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PubMed2002

[Expression and localization of the inducible isoform of nitric oxide synthase in nasal polyps].

Nitric oxide (NO) and peroxynitrite play an important role in pathophysiology of several airway diseases. An inducible isoform of nitric oxide synthase (iNOS) is known to be expressed in the nasal mucosa in allergic and chronic rhinitis. Few reports exist, however, on the expression of iNOS in nasal polyps. We detected and localized iNOS expression in nasal polyp tissue. Nasal polyps were obtained from 10 patients following polypectomy, and divided into allergic and infectious groups based on clinical presentation and laboratory testing. One nasal mucosa of the inferior turbinate was also obtained from a cadaver without nasal disease. iNOS expression was studied by immunohistochemistry under light and electron microscopy. Immunoreactivity for iNOS was localized to the mucosal epithelium, inflammatory cells, vascular endothelium and smooth muscle, and nasal gland. Strong immunoreactivity was shown in the mucosal epithelium of both groups, and weak to moderate reactivity in the mucosal epithelium of the inferior turbinate. Vascular endothelium and smooth muscle of both groups sometimes showed weak to moderate immunoreactivity. Nasal glands of both groups sometimes showed weak immunoreactivity. A significant difference between allergic and infectious groups was observed in predominant types of inflammatory cells. Neutrophils were predominant in the infectious group (p < 0.01), and eosinophils in the allergic group (p < 0.0001). About 50%-53% in allergic and 42% in infectious groups--of inflammatory cells showed positive immunoreactivity for iNOS. Immunoreactive cells were neutrophils, eosinophils, and macrophages. Lymphocytes, plasma cells, and mast cells invariably reacted negatively. A significant difference between allergic and infectious groups was observed in predominant iNOS-immunoreactive cells. Ratios of immunoreactive neutrophils to all neutrophils (p < 0.05) and to all inflammatory cells (p < 0.05) were significantly higher in the infectious group. The ratio of immunoreactive eosinophils to all inflammatory cells was significantly higher in the allergic group (p < 0.0001), while the ratio of immunoreactive eosinophils to all eosinophils did not differ between infectious and allergic groups. The ratios of immunoreactive macrophages to all macrophages and to all inflammatory cells did not differ significantly between groups. Electron microscopy showed that degenerated cells with pyknotic nuclei were located next to immunoreactive eosinophils, suggesting the cytotoxicity of NO, peroxynitrite, or superoxide.

Adult↗
PubMed1989

[Research on the etiology of nasal polyps].

One hundred and seventy patients with nasal polyps were studied. According to the history, skin tests with inhalant allergens, determination of serum nasal secretion and polyp fluid IgE, and X-ray films of nasal sinuses, it was suggested that 93.5% of them might have complicated with allergic diseases, 87.7% with sinusitis. A relationship between local IgE production and the eosinophil infiltration of polyps existed. This study suggests that allergic process acting locally on the mucous membrane of the nose is the etiologic factor and bacterial allergy probably contributes to the development of nasal polyps. In order to prevent the recurrence after polypectomy, antiallergic management combined with antibiotics and drainage of infected sinuses may be necessary in most cases.

Adolescent↗
PubMed2005

Inhibition of nasal polyp mast cell and eosinophil activation by desloratadine.

Nasal polyp tissue which contains mast cells and eosinophils is similar to the inflamed airway mucosa in cellular composition and mediator content. This investigation assessed the effect of desloratadine (DL), on activation of cells in nasal polyp tissue. Polyps were obtained from 22 patients with chronic rhinosinusitis [nine aspirin acetylosalitic acid (ASA)-sensitive and 13 ASA-tolerant]. Polyp tissue was dispersed by digestion, and preincubated with DL and incubated with anti-immunoglobulin E (IgE) or calcium ionophore. LTC4, eosinophil cationic protein (ECP) and tryptase concentrations in supernatants were measured by immunoassays. Desloratadine (1, 10 and 50 microM) inhibited calcium ionophore-induced LTC4 release by a mean of 29%, 50% and 63% respectively, and anti-IgE-induced LTC4 release by a mean of 27%, 35% and 39% respectively. Calcium ionophore-induced tryptase release was inhibited 60% and 69% by 10 and 50 microM of DL, respectively, and anti-IgE-induced tryptase release was inhibited 33%, 47% and 66% for 1, 10 and 50 microM of DL. Desloratadine 10 microM and 50 microM inhibited ECP release by and 45% and 48% respectively. Polyp tissue from ASA-sensitive patients when compared with ASA-tolerant patients released at baseline significantly more ECP (medians 120.0 microg/ml, range: 69.0-182.0 vs 63.4 microg/ml, range: 3.7-172.0; P <0.05), but similar amounts of tryptase and LTC4. This study demonstrated that DL inhibits activation of both eosinophils and mast cells derived from a site of airway mucosal inflammation.

