Curr Allergy Asthma Rep (2010) 10:175180 DOI 10.

1007/s11882-010-0104-4

The Role of Local Steroid Injection for Nasal Polyposis

Marcelo B. Antunes & Samuel S. Becker

Published online: 20 March 2010 # Springer Science+Business Media, LLC 2010

Abstract Sinonasal polyps affect a small but significant percentage of patients with chronic sinusitis. Treatments vary and range from oral and topical medical treatments to surgical removal. Corticosteroids typically have been regarded as the gold standard medical treatment for sinonasal polyps. Delivery of steroids is traditionally via oral or topical means. Over the years, otolaryngologists have also found that intrapolyp injection of corticosteroids is an effective means to treat some patients with sinonasal polyps. This article reviews the prevalence, pathophysiology, and medical treatment options for sinonasal polyps. Focused attention is paid to treatment with steroid injections, including a review of its associated risks and benefits. Keywords Sinus . Polyps . Steroid . Injection . Kenalog

Introduction Sinonasal polyposis (NP) belongs to the spectrum of chronic rhinosinusitis (CRS) and is often considered an end point of an inflammatory process that takes place in the sinonasal mucosa. NP may cause nasal obstruction, chronic sinusitis, and hyposmia. Studies have demonstrated that patients suffering from CRS with NP score worse on

quality-of-life questionnaires than patients with coronary artery disease, chronic obstructive pulmonary disease, and congestive heart failure [1]. Diagnosis is primarily via nasal endoscopy, which allows direct visualization of the polyps. Particular attention is paid to the middle meatusthe space between the middle turbinate and lateral nasal wallas this is the site of origin of most NP. Radiographic studies such as CT complement endoscopy by helping to define the extent of the polyposis and the impact on the surrounding sinuses and skull base. Inflammatory polyposis is typically bilateral; unilateral polyposis raises concern for noninflammatory sources. Although the prevalence of NP is considered low, this remains a matter of debate. Most authors believe the prevalence ranges from 1% to 4% of the population [2, 3]; however, this may be an underestimate, as a much higher prevalence of 32% was reported in an autopsy study [4]. Treatment options vary and range from topical, local, and systemic medications to surgical removal, often including endoscopic sinus surgery.

Pathophysiology of Nasal Polyps Polyps are characterized by their edematous nature in addition to a subepithelial inflammatory infiltrate. Although this inflammatory infiltrate is most commonly eosinophilic in nature [5], in some cases, polyps are primarily neutrophilic [6]. Histologically, polyps present with epithelial damage, a thickened basement membrane, and a reduced number of mucosal glands [7]. The origin of NP is likely multifactorial. Most researchers agree that polyp formation derives from an inflammatory process that begins with mucosal injury at a microscopic level. Mucosal injury stimulates expression of

M. B. Antunes Department of OtorhinolaryngologyHead and Neck Surgery, University of Pennsylvania, Philadelphia, PA, USA S. S. Becker (*) Becker Nose and Sinus Center, 2301 Evesham Road, Suite 404, Voorhees, NJ 08043, USA e-mail: sam.s.becker@gmail.com

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cytokines, chemokines, adhesion molecules, and major histocompatibility complex class II molecules, which assist in immunoregulation and antigen presentation. One such factor in this inflammatory cascade is tumor necrosis factor-, which is expressed to increase epithelium cell permeability [8]. Interleukin (IL)-8 is also a potent chemoattractant for neutrophils and eosinophils, whereas intercellular adhesion molecules and vascular cell adhesion molecules work alongside HLA-DR antigens in T-cell immunoregulation [9, 10]. Several studies suggest that eosinophils are the predominant cell type, constituting up to 80% of the inflammatory cells in the nasal polyps [11]. One of the most important mechanisms for this is the autocrine regulation of cytokines that attract and increase the survival of these cells. IL-5, for instance, plays a major role in this mechanism by recruiting and activating eosinophils, as well as inhibiting eosinophil apoptosis [12]. IL-5 was found to be significantly increased in NP compared with healthy controls and CRS without NP [12, 13]. Moreover, eosinophils themselves may contribute to IL-5 release, perpetuating the inflammatory cycle. Other inflammatory mediators elevated in NP include the eosinophil chemoattractants RANTES (regulated on activation, normal T-cell expressed and secreted) and eotaxin [14, 15]. RANTES is released by macrophages, platelets, fibroblasts, lymphocytes, and epithelial cells. It is a potent attractant to eosinophils and lymphocytes and activates eosinophils [16, 17] Eotaxin is released by macrophages, T lymphocytes, and eosinophils themselves. It is a selective eosinophil attractant that plays an important role in polyp formation [17]. Although the presence of NP is commonly associated with eosinophilia, there exists a subset of polyps characterized by profound glandular hypertrophy, mononuclear cell infiltrate, fibrosis, and mast cells without eosinophilia [18]. A recent study evaluating the gene transcription factor from noneosinophilic polyps found expression of stem cell factor, IL-6, and IL-8 and a lack of upregulation of IL-4, IL-13, and interferon- [19]. A related study found that noneosinophilic polyps have few lymphocytes expressing CCR3 and CCR5, common markers for T-helper type 2 and T-helper type 1 cells, respectively [20]. These studies suggest that patients with noneosinophilic polyps may have a different underlying inflammatory process than those with eosinophilic polyps. Another subset of patients have polyps and aspirin sensitivity. Polyps in these patients are particularly persistent and resistant to treatment. When associated with asthma, the triad is known as Samter s triad. The severity of the disease is well-recognized and often involves all the paranasal sinuses and nasal cavities [21]. The polyps are characterized by marked eosinophilic infiltrationmore so than other types of polypsand several eosinophil-related

