Editorial

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he current issue of the American Journal of Rhinology and Allergy highlights two major themes that frequently confront the allergist/rhinologist: chronic rhinosinusitis with nasal polyps (CRSwNPs) and allergic rhinitis (AR). Also addressed in this issue is the rare clinical occurrence of hereditary angioedema (HAE), which deserves attention because of newly developed therapies to prevent potentially life-threatening consequences. In a series of excellent articles, the basic challenges confronting the allergist/rhinologist regarding definition, diagnosis, and treatments of these disorders are rigorously evaluated.

bothered by side effects of prescription nasal sprays, with a high proportion suggesting that there were no truly effective treatments for AR. It would be interesting to study if this could be related to the low humidity/dry climate found in the Middle East, which could make nasal humidification difficult. These and other authors have suggested that patient and preJacquelynne Perou Corey, M.D. scriber education can improve appropriate use of INCSs. Petty and Blaiss9 review INCS topical characteristics (formulations, vehicles, and side effects) and provide insights to improve patient adherence.

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ALLERGIC RHINITIS The ideal definition of AR would help clinicians and researchers to distinguish it from nonallergic rhinitis (NAR) and mixed rhinitis (AR ⫹ NAR). Bernstein1 points out this may be difficult because of overlapping symptoms. A careful history followed by skin (or in vitro) testing to assess allergic status is recommended. Although Bernstein suggests that therapeutic response may aid diagnosis, more research is needed to determine if this assumption is correct. Providing insight into therapeutic response is the article by Gawlik et al.2, in which the mechanism of action of intranasal azelastine therapy is evaluated in NAR. These authors report that an untreated NAR control group showed greater substance P release in nasal lavage fluids after challenge with hypertonic saline than did an azelastine pretreated group. A different approach to defining AR is taken by Larenas-Linnemann et al.3 who studied patients diagnosed with AR by Mexican allergists. They categorized patients according to U.S. coding practices as seasonal AR and perennial AR and compared it with the European Allergic Rhinitis and Its Impact on Asthma classifications of intermittent versus persistent and mild versus moderate–severe. They observed that the physicians tended to “overdiagnose” perennial AR and intermittent–persistent compared with the patient’s assessment. Comorbidities, risk factors, and physiological triggers of AR are explored by several authors. Haavisto et al.,4 using acoustic rhinometry, measured nasal patency changes induced by physical exercise in AR and asthma and found lower area before and after exercise in the allergic group. All three groups (allergic, asthmatic, and controls) experienced improved (⬃15%) nasal volume/area after exercise. Increased body mass index in AR patients was found by Ciprandi et al.5 to be associated with increased markers of inflammation compared with normal weight controls and may increase risk for early bronchial impairment. In Western countries, the incidence of concomitant AR and asthma is common, with some estimates as high as 50%.1 Hong et al.6 studied the comorbidity of AR and asthma in two southern Chinese cities via a hospital-based cross-sectional survey. The prevalence of concomitant bronchial asthma was only 5.33%.

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Two large population studies within this issue provide insight into the burden of illness and treatment related to AR. Hadi and Rahman7 analyzed surveys of the United States, Latin America, and AsiaPacific compared with the Middle East, and Katelaris et al.8 surveyed Australia. These surveys point out the paradox that, despite a “gold standard” treatment for AR with intranasal corticosteroids (INCSs), these agents remain underutilized. In Australia, most physiciandiagnosed patients were seen by a general practitioner only, and 55% had no diagnostic tests.8 Hadi and Rahman7 noted the relative lack of use of INCSs as well. In addition, there were ethnic and/or possibly racial differences noted. Middle Eastern patients were particularly

Many studies have lumped all types of CRS together, making scientific study and evidence-based care of these patients challenging. Chaaban et al.10 review the literature and divide CRS into two groups: CRSwNPs and CRS without NPs. CRS without NPs is considered neutrophilic and, in Western countries, is mainly associated with cystic fibrosis. CRSwNPs is considered “eosinophilic” and is divided into eosinophilic CRS, allergic fungal rhinosinusitis, and aspirinexacerbated respiratory disease (AERD). Hypotheses for the variance in CRS subtypes have involved fungus, bacteria, superantigens to Staphylococcus, biofilms, and changes in the microbiome. Kim et al.,11 swabbing for staph and performing mucosal biopsies in diseased and normal sinuses, found evidence of greater intramucosal microcolonies in CRS and more activated CD163⫹ macrophages, the latter of which also correlated with disease severity. The role of eosinophilia and its relevance in a non-Western/ non-European countries was studied by Kim et al.12 in 347 Korean patients with CRS. There was no relationship of eosinophilia to surgical outcome, prevalence of asthma and AR, or preoperative LundMackay score between the eosinophilic group and noneosinophilic group, with or without NPs.

