Aspirin-induced Asthma Patients Research Articles

Does aspirin-induced oxidative stress cause asthma exacerbation?

Aspirin-induced asthma (AIA) is a distinct clinical syndrome characterized by severe asthma exacerbations after ingestion of aspirin or other non-steroidal anti-inflammatory drugs. The exact pathomechanism of AIA remains unknown, though ongoing research has shed some light. Recently, more and more attention has been focused on the role of aspirin in the induction of oxidative stress, especially in cancer cell systems. However, it has not excluded the similar action of aspirin in other inflammatory disorders such as asthma. Moreover, increased levels of 8-isoprostanes, reliable biomarkers of oxidative stress in expired breath condensate in steroid-naïve patients with AIA compared to AIA patients treated with steroids and healthy volunteers, has been observed. This review is an attempt to cover aspirin-induced oxidative stress action in AIA and to suggest a possible related pathomechanism.

Effects of omalizumab on eosinophil cationic peptide, 25-hydroxyvitamin-D, IL-1β and sCD200 in cases of Samter's syndrome: 36 months follow-up

Contex: The historic triad of nasal polyposis, asthma and intolerance to aspirin and related chemicals, recently designated as Samter's syndrome, is an inflammatory condition of unknown pathogenesis. This study surveyed the levels of chosen serum eosinophil cationic peptide (ECP), soluble CD200 (SCD200), interleukin (IL)-1β, high sensitive C-reactive protein (hs-CRP) and 25-hydroxyvitamin-D (25(OH)D) in the aspirin-induced asthmatic patients treated with anti-IgE therapy to investigate their roles in the pathogenesis of disease perpetuation and anti-IgE therapy’s impact on them.Methods: Medical history, lung function tests and measurement of fractional exhale nitric oxide concentrations were performed on the same day. Concentrations of IL-1β and SCD200 in the serum samples were quantified using ELISA kits. Total and specific IgE and hs-CRP levels were enumerated by fluoroenzyme immunoassay. Serum levels of 25(OH)D were quantified by a radioimmunoassay.Results: We had three patients of severe persistent allergic asthma with Samter's syndrome. Levels of total IgE, ECP, fractional exhale nitric oxide concentrations, SCD200, IL-1β and hs-CRP were decreased while 25(OH)D was increased after starting the treatment of anti-IgE.Conclusions: To our knowledge, this is the first time an association between omalizumab use and Samter's syndrome has been documented. As a conclusion allergic nasal symptoms (sneezing, postnasal drip) and asthma symptoms were decreased in patients, but no change was seen on nasal polyposis development after omalizumab treatment.

Low prostaglandin E2 and cyclooxygenase expression in nasal mucosa fibroblasts of aspirin‐intolerant asthmatics

Anomalies in the regulation of cyclooxygenase (COX)-1 and -2 have been described in nasal polyps of aspirin-induced asthma (AIA). Whether these anomalies are specific to nasal polyps or affect all the nasal mucosa (NM) of upper airways is still unclear. The objective of this study was to compare the COX pathway in NM of AIA patients with the NM of control subjects. Fibroblasts were isolated from NM of five AIA patients (AIA-NM) and five control subjects (control-NM). Cells were treated with 10 ng/mL interleukin (IL)-1β for up to 72 h. Prostaglandin E2 (PGE2 ) production was measured by enzyme-linked immunosorbent assay (ELISA), expression of COX-1 protein by Western blot and COX-2 protein by ELISA, Western blot and immunofluorescence techniques. IL-1β increased PGE2 production and COX-1 protein expression in control-NM fibroblasts, but no changes were found in AIA-NM. IL-1β provoked a significant time-dependent increase in COX-2 protein expression in control-NM fibroblasts but had a very mild effect on COX-2 protein expression in AIA-NM. Our data suggest that abnormalities in the COX pathway are not a phenomenon exclusive to nasal-polyp mucosa as they are also present in all the NM of AIA patients. These anomalies may be involved in the pathogenesis of airway inflammation and non-steroidal anti-inflammatory drug intolerance in asthma patients with chronic rhinosinusitis and nasal polyposis.

