 12) or with continuation (n = 4) of the ICI. The AEC should be monitored in ICI-treated patients. If required by oncologic indications, continuation of ICI may be an option in asymptomatic hypereosinophilic patients, and in corticosteroid responders.

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Section: Discussionmentioning

confidence: 99%

Moderate-to-severe eosinophilia induced by treatment with immune checkpoint inhibitors: 37 cases from a national reference center for hypereosinophilic syndromes and the French pharmacovigilance database

et al. 2020

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“…Various forms of vasculitis affecting large vessels have been reported, and the corresponding diagnoses include GCA [33,56,57] or periaortitis [58]. Additionally, medium or small vessels can be affected, with cases of granulomatosis with polyangiitis (GPA) [59,60], eosinophilic granulomatosis with polyangiitis (EGPA) [61] and cryoglobulinemic vasculitis [62] having been reported. Cutaneous granulomatous [63,64] and leukocytoclastic vasculitides [65] have also been described.…”

Section: Vasculitismentioning

confidence: 99%

Rheumatic Manifestations in Patients Treated with Immune Checkpoint Inhibitors

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Klavdianou

Filippopoulou

et al. 2020

IJMS

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Immune checkpoint inhibitors (ICIs) are monoclonal antibodies that activate the immune system, aiming at enhancing antitumor immunity. Their clinical efficacy is well-documented, but the side effects associated with their use are still under investigation. These drugs cause several immune-related adverse events (ir-AEs), some of which stand within the field of rheumatology. Herein, we present a literature review performed in an effort to evaluate all publicly available clinical data regarding rheumatic manifestations associated with ICIs. The most common musculoskeletal ir-AEs are inflammatory arthritis, polymyalgia rheumatica and myositis. Non-musculoskeletal rheumatic manifestations are less frequent, with the most prominent being sicca, vasculitides and sarcoidosis. Cases of systemic lupus erythematosus or scleroderma are extremely rare. The majority of musculoskeletal ir-AEs are of mild/moderate severity and can be managed with steroids with no need for ICI discontinuation. In severe cases, more intense immunosuppressive therapy and permanent ICI discontinuation may be employed. Oncologists should periodically screen patients receiving ICIs for new-onset inflammatory musculoskeletal complaints and seek a rheumatology consultation in cases of persisting symptoms.

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“…Tyrosine kinase inhibitors (TKIs) such as axitinib, pazopanib, sorafenib, regorafenib, and sunitinib, as well as interferons, sirolimus, bisphosphonates (pamidronate and zoledronic acid) can induce FSGS. Cytotoxic T-lymphocyte-associated antigen (CTLA)-4 inhibitors such as ipilimumab, can induce MCD or lupus-like glomerular nephritis [26,27]. Other kidney manifestations in patients receiving checkpoint inhibitors (CPIs) are lupus nephropathy, pauci-immune glomerular nephritis, immunoglobulin A (IgA) nephropathy, as well as nephrotic syndrome with FSGS, MCD, and membrane nephropathy [28].…”

Section: Treatment-associated Glomerular Nephritismentioning

confidence: 99%

Acute Kidney Injury in Oncology Patients

Wang

Diao

et al. 2020

J. Cancer

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With rapid progress in cancer diagnosis and treatment in the last two decades, outcomes in oncological patients have improved significantly. However, the incidence of acute kidney injury (AKI) in this population has also increased significantly. AKI complicates many aspects of patients' care and adversely affects their prognoses; thus, accurately diagnosing the risk factors for AKI ensures appropriate management. AKI may be caused by pre-renal, intrinsic renal, and post-renal reasons, as well as for combined reasons. This review summarizes the potential etiologies of AKI according to the three classifications. For each underlying cause of AKI, the cancer itself and/or cancer treatment may contribute to a patient developing AKI. Therefore, we present disease-and treatment-related factors for each cause category, with special focus on immune checkpoint inhibitors, which are being used increasingly more often. It is important for nephrology services to be knowledgeable to provide the best level of care.

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Eosinophilic granulomatosis with polyangiitis (Churg-Strauss) induced by immune checkpoint inhibitors

Abstract: Figure 1 Timeline showing the relationship between serum eosinophil count and treatment with immune checkpoint inhibitors (double arrow: nivolumab 1 mg/kg and ipilimumab 3 mg/kg infusions; single arrow: nivolumab 3 mg/kg infusion).

Cited by 33 publications

References 10 publications

Moderate-to-severe eosinophilia induced by treatment with immune checkpoint inhibitors: 37 cases from a national reference center for hypereosinophilic syndromes and the French pharmacovigilance database

Moderate-to-severe eosinophilia induced by treatment with immune checkpoint inhibitors: 37 cases from a national reference center for hypereosinophilic syndromes and the French pharmacovigilance database

Rheumatic Manifestations in Patients Treated with Immune Checkpoint Inhibitors

Acute Kidney Injury in Oncology Patients

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