Nasal polyposis: clinical course during 20 years

Vento, Seija; Ertama, Liisa; Hytönen, Maija; Wolff, Carl Henrik Johannes; Malmberg, C. H. O.

doi:10.1016/s1081-1206(10)62468-4

Cited by 98 publications

(70 citation statements)

References 14 publications

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“…However, in severe polyposis and asthma comorbidity, repeated courses of intranasal and/or oral corticosteroids are usually insufficient in controlling symptoms. Repeated sinus surgeries may be needed with inconsistent clinical benefits [80]. …”

Section: Severe Allergic and Related Diseasesmentioning

confidence: 99%

Severe Chronic Allergic (and Related) Diseases: A Uniform Approach – A MeDALL – GA<sup>2</sup>LEN – ARIA Position Paper

Bousquet¹,

Antó²,

Demoly³

et al. 2012

Int Arch Allergy Immunol

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Concepts of disease severity, activity, control and responsiveness to treatment are linked but different. Severity refers to the loss of function of the organs induced by the disease process or to the occurrence of severe acute exacerbations. Severity may vary over time and needs regular follow-up. Control is the degree to which therapy goals are currently met. These concepts have evolved over time for asthma in guidelines, task forces or consensus meetings. The aim of this paper is to generalize the approach of the uniform definition of severe asthma presented to WHO for chronic allergic and associated diseases (rhinitis, chronic rhinosinusitis, chronic urticaria and atopic dermatitis) in order to have a uniform definition of severity, control and risk, usable in most situations. It is based on the appropriate diagnosis, availability and accessibility of treatments, treatment responsiveness and associated factors such as comorbidities and risk factors. This uniform definition will allow a better definition of the phenotypes of severe allergic (and related) diseases for clinical practice, research (including epidemiology), public health purposes, education and the discovery of novel therapies.

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Section: Severe Allergic and Related Diseasesmentioning

confidence: 99%

Severe Chronic Allergic (and Related) Diseases: A Uniform Approach – A MeDALL – GA<sup>2</sup>LEN – ARIA Position Paper

Bousquet¹,

Antó²,

Demoly³

et al. 2012

Int Arch Allergy Immunol

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“…Symptom onset most often occurs after puberty through age 40 without a clear genetic predisposition or a known environmental or infectious trigger. Aggressive nasal polyposis is a hallmark of AERD and is characterized by high polyp burden, abundance of eosinophils and mast cells in the polyp tissue, extracellular matrix deposition, and regrowth of polyps as early as several weeks after polypectomy (1). The rapid regrowth of polyps after surgical excision leads to persistent anosmia, impaired sleep, chronic sinusitis, and worsening of lower respiratory disease.…”

mentioning

confidence: 99%

Impaired E Prostanoid₂ Expression and Resistance to Prostaglandin E₂ in Nasal Polyp Fibroblasts from Subjects with Aspirin-Exacerbated Respiratory Disease

Cahill

Raby²,

Zhou³

et al. 2016

Am J Respir Cell Mol Biol

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Recurrent, rapidly growing nasal polyps are hallmarks of aspirin-exacerbated respiratory disease (AERD), although the mechanisms of polyp growth have not been identified. Fibroblasts are intimately involved in tissue remodeling, and the growth of fibroblasts is suppressed by prostaglandin E 2 (PGE 2 ), which elicits antiproliferative effects mediated through the E prostanoid (EP) 2 receptor. We now report that cultured fibroblasts from the nasal polyps of subjects with AERD resist this antiproliferative effect. Fibroblasts from polyps of subjects with AERD resisted the antiproliferative actions of PGE 2 and a selective EP 2 agonist (P , 0.0001 at 1 mM) compared with nasal fibroblasts from aspirin-tolerant control subjects undergoing polypectomy or from healthy control subjects undergoing concha bullosa resections. Cell surface expression of the EP 2 receptor protein was lower in fibroblasts from subjects with AERD than in fibroblasts from healthy control subjects and aspirin-tolerant subjects (P , 0.01 for both). Treatment of the fibroblasts with trichostatin A, a histone deacetylase inhibitor, significantly increased EP 2 receptor mRNA in fibroblasts from AERD and aspirin-tolerant subjects but had no effect on cyclooxygenase-2, EP 4 , and microsomal PGE synthase 1 (mPGES-1) mRNA levels. Histone acetylation (H3K27ac) at the EP 2 promoter correlated strongly with baseline EP 2 mRNA (r = 0.80; P , 0.01). These studies suggest that the EP 2 promotor is under epigenetic control, and one explanation for PGE 2 resistance in AERD is an epigenetically mediated reduction of EP 2 receptor expression, which could contribute to the refractory nasal polyposis typically observed in this syndrome.