cytokines are demonstrated to be present [22]. The pathogenic process in the development of these polyps is notable for arachidonic acid metabolism abnormalities and decreased eosinophilic apoptosis [23]. For instance, these patients often display a lower level of anti-inflammatory prostaglandin E2, which has an inhibitory effect on eosinophils [24], as well as an upregulation of enzymes involved in the production of leukotriene metabolites [25]. Although the past decade has witnessed great strides being made in our understanding of the inflammatory cascade that stimulates polyp formation, the initial trigger for this inflammatory cascade remains unknown. Several hypotheses regarding this initial event have been proposed, including allergy, fungal and bacterial infections, superantigens, and bacterial biofilms. The relationship of allergy and nasal polyps has long been a matter of debate. Among patients with allergic rhinitis, 0.5% to 4.5% have been found to have NP [26, 27]. On the other hand, authors have reported a prevalence of allergic rhinitis in NP patients ranging from 10% to 64% [28, 29]. The proposed role of fungus as a source of NP derives from the premise that a local immune response to the fungal elements starts an inflammatory cascade that peaks with the formation of polyps. In one proposed mechanism, it has been suggested that a non-IgE mechanism is responsible for the eosinophilic infiltrate [30]. Bacteria and superantigens also may be involved in this inflammatory process. Superantigens bind to T-cell receptors and initiate an exuberant inflammatory response. Interactions between Staphylococcus aureus superantigens and lymphocytes in polyps have been demonstrated [31].

Medical Management of Nasal Polyps Patients with NP often present to a physician when the bulk of their disease is of high severity. The severity and chronicity at the time of presentation can make this a difficult state to manage. Medical interventions vary and include topical and systemic steroids, antimicrobials, antihistamines, leukotriene antagonists, diuretics, and aspirin desensitization. Other approaches include IgE antagonists [32]; (IL-5) [33], IL-4, and IL-13 antagonists [34]; eotaxin antagonists [35]; and CCR3 antagonists [36]. These treatments vary in their availability and efficacy. Antimicrobials traditionally have been part of the treatment of chronic sinusitis with nasal polyps. Antibiotics may be used to decrease colonization or to treat an associated sinus infection, as polyps may block the sinus outflow pathway. In fact, nearly 70% of patients with nasal polyps were cultured positive for S. aureus in one study [37]. Recent studies suggested that macrolide therapy may not only decrease microbial colonization but may also act

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as an anti-inflammatory agent, decreasing IL-8 levels and inhibiting fibroblast proliferation [38, 39]. Studies diverge, however, with regard to the efficacy of macrolide use in the treatment of nasal polyps. Antihistamines are used in patients with allergic rhinitis, but their use in nasal polyps has not been extensively studied to the point of making a formal recommendation, even though theoretically, these patients may benefit. Leukotriene antagonists affect the metabolism of arachidonic acid, which may be involved in the pathophysiology of nasal polyps, especially in patients with aspirin sensitivity. As with antihistamines, the efficacy of leukotriene antagonists for treatment of nasal polyposis remains uncertain. In patients with NP and aspirin sensitivity, it has been suggested that desensitization may help reduce polyp formation. Aspirin desensitization consists of administering incremental oral doses until one can reach a maintenance dose inducing a refractory period. The treatment is often continued for several years. One study demonstrated that desensitization reduced the number of sinus infections, asthma hospitalizations, use of corticosteroids, and need for sinus surgery [40].

reducing polyp size and nasal symptoms score and in improving nasal expiratory peak flow. Two placebocontrolled trials have demonstrated significant improvement in patient nasal symptoms and polyp size via endoscopic and radiologic imaging [51, 52]. Of concern with long-term steroid use are the effects on the hypothalamic-pituitary-adrenal axis, cataract and glaucoma formation, osteoporosis, and growth retardation in children [53]. Systemic and topical steroids are also used after surgical removal of polyps. Their decrease in recurrence rate is well-documented.