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A WORLDLY VIEW OF AR TREATMENT: INTRANASAL CORTICOSTEROIDS SHOULD TOP LIST

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CRSwNPs: THE EOSINOPHIL IS/ISNⴕT IMPORTANT

CRSwNP TREATMENT—EVIDENCE-BASED MEDICINE: STEROIDS SHOULD TOP LIST Schlosser and Soler13 make a strong case for evidence-based treatment of CRSwNPs in their review, which evaluates medical and surgical treatments with a focus on the highest levels of evidence. They provide an excellent summary of recommendations in table form. While there is strong evidence to support recommendations for use of oral short-term and perioperative steroids, INCS sprays, postoperative antibiotics, anti-IL-5 monoclonal antibody and for leukotriene antagonists (LTA’s) in CRSwNPs, there is strong evidence not to use oral/topical antifungals. Insight into why antibiotics may have varying effectiveness in different types of CRS is elucidated by Kennedy and Borish.14 Bacteria present in biofilms are not capable of being eradicated with antibiotics at doses that they can be used. Bacteria in the biofilms have their “core” metabolic activity down-regulated, decreasing oxygen concentration and altering the pH. Additional evidence for the use of LTA, with or without INCS in CRSwNPs, comes from a meta-analysis by Wentzel et al.15 They

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suggest that LTAs may be an effective tool for treating CRSwNPs, with limited benefit as an adjunctive agent. Concomitant asthma, AERD, or atopy does not appear to affect the response to LTA. Wang et al.16 noted that lower levels of vitamin D were associated with CRSwNPs, with a lower level being associated with higher polyp grade. Subcategorization of AERD, which has a particularly poor prognosis in all patients, has been difficult, particularly because clinical tests have been lacking and history alone is insufficient. Forer et al.17 found that nasal eosinophils and serum LTE4 were elevated in CRSwNP patients with positive aspirin challenge. When medical therapy fails, surgery for CRS is recommended.13 Studies suggest that benefits are improved for extensive disease when sinuses are opened widely and used with adjunctive therapies postoperatively. Although most surgery can not be performed “blindly,” Tirelli et al.18 randomly assigned left and right sides of surgical patients with CRSwNPs to either microdebrider or Blakely forceps. They found that the manual instrument showed a lower rate of NP recurrence.

proves postoperative pain control. Wang et al.23 noted that patients with CRS have a 1.48 higher risk of acute MI within 6 years. Albu et al.24 noted that lumbar drains did not affect the success of cerebrospinal fluid leak repair; the presence of increased intracranial pressure preoperatively was most predictive of recurrence. It is important to note that in addition to the “negative results” that are presented here, the two meta-analyses in this issue13,15 include articles that show negative results in one study but show overall positive results when the full body of literature is analyzed.

THERAPY FOR CRS: INCS—“DO WHAT I SAY, NOT WHAT I DO” Bhattacharyya and Kepnes19 found that despite the strong recommendation for INCS in CRSwNPs, in a large population survey of office visits for NPs, only 43% were prescribed INCS, 27% were prescribed oral steroids, 26% were prescribed antibiotics, and 18.5% were prescribed oral antihistamines. Otolaryngologists were less likely 36% versus 57% than nonotolaryngologists to prescribe INCS, and less likely to prescribe oral steroids, antibiotics, and oral antihistamines. According to evidence-based medicine,7 we should be happy we’re prescribing fewer antibiotics and antihistamines, but not so happy about prescribing fewer INCSs or oral steroids.