Upregulation of CD11b on Eosinophils in Aspirin Induced Asthma

Although a challenge test using non-steroidal anti-inflammatory drugs (NSAIDs) is crucial for diagnosis of aspirin-induced asthma (AIA), it also has drawbacks in terms of possible side effects. Therefore, alternative in-vitro diagnostic methods for AIA are awaited. Nineteen stable non-AIA patients (9 males and 10 females; mean age, 49.4 ± 4.8 years), and 20 AIA patients (9 males and 11 females; mean age, 51.1 ± 4.8 years) were enrolled in this study. CD11b and CD16 expressions on the peripheral-blood granulocytes after administration of aspirin and different concentrations of PGE2 in vitro were examined using flowcytometry. Aspirin induced a significant increase in CD11b expression on eosinophils (CD16 negative granulocytes) in 19 AIA patients and one non-AIA patient. Increase in CD11b expression on eosinophils by aspirin administration was suppressed by PGE2 in a dose-dependent manner. The measurement of CD11b expression on peripheral-blood eosinophils showed very high sensitivity and specificity of (-95%) in diagnosing AIA. Although this method requires laboratory facilities for flowcytometry, it may be very useful in diagnosis of AIA without side effects. In addition, PGE2 may be involved in regulation of CD11b expression on eosinophils by aspirin administration.

Signal Transduction Pathways (MAPKs, NF-κB, and C/EBP) Regulating COX-2 Expression in Nasal Fibroblasts from Asthma Patients with Aspirin Intolerance

BackgroundRecent studies have revealed that cyclooxygenase-2 (COX-2) expression is down-regulated in aspirin-induced asthma (AIA). Various signal pathways (MAPKs, NF-κB and C/EBP) are involved in COX-2 regulation.ObjectiveTo investigate the regulation of COX-2 expression through MAP-kinase pathway activation and nuclear factor translocation in aspirin-induced asthma (AIA).MethodsFibroblasts were isolated from specimens of nasal mucosa (NM, N = 5) and nasal polyps (NP, N = 5). After IL-1β (1 ng/ml) incubation, COX-2 and phosphorylated forms of ERK, JNK and p38 MAPK were measured by Western blot. MAPK’s role in IL-1β-induced COX-2 expression was assessed by treating cells with ERK (PD98059), JNK (SP600125) and p38 MAPK (SB203580) inhibitors (0.1–10 µM) prior to IL-1β exposure. NF-κB and C/EBP nuclear translocation was measured by Western blot and TransAM® after IL-1β (10 ng/ml) exposure.ResultsNo differences were observed in the MAPK phosphorylation time-course between NM and NP-AIA fibroblasts. The p38 MAPK inhibitor at 10 µM significantly reduced IL-1β-induced COX-2 expression in NM fibroblasts (85%). In NP-AIA fibroblasts the COX-2 inhibition (65%) at 1 and 10 µM was not statistically significant compared to non-treated cells. ERK and JNK inhibitors had no significant effect in either the NM or NP-AIA cultures. The effect of IL-1β on NF-κB and C/EBP subunits’ nuclear translocation was similar between NM and NP-AIA fibroblasts.ConclusionsThese results suggest that p38 MAPK is the only MAPK involved in IL-1β-induced COX-2 expression. NM and NP-AIA fibroblasts have similar MAPK phosphorylation dynamics and nuclear factor translocation (NF-κB and C/EBP). COX-2 downregulation observed in AIA patients appears not to be caused by differences in MAPK dynamics or transcription factor translocation.

Strategy for NSAID administration to aspirin-intolerant asthmatics in combination with PGE2 analogue: a theoretical approach

Aspirin-induced asthma (AIA) is a severe inflammatory disease, which affects aspirin-intolerant patients after ingestion of aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs). In this article, a mathematical model describing arachidonic acid metabolism and its interaction with NSAIDs, is used to study the strategy for safe managing of NSAIDs to AIA patients. Three different AIA patient populations are taken into consideration. First, the values of aspirin and ibuprofen limiting doses that might induce symptoms of AIA are calculated and compared to experimentally observed threshold doses to enlighten which AIA patient population is susceptible to aspirin and ibuprofen. Second, the methodology of NSAID administration is studied on AIA populations susceptible to aspirin and ibuprofen by using 1,000 mg dose of aspirin and 200 or 400 mg dose of ibuprofen followed by PGE(2) analogue dosing. Our model results show that successive doses of PGE(2) analogue applied at appropriate time after aspirin or ibuprofen ingestion would enable administration of both NSAIDs to AIA patients. PGE(2) analogue doses and the corresponding times of their applications are calculated. The model is also used to estimate the duration of symptoms of AIA for different aspirin and ibuprofen doses.