Steroid Injection in Nasal Polyps Intrapolyp steroid injections have been used to deliver a higher concentration of corticosteroids to polyp tissue while at the same time limiting the systemic effects associated with these medications. A steroid injection is thought to combine the efficacy of oral steroids with the limited side effect profile of topical steroids and is typically performed in the clinic setting. This practice was first described in the 1950s, when several authors described their experience injecting steroids intranasally into polyps and turbinates [5458]. The practice gained popularity until 1962, when the first reported case of blindness following steroid injection of hydrocortisone was published [59]. Another three reports of visual loss were published in the following years, further raising the concern with this practice [6062]. In a thorough review, Mabry [63] identified another 10 cases, one of which was from an intrapolyp injection, whereas the remaining nine resulted from inferior turbinate injections. The pathogenesis of visual loss may be via embolization of the steroid particles or vasospasm of the retinal artery. Embolization occurs by retrograde flow of the steroid particles from the ethmoid arteries, which supply the nasal lining into the ophthalmic artery and the retinal artery [63, 64]. It has been suggested that the risk of blindness from embolization may be decreased by the use of a suspension of small steroid particles, which would be less likely to embolize. It also has been proposed that the risk of blindness from vasospasm may be diminished if topical vasoconstriction is performed prior to the intrapolyp injection [65]. Care should be taken to inject directly into the polyp and not into the more vascular surrounding sinonasal mucosa. Since these initial publications, several authors have published their results representing more than 100,000 intranasal corticosteroid injections (polyp or nonpolyp injection), with no episodes of reported visual loss [66 70]. Likewise, Becker et al. [71] reviewed the results of 189 patients who received nearly 1,500 injections and

Topical and Systemic Steroids Currently, topical and systemic steroids are considered firstline therapy for NP. Steroids act via their interaction with the glucocorticoid receptor (GR). They enter the cytoplasm of target cells and bind to this receptor, which is highly expressed in the airway mucosa. There are two isoforms: GR- and GR- [41]. The complex then moves to the nucleus, where gene transcription is affected. GR- generates transcription factors that enhance anti-inflammatory and repress pro-inflammatory gene transcription [42]. The clinical efficacy of corticosteroids relies on their ability to reduce eosinophilic infiltration by preventing their activation and decreasing their survival. This is achieved at the cellular level and by reducing cytokines and chemokines secreted by the epithelium [4345]. The use of steroids in CRS and NP has been extensively studied. The use of topical steroids in their various preparations has been documented to be efficacious in reducing nasal polyps size and in improving nasal blockage and congestion. Topical steroids have not been shown to be as effective in restoration of patients sense of smell [46, 47, 48, 49]. The systemic absorption of topical steroids is still undetermined, with data ranging from less than 1% to 50% [50]. However, at recommended dosages, no significant effects have been identified in the hypothalamic-pituitary-adrenal axis or any other organ system. Systemic steroids traditionally have been used as the mainstay treatment of nasal polyps. They are effective in

