Sustained response to mepolizumab in refractory Churg-Strauss syndrome

Kahn, Jean‐Emmanuel; Grandpeix-Guyodo, Catherine; Marroun, Ibrahim; Catherinot, Émilie; Mellot, François; Roufosse, Florence; Blëtry, O.

doi:10.1016/j.jaci.2009.10.014

Cited by 105 publications

(60 citation statements)

References 8 publications

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“…These results have made possible the use of anti-IL-5 therapy in EGPA, initially with efficacy in one case of EGPA refractory to other treatments [96].…”

Section: Biological Therapies (Monoclonal Antibodies)mentioning

confidence: 97%

Churg-Strauss Syndrome or Eosinophilic Granulomatosis with Polyangiitis

et al. 2015

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Eosinophilic granulomatosis with polyangiitis (Churg-Strauss, EGPA) is a systemic small-to-medium-sized vasculitis associated with asthma and eosinophilia. Histologically EGPA presents tissue eosinophilia, necrotizing vasculitis, and granulomatous inflammation with eosinophil tissue infiltration. EGPA commonly involves the upper airway and lung parenchyma, peripheral neuropathy, cardiac disorders, and skin lesions. The anti-neutrophil cytoplasmic antibodies (ANCA) are positive in 40% of cases, especially in those patients with clinical signs of vasculitis. The pathogenesis of EGPA is multifactorial. The disease can be triggered by exposure to a variety of allergens and drugs, but a genetic background has also been described, particularly an association with HLA-DRB4. Th2 response is of special importance in the upregulation of different interleukins such as IL-4, IL-13, and IL-5. Th1 and Th17 responses are also of significance. Activated eosinophils have a prolonged survival and probably cause tissue damage by releasing eosinophil granule proteins, while their tissue recruitment can be regulated by chemokines such as eotaxin-3 and CCL17. Humoral immunity is also OPEN ACCESSSinusitis 2016, 1 25 abnormally regulated, as demonstrated by excessive responses of IgG4 and IgE. EGPA has a good respond to glucocorticoids, although the combination of glucocorticoids and immunosuppressants (e.g., cyclophosphamide, azathioprine) is needed in most of cases. Newer treatment options include anti-IL-5 antibodies (mepolizumab), whose efficacy has been described in clinical trials, and anti-CD-20, a B cell-depleting agent (rituximab), reported in several case series.

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“…These results have made possible the use of anti-IL-5 therapy in EGPA, initially with efficacy in one case of EGPA refractory to other treatments [96].…”

Section: Biological Therapies (Monoclonal Antibodies)mentioning

confidence: 97%

Churg-Strauss Syndrome or Eosinophilic Granulomatosis with Polyangiitis

et al. 2015

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“…Moreover, rituximab can be also used as maintenance therapy but the level of evidence is low (grade 3C). Finally, studies including biological agents such as etanercept, adalimumab, abatacept, altemtuzumab, and mepolizumab either did not include patients with neurological involvement, or the results were inconclusive [137][138][139].…”

Section: Antineutrophil Cytoplasmic Antibody-positive Vasculitidesmentioning

confidence: 99%

Immunotherapies for Neurological Manifestations in the Context of Systemic Autoimmunity

et al. 2016

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Neurological involvement is relatively common in the majority of systemic autoimmune diseases and may lead to severe morbidity and mortality, if not promptly treated. Treatment options vary greatly, depending on the underlying systemic pathophysiology and the associated neurological symptoms. Selecting the appropriate therapeutic scheme is further complicated by the lack of definite therapeutic guidelines, the necessity to differentiate primary neurological syndromes from those related to the underlying systemic disease, and to sort out adverse neurological manifestations caused by immunosuppressants or the biological agents used to treat the primary disease. Immunotherapy is a sine qua non for treating most, if not all, neurological conditions presenting in the context of systemic autoimmunity. Specific agents include classical immune modulators such as corticosteroids, cyclophosphamide, intravenous immunoglobulin, and plasma exchange, as well as numerous biological therapies, for example antitumor necrosis factor agents and monoclonal antibodies that target various immune pathways such as B cells, cytokines, and co-stimulatory molecules. However, experience regarding the use of these agents in neurological complications of systemic diseases is mainly empirical or based on small uncontrolled studies and case series. The aim of this review is to present the state-of-the-art therapies applied in various neurological manifestations encountered in the context of systemic autoimmune diseases; evaluate all treatment options on the basis of existing guidelines; and compliment these data with our personal experience derived from a large number of patients.

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“…Anti-IL6 and IL-6R are now being tested in lupus nephritis. A phase II trial of sirukumab (an antiIL6 monoclonal antibody) in lupus nephritis reported negative findings, with a high incidence of infectious complications [50]. A small study of tocilizumab (an antiIL6R monoclonal antibody) in SLE nephritis yet to give result.…”

Section: Brief On Other Monoclonal Antibodiesmentioning

confidence: 99%

Glomerulonephritis – Do We Have Promising Role of Monoclonal Antibodies?

Sharma¹,

Saxena²

2016

J Clin Exp Nephrol

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In present era, drugs like steroids, cytotoxic drugs and calcineurin inhibitors are the backbone to treat immune mediated glomerular diseases. Failure of these therapies often results in persistence of proteinuria, refractory illness and later chronic kidney diseases. The quests to find an answer to such diseases have resulted in the introduction of monoclonal antibodies or target specific drugs. Rituximab is the first monoclonal antibody, which was studied extensively in pauci-immune glomerulonephritis and is now approved for its role in refractory and new onset renal vasculitis. Belimumab has shown role in active systemic lupus erythematous (SLE). With increasing insight in glomerular pathophysiology, many new monoclonal antibodies are now being under trial. Their encouraging results allowed further research on target cytokines, inflammatory mediators and different lymphocyte populations. This review shall discuss monoclonal and their emerging role in glomerulonephritis.

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Sustained response to mepolizumab in refractory Churg-Strauss syndrome

Cited by 105 publications

References 8 publications

Churg-Strauss Syndrome or Eosinophilic Granulomatosis with Polyangiitis

Churg-Strauss Syndrome or Eosinophilic Granulomatosis with Polyangiitis

Immunotherapies for Neurological Manifestations in the Context of Systemic Autoimmunity

Glomerulonephritis – Do We Have Promising Role of Monoclonal Antibodies?

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