Matrix Metalloproteinase-9 Promoter Gene Polymorphism (–15620T) in Nasal Polyposis

Expression of matrix metalloproteinase (MMP)-9 increases in nasal polyp tissues. However, the impact of MMP-9 genotypes on the development of nasal polyposis (NP) is unknown. The aim of this study was to examine a potential association of MMP-9 promoter gene polymorphism with the development of NP. A prospective and case-control study was performed on 93 patients with NP and 115 controls without sinonasal disease. Genotypes of MMP-9 (-1562C>T) were identified by restriction fragment length polymorphism analyses after polymerase chain reaction. The frequency of -1562CT genotype of MMP-9 was significantly high in NP patients with aspirin-induced asthma (p = 0.014). Distribution of T allele was significantly high in NP patients with aspirin-induced asthma (p = 0.013). MMP-9 genotypes were not associated with gender or the presence of atopy. In this study, MMP-9 -1562CT genotype was associated with susceptibility to NP in aspirin-induced asthmatic patients. Because this report is a population-based study, further research should be performed on larger study subjects to reveal the precise role of MMP-9 promoter gene polymorphism in the development of NP.

Sinonasal Outcomes After Endoscopic Sinus Surgery in Asthmatic Patients With Nasal Polyps: A Difference Between Aspirin‐Tolerant and Aspirin‐Induced Asthma?

Aspirin-sensitivity, asthma, and nasal polyposis (NP) comprise the clinical entity of Samter's triad. The aim of this study is to report the sinonasal outcomes of endoscopic sinus surgery (ESS) in treating NP in asthmatic patients, comparing aspirin-induced asthmatic (AIA) patients with aspirin-tolerant asthmatics (ATA). Retrospective chart review. The records of 66 patients with NP and asthma were retrospectively reviewed. Forty-one AIA patients were compared with 25 ATA patients. For each patient, a Lund-Mackay computed tomography (CT) score of the preoperative scans and the available postoperative CT scans in a period of 18 months were calculated and used as primary endpoint. Sinonasal improvement assessed by patients and reported with a symptoms scale was used as the secondary endpoint for the comparison immediately before surgery and 6 months and 12 months following ESS. Preoperative CT scores in AIA patients compared with ATA patients were significantly higher 19 (standard deviation, 4.82) vs. 14 (standard deviation, 6.8), respectively (P = .006). This difference was sustained for the available postoperative CT scans (P < .0001). During the period of 18 months follow-up, 63.4% of AIA patients vs. 96% of ATA patients had CT improvement with a statistically significant difference between the two groups (P = .003). At 6 months following ESS, 63.4% of AIA patients vs. 56% of ATA patients had symptomatic improvement. At 12 months, 68.3% of AIA patients vs. 60% of ATA patients had symptomatic improvement, with no significant difference between the two groups. AIA patients had more extensive sinonasal disease than ATA patients. Both groups showed statistically significant improvement in sinonasal outcomes after ESS. The difference between the two groups was statistically significant for patients' CT improvement with worse CT scores being seen in AIA patients.

Asthma Outcomes after Endoscopic Sinus Surgery in Aspirin-Tolerant versus Aspirin-Induced Asthmatic Patients

Certain diseases affect both upper and lower airways. Aspirin-induced asthma (AIA) is a clinical entity characterized by asthma, nasal polyposis, and aspirin intolerance. To understand the response of the lower airway to surgical treatment of the sinuses, we examined asthma outcomes in AIA compared with a second group of aspirin-tolerant asthmatic (ATA) patients to establish if there were any differences between the two groups after endoscopic sinus surgery (ESS). A retrospective record review was performed of 91 asthmatic subjects with chronic rhinosinusitis. Forty-one subjects had AIA and 50 subjects had ATA. Subjective and objective asthma outcome parameters were used to compare between the two groups at three time points: immediately before ESS and 6 and 12 months after ESS. Preoperatively, AIA patients had significantly higher asthma severity (p<0.0001) and lower forced expiratory volume in 1 second values (p=0.04). At 12 months after ESS, a statistically significant difference between the two groups with better results in AIA patients was seen in asthma severity improvement (p=0.010) and in the decrease of ICS doses (p<0.0001), without significant differences between the two groups in other asthma outcome parameters. AIA patients usually present with more severe asthma. The asthmatic complaints of AIA and ATA patients continue to improve significantly over 6 and 12 month after ESS. Although ESS helped both groups of patients, AIA had statistically significant better results compared with ATA patients in asthma severity scores and decreased need for ICS.

