The Role of Omalizumab in NSAID-Exacerbated Respiratory Disease: A Narrative Review

Taniguchi, Masami; Heffler, Enrico; White, Andrew A.; Côrte-Real, Joana; Olsson, Petter; Lazarewicz, Slawomir

doi:10.1016/j.jaip.2022.06.016

Cited by 9 publications

(6 citation statements)

References 94 publications

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“…In the pathogenesis of N-ERD, mast cells, basophils and eosinophils triggered by an increase in proinflammatory mediators such as cysteinyl leukotrienes (CysLTs) and prostaglandin D2 (PGD2) and a decrease in anti-inflammatory metabolites such as prostaglandin E2 (PGE2) and lipoxin A4, due to cyclooxygenase-1 (COX-1) inhibition induced by NSAIDs play a role. 6 , 7 …”

Section: Introductionmentioning

confidence: 99%

“…It has been demonstrated that omalizumab (anti-IgE) improved nasal symptoms in patients with nasal polyps including N-ERD in a randomized controlled study, and both nasal and asthma symptoms in patients with N-ERD accompanied by severe asthma in an open-label study. 7 , 13 , 14 Omalizumab reduces the free IgE in the circulation and inhibits the interaction of the high-affinity receptors for the Fc region (FcεRI) with IgE, resulting in reduced mast cell activation and thus reducing the synthesis of the cysteinyl leukotrienes (CysLTs). 15 …”

Section: Introductionmentioning

confidence: 99%

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Does NSAID exacerbated respiratory disease (N-ERD) accompanying severe asthma affect biological treatment response? Efficacy of omalizumab and mepolizumab in N-ERD

Tepetam,

Özden,

Kılıç

et al. 2023

World Allergy Organization Journal

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Does NSAID exacerbated respiratory disease (N-ERD) accompanying severe asthma affect biological treatment response? Efficacy of omalizumab and mepolizumab in N-ERD

Tepetam,

Özden,

Kılıç

et al. 2023

World Allergy Organization Journal

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“…group recently published results showing that succinate receptor 1 (SUCNR1) is abundant in human mast cells and that succinate causes mast cell activation (36). Many reports have already shown that mast cell activation persists even during the stable phase as a characteristic pathology of N-ERD (42)(43)(44)(45)(46)(47)(48). N-ERD is more hypersensitive to adenosine inhalation, which stimulates mast cells (49), and the mast cell stabilizer cromolyn improves lung function only in stable adult asthmatics with N-ERD (50).…”

Section: Discussionmentioning

confidence: 99%

“…N-ERD is more hypersensitive to adenosine inhalation, which stimulates mast cells (49), and the mast cell stabilizer cromolyn improves lung function only in stable adult asthmatics with N-ERD (50). Furthermore, omalizumab, an anti-IgE agent, has been demonstrated to significantly improve airway symptoms and aspirin sensitivity in N-ERD, in addition to inhibiting mast cell activation (48,(50)(51)(52). We hypothesized that when succinate ester preparations are rapidly administered to patients with N-ERD, their breakdown produces large amounts of succinate, which strongly activates mast cells via SUCNR1.…”

Section: Discussionmentioning

confidence: 99%

Hypersensitivity to intravenous succinate corticosteroids in patients with nonsteroidal anti-inflammatory drug-exacerbated respiratory disease

Taniguchi,

Sato,

Mita

2023

Front. Allergy

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Although there are many case reports of asthma exacerbations with intravenous corticosteroids, especially hydrocortisone succinate, in nonsteroidal anti-inflammatory drug-exacerbated respiratory disease (N-ERD), the frequency and mechanism remain unclear. We hypothesized that N-ERD patients are potentially hypersensitive to succinates, especially succinate corticosteroids, based on the results of previous provocation studies and considered specific mechanisms. The objective of this study was to determine the frequency and mechanism of succinate corticosteroids hypersensitivity in patients with N-ERD. Eleven patients with stable, moderate to severe N-ERD were tested with hydrocortisone sodium succinate (HCs), hydrocortisone sodium phosphate (HCp), methylprednisolone sodium succinate (MPSLs), prednisolone sodium succinate (PSLs), and chloramphenicol sodium succinate (CPs, without a steroidal chemical structure) at doses below the normal dose through intravenous administration using a single-blind test. As a comparison, seven patients with aspirin-tolerant asthma (ATA) also underwent an intravenous provocation test of HCs. The positive intravenous provocation test rates of HCs 100–500 mg, HCp 500 mg, MPSLs 80 mg, PSLs 20 mg, and CPs 500 mg in N-ERD patients were 82% (9/11), 9% (1/11), 50% (5/10), 33% (1/3), and 86% (6/7), respectively. Most positive reactions began with a severe cough within 5 min of intravenous injection. The course of these hypersensitivity symptoms differed from those seen with the usual aspirin challenge test. The HCs 100–500 mg intravenous test was negative in all seven patients with ATA. In conclusion, patients with N-ERD have high rates of potential hypersensitivity to the succinate ester structure, which is not linked to the corticosteroid structure, but to the succinate ester structure. We hypothesized that the mechanism of hypersensitivity observed during rapid intravenous administration of succinate corticosteroids is mast cell activation via succinate receptor stimulation, rather than due to the corticosteroid itself.

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“…The combination of zileuton and LTRA or celecoxib may have a synergistic effect in patients with NERD. However, it is less desirable than LTRA because of concerns regarding side effects, such as hepatotoxicity [90].…”

Section: Lt Modifiermentioning

confidence: 99%

Can we apply biomarkers in the management of non-steroidal anti-inflammatory drug exacerbated respiratory disease?

Rhyou,

Nam,

Park

2023

Explor Asthma Allergy

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Non-steroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (NERD) is characterized by adult-onset asthma, chronic rhinosinusitis with nasal polyps (CRSwNPs), and aspirin/NSAID hypersensitivity, presenting recurrent asthma exacerbation and poor clinical outcomes. Patients with NERD have heterogeneous clinical phenotypes/endotypes, and the management of NERD remains challenging. Dysregulation of arachidonic acid (AA) metabolism and persistent eosinophilic airway inflammation are the major pathogenic mechanisms in the upper and lower airways of NERD. To date, increased levels of urinary leukotriene E4 (uLTE4) [a terminal metabolite of the lipoxygenase (LOX) pathway] have been the most relevant biomarker for NERD. It is demonstrated that mast cells, platelets, and epithelial cells can amplify upper and lower airway inflammation in NERD, and several potential biomarkers based on these complicated and heterogeneous mechanisms have been suggested. This review summarizes potential biomarkers for application in the management of NERD.

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The Role of Omalizumab in NSAID-Exacerbated Respiratory Disease: A Narrative Review

Cited by 9 publications

References 94 publications

Does NSAID exacerbated respiratory disease (N-ERD) accompanying severe asthma affect biological treatment response? Efficacy of omalizumab and mepolizumab in N-ERD

Does NSAID exacerbated respiratory disease (N-ERD) accompanying severe asthma affect biological treatment response? Efficacy of omalizumab and mepolizumab in N-ERD

Hypersensitivity to intravenous succinate corticosteroids in patients with nonsteroidal anti-inflammatory drug-exacerbated respiratory disease

Can we apply biomarkers in the management of non-steroidal anti-inflammatory drug exacerbated respiratory disease?

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