Statins and Nasal Polyps
Authors: Caterina Bucca, Andrea Marsico, Erika Panaro, Patrizia Bigo, Luisa Brussino
Journal: Annals of Internal Medicine (2005)

Letters15 February 2005Statins and Nasal PolypsCaterina Bucca, MD, Andrea Marsico, MD, Erika Panaro, MD, Patrizia Bigo, MD, and Luisa Brussino, MDCaterina Bucca, MDFrom University of Turin, 10128 Turin, Italy, and St. Giovanni Battista Hospital; 10126 Turin, Italy., Andrea Marsico, MDFrom University of Turin, 10128 Turin, Italy, and St. Giovanni Battista Hospital; 10126 Turin, Italy., Erika Panaro, MDFrom University of Turin, 10128 Turin, Italy, and St. Giovanni Battista Hospital; 10126 Turin, Italy., Patrizia Bigo, MDFrom University of Turin, 10128 Turin, Italy, and St. Giovanni Battista Hospital; 10126 Turin, Italy., and Luisa Brussino, MDFrom University of Turin, 10128 Turin, Italy, and St. Giovanni Battista Hospital; 10126 Turin, Italy.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-142-4-200502150-00024 SectionsAboutVisual AbstractPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Background: Chemotaxis of eosinophils is the crucial event in the development of nasal polyposis related to chronic hyperplastic eosinophilic sinusitis (1, 2). Several statins, including atorvastatin, inhibit T-helper 1 differentiation and induce T-helper 2 polarization and production of T-helper 2 cytokines, such as interleukin (IL)-5, that promote the activation and chemotaxis of eosinophils.Methods and Findings: A 57-year-old woman with nonallergic rhinosinusitis (low serum levels of total and specific IgE, negative results on skin prick tests, and neutrophils and Staphylococcus aureus in nasal lavage), asthma, and no aspirin sensitivity presented in May 2002 for recent onset of rhinosinusitis associated with asthma attacks. She had no systemic disease. After a 2-week course of amoxicillin–clavulanate and long-term treatment with intranasal and inhaled corticosteroids plus inhaled long-acting β2-agonist, the patient's condition nearly normalized.Six months later, the patient returned because of severe persistent nasal obstruction with extensive bilateral polyposis, mild airway obstruction, and increased levels of exhaled nitric oxide despite long-term treatment with intranasal and inhaled corticosteroids. Eosinophilia was noted in nasal scrapings and in peripheral blood (969 eosinophils/mL). The Figure shows FEV1, exhaled nitric oxide, and nasal cytologic characteristics throughout follow-up. Computed tomography showed extensive opacification of all paranasal sinuses; right maxillary and frontal sinuses were completely stuffed by polypoid tissue.Figure. FEV 1 , exhaled nitric oxide, and nasal cytologic characteristics during treatment with statins and after statin withdrawal. Download figure Download PowerPoint An otolaryngologist surgically removed the polyps, and histologic examination showed relevant edema and inflammatory infiltrate, with predominant eosinophils. Nasal polyps returned within 1 month after surgery and were associated with persistent eosinophilia. The patient reported taking atorvastatin, which her practitioner had prescribed in October 2002 for hyperlipemia. Three weeks after atorvastatin withdrawal, nasal symptoms had dramatically improved, nasal polyps had disappeared, and only a few neutrophils and eosinophils were found in nasal scrapings. Suspecting that atorvastatin was responsible for the development of eosinophilic polyposis, we asked the patient to resume atorvastatin therapy. Nasal symptoms and polyps recurred shortly thereafter, together with nasal eosinophilia. The patient improved again soon after drug withdrawal. Of note, the patient returned 6 months later for recurrence of polyps: Her general practitioner had prescribed simvastatin. We have seen 2 other patients, one 68 years of age and one 74 years of age, who had nonatopic chronic obstructive pulmonary disease and reported having severe nasal obstruction since the start of statin therapy (6 months and 6 years, respectively). Both patients were former smokers. In both cases, nasal lavage showed eosinophilia and nasal biopsies confirmed the presence of eosinophilic nasal polyposis. Polyps resolved in both patients after statin withdrawal.Discussion: To our knowledge, this is the first report of nasal polyposis associated with statin treatment. Growing evidence suggests that statins, besides their lipid-lowering effect, also have anti-inflammatory and immunomodulatory properties (3-5). These properties involve inhibition of T-helper 1 differentiation and T-helper 2 polarization, with increased production of T-helper 2 cytokines (IL-4, IL-5, and IL-10) that promote activation and chemotaxis of eosinophils. The latter mechanism is the crucial event in the development of chronic hyperplastic eosinophilic sinusitis (1, 2).Conclusion: Statins may lead to development of eosinophilic polypoid rhinosinusitis by switching inflammation from the T-helper 1 phenotype to the T-helper 2 phenotype.References1. Bachert C, Van Cawenberge P. Nasal polyps and sinusitis.. In: Adkinson NF, Yunginger JW, Busse WB, Bochner BS, Holgate ST, Simons FE, eds. Middleton's Allergy. Principles & Practice, 6th Edition. St. Louis: Mosby; 2003:1421-36. Google Scholar2. Steinke JW, Bradley D, Arango P, Crouse CD, Frierson H, Kountakis SE, et al. Cysteinyl leukotriene expression in chronic hyperplastic sinusitis-nasal polyposis: importance to eosinophilia and asthma. J Allergy Clin Immunol. 2003;111:342-9. [PMID: 12589355] CrossrefMedlineGoogle Scholar3. Hakamada-Taguchi R, Uehara Y, Kuribayashi K, Numabe A, Saito K, Negoro H, et al. Inhibition of hydroxymethylglutaryl-coenzyme a reductase reduces Th1 development and promotes Th2 development. Circ Res. 2003;93:948-56. [PMID: 14563711] CrossrefMedlineGoogle Scholar4. Nath N, Giri S, Prasad R, Singh AK, Singh I. Potential targets of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor for multiple sclerosis therapy. J Immunol. 2004;172:1273-86. [PMID: 14707106] CrossrefMedlineGoogle Scholar5. Youssef S, Stuve O, Patarroyo JC, Ruiz PJ, Radosevich JL, Hur EM, et al. The HMG-CoA reductase inhibitor, atorvastatin, promotes a Th2 bias and reverses paralysis in central nervous system autoimmune disease. Nature. 2002;420:78-84. [PMID: 12422218] CrossrefMedlineGoogle Scholar Comments0 CommentsSign In to Submit A Comment Author, Article, and Disclosure InformationAffiliations: From University of Turin, 10128 Turin, Italy, and St. Giovanni Battista Hospital; 10126 Turin, Italy. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByAssociation between Dyslipidemia and Chronic Rhinosinusitis in a Korean PopulationSystemic Therapies in Managing Sinonasal InflammationNew insights into airway remodelling in asthma and its possible modulationDoes the prevalence of nasal polyps increase in patients using statins?Statin-associated adverse effects beyond muscle and liver toxicitySimvastatin does not exhibit therapeutic anti-inflammatory effects in asthmaCurrent World LiteratureAdverse effects of statins 15 February 2005Volume 142, Issue 4Page: 310-311KeywordsAsthmaChemotaxisCytokinesEosinophiliaEosinophilsNeutrophilsNitric oxidePhenotypesStatinsSystemic diseases ePublished: 15 February 2005 Issue Published: 15 February 2005 CopyrightCopyright © 2005 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...