Beyond Our Pages

Beyond Our Pages

Pathogenesis of nonsteroidal antiinflammatory drug-induced asthma

To summarize recent findings related to the pathogenic mechanisms of aspirin-induced asthma with emphasis on molecular genetic mechanisms. The overproduction of cysteinyl leukotrienes with the increased expression of cysteinyl leukotriene receptor 1 (CYSLTR1) is a consistent finding in aspirin-induced asthma patients. Recent data have suggested a dysregulation of cyclooxygenase-2 and prostaglandin E2, increased levels of 15-hydroxyeicosatetranoic acid, and decreased lipoxin generation as characteristics of the condition. The HLA allele DPB10301 was documented as a strong genetic marker for susceptibility in an Asian population. Leukotriene C4 synthase has been established as a key genetic determinant of aspirin-induced asthma, but recent studies have demonstrated that several single nucleotide polymorphisms in the promoters of prostaglandin E2 receptor subtype 2, CYSLTR1 and CYSLTR2 and T-box expressed in T cells (TBX21) could increase risk for the condition. Although cyclooxygenase-2 and thromboxane A2 receptor polymorphisms were not associated with aspirin-induced asthma phenotype, they may exert functional effects. The identification of genetic markers for aspirin-induced asthma susceptibility along with in-vitro functional studies would help to elucidate the pathogenesis of the condition. Further studies of the interactions among genes and between genes and the environment will be essential.

Comparison of Plasma Eotaxin Family Level in Aspirin-Induced and Aspirin-Tolerant Asthma Patients

Eosinophilic infiltration of airway tissue is a central feature of aspirin-induced asthma (AIA). Eotaxins belong to the family of CC chemokines, which coordinate the recruitment of inflammatory cells bearing chemokine (C-C motif) receptor-3 to sites of allergic inflammation. In the present study, the levels of eotaxin-1, eotaxin-2, and eotaxin-3 following an oral aspirin provocation test (APT) were measured, and the relationship between the eotaxin level and clinical parameters in patients with asthma was evaluated. An APT was performed in patients with asthma. Twenty AIA patients and 23 aspirin-tolerant asthma (ATA) patients were identified. Plasma levels of eotaxin-1, eotaxin-2, and eotaxin-3 levels were measured by enzyme-linked immunosorbent assay in the 43 patients with asthma and in 39 control subjects. The proportion of blood eosinophils was significantly higher in asthmatic patients than in control subjects. Nasal polyps were more common in AIA patients than in ATA patients (p < 0.05). In addition, the eotaxin-1 level was higher in AIA and ATA patients than in control subjects (p < 0.01 for each). The eotaxin-2 level was higher in ATA patients than in either the AIA patients (p < 0.05) or control subjects (p < 0.01). Similarly, the eotaxin-3 level was higher in ATA patients than in control subjects. A trend toward higher plasma levels of eotaxin-1 and eotaxin-3 at baseline and at 4 h after APT administration in the ATA group was noted but was not significant. Eotaxin-2 was also higher in ATA patients than in AIA patients at baseline and at 4 h after the APT. This study shows that eotaxin-2 is differentially secreted in patients with asthma according to aspirin intolerance, and that secretion is not time-dependent in response to the APT in AIA and ATA patients. It therefore appears that eotaxin-2 may be up-regulated and may act differentially in patients with ATA.

Pharmacological Inhibitors of Cysteinyl Leukotrienes Biosynthesis: Therapeutic Implications

Cysteinyl leukotrienes (cys-LTs) have emerged as important mediators of inflammation. Interest in these molecules have been amplified by recent introduction of the drugs which can either inhibit their biosynthesis or interfere with their binding to specific receptors. Biosynthesis of cys-LTs starts with the action of 5-lipoxygenase on arachidonic acid, liberated from membrane phospholipids and leads to formation of leukotriene A4 (LTA4). Cells, which express leukotriene C4 synthase (LTC4S), conjugate LTA4 with reduced glutathione to leukotriene C4 (LTC4), the first derivative of the family of cysteinyl leukotrienes. This in turn can be converted to leukotriene D4 (LTD4) and then to leukotriene E4 (LTE4). Cys-LTs powerfully affect cardiopulmonary functions. Thus, they contribute to bronchoconstriction, mucous secretion, edema migration of eosinophils into airways, and constriction of vessels including coronary arteries. A welldefined clinical syndrome, which affects about 10 % of adult asthmatics, i.e. called aspirin-induced asthma (AIA), is characterized by overproduction of cys-LTs. Chronic treatments of AIA patients with leukotriene biosynthesis inhibitors produce clinical benefits and improvement in pulmonary function tests. 5-LO inhibitors can be classified into several classes of compounds; redox, and non-redox inhibitors, first and second generation N-hydroxyurea derivatives, and FLAP inhibitors. From the clinical point of view, the most important group of inhibitors are the first N-hydroxyurea derivatives e.g. zileuton. They show clinical efficacy in asthma and provide a rationale for envisioning novel leukotriene - based approaches in therapy. Keywords: 5-lipoxygenase, cysteinyl leukotrienes, zileuton, aspirin-induced asthma