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Curr Allergy Asthma Rep (2010) 10:175180 5. Bachert C, Gevaert P, Holtappels G, et al.: Nasal polyposis: from cytokines to growth. Am J Rhinol 2000, 14:279290. 6. Payne SC, Han JK, Huyett P, et al.: Microarray analysis of distinct gene transcription profiles in non-eosinophilic chronic sinusitis with nasal polyps. Am J Rhinol 2008, 22:568580. This is an insightful article that characterizes and groups polyps in patients with noneosinophilic sinusitis on a molecular level. 7. Tos M, Sasaki Y, Ohnishi M, et al.: Fireside conference 2. Pathogenesis of nasal polyps. Rhinol Suppl 1992, 14:181185. 8. Krunkosky TM, Fischer BM, Martin LD, et al.: Effects of TNFalpha on expression of ICAM-1 in human airway epithelial cells in vitro. Signaling pathways controlling surface and gene expression. Am J Respir Cell Mol Biol 2000, 22:685692. 9. Murphy PM: The molecular biology of leukocyte chemoattractant receptors. Annu Rev Immunol 1994, 12:593633. 10. Hershberg RM, Cho DH, Youakim A, et al.: Highly polarized HLA class II antigen processing and presentation by human intestinal epithelial cells. J Clin Invest 1998, 102:792803. 11. Stoop AE, van der Heijden HA, Biewenga J, et al.: Eosinophils in nasal polyps and nasal mucosa: an immunohistochemical study. J Allergy Clin Immunol 1993, 91:616622. 12. Bachert C, Wagenmann M, Hauser U, et al.: IL-5 synthesis is upregulated in human nasal polyp tissue. J Allergy Clin Immunol 1997; 99:837842. 13. Lee CH, Rhee CS, Min YG: Cytokine gene expression in nasal polyps. Ann Otol Rhinol Laryngol 1998, 107:665670. 14. Jahnsen FL, Haye R, Gran E, et al.: Glucocorticosteroids inhibit mRNA expression for eotaxin, eotaxin-2, and monocytechemotactic protein-4 in human airway inflammation with eosinophilia. J Immunol 1999, 163:15451551. 15. Bartels J, Maune S, Meyer JE, et al.: Increased eotaxin-mRNA expression in non-atopic and atopic nasal polyps: comparison to RANTES and MCP-3 expression. Rhinology 1997, 35:171174. 16. Meyer JE, Bartels J, Grgh T, et al.: The role of RANTES in nasal polyposis. Am J Rhinol 2005, 19:1520. 17. Shin SH, Lee SH, Jeong HS, et al.: The effect of nasal polyp epithelial cells on eosinophil activation. Laryngoscope 2003, 113:13741377. 18. Early SB, Han J, Borish L, et al.: Histologic examination reveals distinct disease subsets of chronic sinusitis. J Allergy Clin Immunol 2007, 119:S243. This is a well-written article that classifies chronic sinusitis based on histopathologic findings. It provides a useful way to think about a broad-based disease. 19. Payne SC, Han JK, Huyett P, et al.: Microarray analysis of distinct gene transcription profiles in non-eosinophilic chronic sinusitis with nasal polyps. Am J Rhinol 2008, 22:568581. 20. Kim JW, Hong SL, Kim YK: Histological and immunological features of non-eosinophilic nasal polyps. Otolaryngol Head Neck Surg 2007, 137:925930. This is an insightful overview of characteristics of the less common noneosinophilic polyps. 21. Kowalski ML: Rhinosinusitis and nasal polyposis in aspirin sensitive and aspirin tolerant patients: are they different? Thorax 2000, 55(Suppl 2):S84S86. 22. Pods R, Ross D, van Hlst S, et al.: RANTES, eotaxin and eotaxin-2 expression and production in patients with aspirin triad. Allergy 2003, 58:11651170. 23. Kowalski ML, Grzegorczyk J, Pawliczak R, et al.: Decreased apoptosis and distinct profile of infiltrating cells in the nasal polyps of patients with aspirin hypersensitivity. Allergy 2002, 57:493500. 24. Kowalski ML, Pawliczak R, Wozniak J, et al.: Differential metabolism of arachidonic acid in nasal polyp epithelial cells cultured from aspirin-sensitive and aspirin-tolerant patients. Am J Respir Crit Care Med 2000, 161:391398. 25. Sousa AR, Parikh A, Scadding G, et al.: Leukotriene-receptor expression on nasal mucosal inflammatory cells in aspirinsensitive rhinosinusitis. N Engl J Med 2002, 347:14931499.

found one case of temporary diplopia, with no cases of vision loss. Patients in this series received injections using Kenalog-40 (Bristol-Myers Squibb, New York, NY) drawn with a 1-mL syringe and injected under endoscopic visualization with a 25-gauge needle after appropriate topical vasoconstriction. Empirically speaking, the steroid effect seems to last for about 6 to 8 weeks. In terms of systemic effects from intrapolyp steroid injection, it is mostly thought to be nonsignificant, although one study measuring plasma cortisol demonstrated a transient and mild amount of systemic absorption without lasting adrenal suppression [72].

Conclusions Physicians have a large armamentarium with which to treat NP. Although surgical treatment may be needed when the bulk of polyps is excessive, medical therapy can be used to manage most cases successfully. For patients with polyps refractory to management with oral and topical corticosteroids, intrapolyp steroid injection can be considered. Steroid injection seems to be an effective method of treatment; however, there are insufficient data to attest to its true efficacy and absorption compared with other means of steroid delivery. Patients should be advised that this is an off-label use of medications, and the risks and benefits should be reviewed in detail prior to performing a steroid injection. Written informed consent should be obtained prior to administration.
Disclosure No potential conflicts of interest relevant to this article were reported.

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