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“…Long-term success of surgery has been variable based on published studies [51,52,53]. A prospective cohort study in the UK in 3,128 patients showed that revision surgery was conducted in 11.4% of patients within 3 years [51].…”

Section: Resultsmentioning

confidence: 99%

Evidence-Based Management of Nasal Polyposis by Intranasal Corticosteroids: From the Cause to the Clinic

Bachert¹

2011

Int Arch Allergy Immunol

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Background: Nasal polyposis is an inflammatory disorder involving the mucosa of the nose and paranasal sinuses and affecting approximately 2–4% of the general population. Methods: A literature search of Medline and Embase was conducted to obtain an overview of the epidemiology, pathophysiology, and current treatment of nasal polyposis, focusing on evidence-based efficacy of intranasal corticosteroids (INSs) as primary and postoperative therapy. Recent research on INSs in nasal polyp treatment, along with notable historic findings, was reviewed. Results: Nasal polyps are mostly characterized by eosinophil infiltration, a complex inflammation of nasal mucosa, and possibly production of polyclonal IgE. Current treatment modalities include INSs, oral corticosteroids, and surgery; surgery is generally limited to those with an insufficient response to medical treatment. Because of their effects on eosinophil-dominated inflammation, INSs and oral corticosteroids are the primary medical treatment strategies. The very low (≤1%) systemic bioavailability of newer INSs minimizes the systemic adverse effects seen with oral corticosteroids. Conclusion:Based on randomized, controlled trials, guidelines recommend INSs as first-line therapy for nasal polyps and for care after polypectomy. Clinical data suggest INSs are effective in reducing polyp size and relieving nasal symptoms. INS treatment has also reduced nasal polyp recurrence in patients undergoing functional endoscopic sinus surgery. Treatment with these mainstay options has been found to improve quality of life, which, along with symptom improvement, is a key factor in disease treatment.

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Nasal polyposis: clinical course during 20 years

Cited by 98 publications

References 14 publications

Severe Chronic Allergic (and Related) Diseases: A Uniform Approach – A MeDALL – GA<sup>2</sup>LEN – ARIA Position Paper

Severe Chronic Allergic (and Related) Diseases: A Uniform Approach – A MeDALL – GA<sup>2</sup>LEN – ARIA Position Paper

Impaired E Prostanoid₂ Expression and Resistance to Prostaglandin E₂ in Nasal Polyp Fibroblasts from Subjects with Aspirin-Exacerbated Respiratory Disease

Evidence-Based Management of Nasal Polyposis by Intranasal Corticosteroids: From the Cause to the Clinic

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Nasal polyposis: clinical course during 20 years

Cited by 98 publications

References 14 publications

Severe Chronic Allergic (and Related) Diseases: A Uniform Approach – A MeDALL – GA<sup>2</sup>LEN – ARIA Position Paper

Severe Chronic Allergic (and Related) Diseases: A Uniform Approach – A MeDALL – GA<sup>2</sup>LEN – ARIA Position Paper

Impaired E Prostanoid2 Expression and Resistance to Prostaglandin E2 in Nasal Polyp Fibroblasts from Subjects with Aspirin-Exacerbated Respiratory Disease

Evidence-Based Management of Nasal Polyposis by Intranasal Corticosteroids: From the Cause to the Clinic

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Product

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Impaired E Prostanoid₂ Expression and Resistance to Prostaglandin E₂ in Nasal Polyp Fibroblasts from Subjects with Aspirin-Exacerbated Respiratory Disease