Montelukast protects against nasal lysine-aspirin challenge in patients with aspirin-induced asthma

Rationale We evaluated the dose-response for montelukast (ML) against nasal lysine-aspirin (L-ASA) challenge in patients with aspirin-induced asthma (AIA). Methods 12 AIA patients were randomized in double-blind cross-over fashion to receive single doses of ML 10 mg (ML10), ML 40 mg (ML40), or placebo (PL), with L-ASA challenge performed 12 hours post-dosing. Measurements of peak nasal inspiratory flow (PNIF), nasal blockage visual analogue scale (VAS) and FEV 1 were made over 120 minutes after L-ASA challenge. Results Pre-challenge values for mean (SEM) PNIF (l/min) were not significantly different comparing all groups; ML10: 132 (10), ML40: 125 (12) and PL: 132 (11). The maximum % PNIF fall from baseline was significantly greater ( p<0.05) with PL: 45 (6) vs. ML10: 34 (6) or ML40: 32 (5). There was also a significantly greater ( p<0.05) average % PNIF response over 120 minutes after L-ASA challenge for PL: 26 (7) vs. ML10: 14 (6) or ML40: 17 (6). There were no significant differences for the maximum or average % PNIF fall from baseline comparing ML10 vs. ML40. There was a significant increase ( p<0.05) in VAS between baseline and 60 minutes or 120 minutes with PL, but not with ML10 or ML40. There were no significant differences for either the maximum or average % FEV 1 over 120 minutes as change from baseline comparing all groups. Conclusion A single dose of ML 10mg partially protected against the local effects of nasal L-ASA challenge, without further benefit at 40 mg. Nasal L-ASA challenge appeared to be a reproducible and safe method in assessing patients with AIA.

Characterization of six base pair deletion in the putative HNF1-binding site of human PXR promoter.

Pregnane X receptor (PXR) regulates transcription of drug metabolism genes such as CYP3A4 and MDR1. Several species of PXR transcripts have been reported, including hPAR-2 with an extended amino-terminus. Database search identified a 6-bp deletion at the putative HNF1 binding element on the proximal region flanking to the hPAR-2 transcription start site. Aspirin-induced asthma (AIA) is a typical drug-induced phenotype due to aspirin or nonsteroidal antiinflammatory drugs, and these drugs are metabolized by CYP2C9 and UGT1A6, which are regulated by PXR. We examined a possible association between the 6-bp deletion variant and AIA; 129 AIA patients and 117 controls were genotyped, and no allelic association was observed. Characterization of the hPAR-2 promoter revealed that the proximal region of 1.5-kb from the transcription start site conferred a promoter activity and that the 6-bp deletion diminished the activity. These results suggest that the putative HNF1 binding element is essential for the transcriptional activity of hPAR-2 and also, that substantial numbers of Japanese are in a deficient state. Because of the biological significance of the 6-bp deletion of PXR, the variant might potentially associate with as yet unknown phenotype.

Glutathione peroxidase activity in blood cells from aspirin-induced asthma patients.