LARYNGEAL HAE

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An important function of scientific research and guidelines is to translate the science to clinical care, and then back again, to see how real-life outcomes in real patients live up to the scientific ideal. Forward steps with basic science, pathophysiology,25 clinical trials, clinical guidelines, and evidence-based medicine1,2,4,5,10,11,13,14–17,20,21 and one step back with analysis of real-life outcomes (including analysis of failures)3,6,7,9,12,13,18,19,23,24 will keep us progressing in the right direction, toward better patient care. Although INCSs are highly recommended for AR and CRSwNPs, their relatively poor utilization by patients presents a challenge to us all. There are many factors that influence the use of appropriate treatments, other than scientific validity and patient or physician education: socioeconomic factors such as cost; accessibility to care; and other cultural, environmental, and socioeconomic barriers. The upcoming availability of INCSs without a prescription in the United States, as well as changes in access to healthcare, present us with additional challenges to meet in order to provide patients with AR and CRS with top quality care.

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Otolaryngologists and allergists are frequently called on to evaluate and treat patients with HAE, a disorder that manifests as repeated attacks of swelling of the skin, face, larynx, gastrointestinal tract, and other organs. The otolaryngologist may be called on in the emergency room for a difficult intubation; the allergist may receive a consult to rule out allergy. Both may be consulted for perioperative management for dental or other surgical procedures. Minor trauma or manipulation of the face, mouth, or upper airway may also trigger acute attacks in this disorder.20 C1 esterase inhibitor levels are low or nonfunctional, leading to excessive release of bradykinin, which leads to vasodilation, vascular permeability, and edema, with dysregulation of the complement, contact, and fibrinolytic pathways. Laryngeal edema is the most dangerous manifestation, potentially leading to difficult intubation and asphyxiation if unsuccessful. Bernstein,20 in his review of newly available therapies for HAE, points out that an improved understanding of pathophysiology has led to advancements in lifesaving treatments. Riedel et al.21 were able to relieve potentially life-threatening laryngeal angioedema by prompt administration of nanofiltered C1 esterase inhibitor. When administered within 4 hours of symptom onset, clinical relief was seen in 94% of attacks within 4 hours of treatment. Other newly available treatments include icatibant, a bradykinin B2-receptor antagonist, or ecallantide, a kallikrein inhibitor. Although HAE is rare, acquired angioedema from angiotensin-converting enzyme inhibitors, is common, comprising 30% of all emergency room visits for angioedema.

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PROGRESS

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PERSONAL NOTES My father, Maurice Perou, M.D., is a retired pathologist. In his lifetime, he went from losing the tip of a finger caused by lack of antibiotics (penicillin wasn’t even invented), through the invention of laboratory diagnostics, near eradication of small pox with vaccination, the HIV epidemic, stem cell transplants, and genetic markers for cancer, with just as drastic socioeconomic changes in the practice of medicine; Medicare; Medicaid; Social Security; electronic medical records; Affordable Care Act; and Public Health advances in sanitation, food safety, vaccination, and water and air quality. He has, and continues to, inspire me to keep learning. Jacquelynne Perou Corey, M.D.

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QUICK CLINICAL PEARLS AND THE VALUE OF NEGATIVE RESULTS

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From the exclusively e-published articles within this issue, which are represented by abstracts printed herein, some clinical pearls are gathered. Mo et al.22 found that soaking nasal packing in lidocaine im-

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Bernstein JA. Characterizing rhinitis subtypes. Am J Rhinol Allergy 27:457–460, 2013. Gawlick R, Jawor B, Rogala B, et al. Effect of intranasal azelastine on substance P release in perennial nonallergic rhinitis patients. Am J Rhinol Allergy 27:514–516, 2013. Larenas-Linnemann S, Dinger H, Shah-Hosseini K, et al. Over diagnosis of persistent allergic rhinitis in perennial allergic rhinitis patients: A nationwide study in Mexico. Am J Rhinol Allergy 27:495– 501, 2013. Haavisto LE, Lukkarinen M, Lukkerinen H, et al. Physical exercise increases nasal patency in asthmatic and atopic preschool children. Am J Rhinol Allergy 27:451–456, 2013. Ciprandi G, Ricciardolo FLM, Dignori A, et al. Increased body mass index and bronchial impairment in allergic rhinitis. Am J Rhinol Allergy 27:e195–e201, 2013. Hong H, Yang Q, Zuo K, et al. A hospital-based survey on the prevalence of bronchial asthma in patients with allergic rhinitis in southern China. Am J Rhinol Allergy 27:502–505, 2013. Hadi UH, and Rahman HA. The impact and treatment of allergic rhinitis in the Middle East: A comparison with the landmark allergy surveys from other worldwide regions. Am J Rhinol Allergy 27:490–494, 2013.