Aspirin and other inhibitors of cyclo-oxygenase precipitate acute bronchospasm in about 10% of adult asthmatics. It has been assumed that cyclo-oxygenase is involved in the pathogenesis of bronchospasm, but the precise mechanism remains poorly understood. The oxygenation products of arachidonic acid include hydroperoxyeicosatetraenoic acid and cyclic endoperoxides. Glutathione peroxidase (GPX) reduces semi-stable hydroperoxides to less reactive alcohols and removes H(2)O(2) involved in inflammation. GPX could, therefore, modulate oxidation of arachidonic acid in the cyclo-oxygenase and lipoxygenase pathways, but the involvement of GPX in the pathogenesis of asthma has received little attention. We measured GPX activity in platelets, peripheral blood lymphocytes (PBL), red blood cells (RBC) and plasma from 13 patients with aspirin-induced asthma (AIA). Age- and sex-matched healthy individuals served as the comparison group. The patients had significantly higher GPX activity in platelets (P = 0.05) and tended to have high GPX activity (P = 0.08) in plasma but not in RBC or PBL. The results suggest that the increased GPX activity may be an adaptive advantage in AIA to protect against increased free radical production by inflammatory cells. That the higher GPX activity was not evident in all cell types studied may indicate a differential role played by them as effector cells in the pathogenesis of AIA.

The editors' choice

The editors' choice

Analgesics and asthma.

The incidence of asthma is increasing throughout the world, which presents both public health and economic concerns. It is widely recognized that in some adult patients with asthma, aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit cyclooxygenase (COX)-1 exacerbate the condition. This is a distinct clinical syndrome called aspirin-induced asthma (AIA). The disease develops according to a characteristic pattern of symptoms. Persistent eosinophilic rhinosinusitis precedes development of nasal polyposis, aspirin hypersensitivity, and asthma. There is no in vitro test, and diagnosis can only be established by provocation tests with aspirin. At the biochemical level, AIA is characterized by a chronic overproduction of cysteinyl leukotrienes. The key enzyme, leukotriene C4 synthase, is overexpressed in bronchi, and its messenger RNA is upregulated in peripheral blood eosinophils. This can be partly related to the genetic polymorphism of the enzyme. The disease runs a protracted course, even if COX-1 inhibitors are avoided. The course of AIA is often severe, and at least half of the patients need systemic corticosteroids to control their asthma. To prevent life-threatening reactions, patients with AIA should avoid aspirin and other analgesics that inhibit COX-1. The incidence of cross-sensitivity to paracetamol in AIA patients is low and, when a reaction does occur, the symptoms experienced are shorter and milder than if the reactions were evoked by an NSAID. Rapidly growing evidence indicates that highly specific COX-2 inhibitors, known as coxibs, are well tolerated and can be safely used by AIA patients.

Serum interleukin-5 in aspirin-induced asthma.

Eosinophilopoetic cytokine IL-5 enhances cysteinyl-leukotriene (cys-LT) synthesis in eosinophils in vitro. In patients with aspirin-induced asthma (AIA) bronchial biopsies revealed eosinophil infiltration and a marked increase in IL-5 positive cells. We wondered whether in AIA patients the bronchial IL-5 increase is reflected in peripheral blood, and if so, whether it is related to overproduction of cys-LT. In 11 stable patients with AIA, 32 with ATA (aspirin-tolerant asthma) and in 16 controls we measured serum IL-5 concentrations and urinary LTE4, believed to reflect global cys-LT production. Serum IL-5 was detectable in 12 of 43 asthmatics, but in none of the control subjects. It was highest in the ATA group and differed significantly from the controls. There was no significant difference in IL-5 levels between: (i) the asthmatic groups studied, and (ii) AIA patients and controls. No relationship was found between serum IL-5 and urinary cys-LT. Overexpression of IL-5 reported in the airways of aspirin-sensitive patients with asthma was not reflected in their blood. If IL-5 affects cys-LT production, it is rather in the bronchi of the patients than in the blood.

Effects of Sinus Surgery on Asthma in Aspirin Triad Patients

The aspirin triad (nasal polyposis, asthma and sensitivity to aspirin) is a well-recognized clinical entity, also known as aspirin-induced asthma (AIA). The sinusitis associated with AIA is often difficult to treat and aggravates the asthmatic symptoms. In order to evaluate the surgical treatment of sinusitis in AIA, 22 patients who underwent sinus surgery were studied. Twenty patients (90.9%) got any relief of their asthma symptoms from sinus surgery. Postoperative pulmonary function test 1 year after surgery showed statistically significant improvement over the preoperative one. Three of 5 patients (60%) who used systemic steroids were able to eliminate or reduce their dosages. Also, 8 of 17 patients (47.1%) who were using inhaled topical steroids reduced their dosages and statistical analysis showed a significant difference in the doses of topical steroid used before and after surgery. Subjective evaluation of 20 patients (90.9%) indicated that the sinus surgery was effective for their asthma condition; showing from mild to marked improvement. For AIA patients aggravated by sinus disease, we recommend sinus surgery to improve the quality of life.