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Katelaris CH, Sacks R, and Theron PN. Allergic rhinoconjunctivitis in the Australian population: Burden of disease and attitudes to intranasal corticosteroid treatment. Am J Rhinol Allergy 27:506–509, 2013. Petty DA, and Blaiss MS. Intranasal corticosteroids topical characteristics: Side effects, formulation, and volume. Am J Rhinol Allergy 27:510–513, 2013. Chaaban MT, Walsh ME, Woodworth BA. Epidemiology and differential diagnosis of nasal polyps. Am J Rhinol Allergy 27:473–478, 2013. Kim RJT, Yin T, Chen C-JJ et al. The interaction between bacteria and mucosal immunity in chronic rhinosinusitis: A prospective crosssectional analysis. Am J Rhinol Allergy 27:e183–e189, 2013. Kim SY, Park JH, Rhee C-S, et al. Does eosinophilic inflammation affect the outcome of endoscopic sinus surgery in chronic rhinosinusitis in Koreans? Am J Rhinology Allergy 27:e166–e169, 2013. Schlosser RJ, and Soler ZM. Evidence-based treatment of chronic rhinosinusitis with nasal polyps. Am J Rhinol Allergy 27:461–466, 2013. Kennedy JL, and Borish L. Chronic rhinosinusitis and antibiotics: The good, the bad, and the ugly. Am J Rhinol Allergy 27:467–472, 2013. Wentzel JL, Soler ZM, DeYoung K, et al. Leukotriene antagonists in nasal polyposis: A meta-analysis and systematic review. Am J Rhinol Allergy 27:482–489, 2013. Wang L-F, Lee C-H, Chien C-Y, et al. Serum 25-hydroxyvitamin D levels are lower in chronic rhinosinusitis with nasal polyposis and are correlated with disease severity in Taiwanese patients. Am J Rhinol Allergy 27:e162–e165, 2013.

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Forer B, Landsberg R, and Kivity S. Aspirin challenge in patients with chronic rhinosinusitis with polyps correlates with local and systemic inflammatory markers. Am J Rhinol Allergy 27:e170–e173, 2013. Tirelli G, Gatta A, Spinato G, et al. Surgical treatment of nasal polyposis: A comparison between cutting forceps and microdebrider. Am J Rhinol Allergy 27:e202–e206. Bhattacharyya N, and Kepnes LJ. Medications prescribed at ambulatory visits for nasal polyposis. Am J Rhinol Allergy 27:479–481, 2013. Bernstein JA. Managing hereditary angioedema patients undergoing otolaryngeal procedures. Am J Rhinol Allergy 27:522–527, 2013. Riedl AM, Lumry WR, Li HH, et al. Nanofiltered C1 esterase inhibitor for treatment of laryngeal attacks in patients with hereditary angioedema. Am J Rhinol Allergy 27:517–521, 2013. Mo J-H, Park Y-M, Chung Y-J. Effect of lidocaine-soaked nasal packing on pain relief after endoscopic sinus surgery. Am J Rhinol Allergy 27:e174–e177, 2013. Wang P-C, Lin H-C, and Kang J-H. Chronic rhinosinusitis confers an increased risk of acute myocardial infarction. Am J Rhinol Allergy 27:e178–e182, 2013. Albu S, Emanuelli E, Trombitas V, et al. Effectiveness of lumbar drains on recurrence rates in endoscopic surgery of cerebrospinal fluid leaks. Am J Rhinol Allergy 27:e190–e194, 2013. Dimitrijevic I, and Edvinsson L. Increased endothelin 1 type B receptors in nasal lesions of patients with granulomatosis with polyangiitis. Am J Rhinol Allergy 27:444–450, 2013. e

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Chronic rhinosinusitis with nasal polyps (CRSwNPs) and allergic rhinitis (AR).

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