Adult↗
PubMed1977

Nasal polyps in asthma and rhinitis. A review of 6,037 patients.

Data from records of patients with asthma and rhinitis in the Rhode Island Hospital Adult Allergy Clinic and in an adult allergy private were reviewed. The frequency of nasal polyps in the total population of 4,986 was 4.2%; in the asthmatic portion of the population the frequency was 6.7%, and in the rhinitis alone group the frequency was 2.2%. Asthmatics with negative allergy skin tests to inhalant allergers had significantly more nasal polyps than asthmatics with positive skin tests, 12.5% vs 5.0%, p less than 0.01. The frequency of nasal polyps increased with advancing years. Of the total 211 cases of nasal polyps, 71% had asthma and 29% had rhinitis alone. Also, 14% of the patients with nasal polyps had aspirin intolerance, primarily of the bronchospastic type. In addition, 1,051 patients with asthma and rhinitis from the Pediatric Allergy Clinic with a mean age of 6 yr were similarly evaluated. Only 1 (0.1%) of these pediatric patients had nasal polyps.

Adolescent↗
PubMed1997

Inflammatory cytokine expression on nasal polyps developed in allergic and infectious rhinitis.

To investigate the expression of cytokine mRNAs in nasal polyps and the role of allergy in the pathogenesis of nasal polyposis, we studied the expression of IL-4, IL-5, and IFN-gamma mRNAs using the RT-PCR and Southern blot. Nasal polyp specimens were obtained from 14 patients with infectious rhinitis and 5 patients with perennial allergic rhinitis. Turbinate mucosa specimens were obtained from 10 patients with allergic rhinitis and from 10 healthy subjects as controls. IL-4, IL-5 and IFN-gamma mRNA were expressed in most specimens of allergic turbinate mucosa. The expression of these cytokines was less frequent in normal healthy turbinate mucosa. The density ratios of IL-4, IL-5 and IFN-gamma to beta-actin were individually determined in both polyp and turbinate tissues. The density ratio for each cytokine was relatively higher in polyp tissues than in healthy turbinate mucosa; however, there was no significant difference in the density ratios determined for polyps associated with allergic rhinitis as compared with polyps associated with infectious rhinitis. These findings indicate that nasal polyposis may differ from allergic rhinitis in the mechanism by which IL-4 and IL-5 are increased. It is concluded that allergy may have an insignificant role in the development of nasal polyps.

Adult↗
PubMed2004

Vascular endothelial growth factor in nasal polyps: a comparison of asthmatic and non-asthmatic patients.

The cause of nasal polyps remains unknown, although there is a well-recognized clinical association between nasal polyposis and asthma. The characteristic histological features of nasal polyps include large quantities of extracellular fluid. Vascular endothelial growth factor (VEGF) is a potent mediator of angiogenesis and vascular permeability. This study aimed to compare expression of VEGF in nasal polyps from patients with asthma and those with no apparent respiratory disease. Twenty-four asthmatic and 35 non-asthmatic patients were studied using immunohistochemistry for VEGF. VEGF expression was identified in endothelial, inflammatory and epithelial cells. There was significantly greater endothelial expression of VEGF in asthmatic patients (P < 0.05). Greater epithelial expression was observed in asthmatic patients but this did not reach statistical significance (P = 0.07). There was no difference in the density of inflammatory cells expressing VEGF. Differences between the two groups may reflect differences in disease severity or in the nature of the inflammatory process.

Adult↗
PubMed2001

Localization of cystic fibrosis transmembrane conductance regulator in epithelial cells of nasal polyps and postoperative polypoid mucosae.

Cystic fibrosis transmembrane conductance regulator (CFTR) is a chloride channel protein that plays an important role in electrolyte and water transport through the respiratory epithelial cells. In order to understand the possible role of CFTR in the pathogenesis of nasal polyps and postoperative polypoid mucosae, we aimed to characterize the localization of CFTR in the epithelia of nasal polyps and postoperative polypoid mucosae of subjects who did not manifest the phenotypic expression of cystic fibrosis. Immunohistochemical staining for CFTR, using monoclonal mouse anti-human CFTR, was performed on tissue sections of 4 normal turbinates and nasal polyps and postoperative polypoid mucosae from 10 patients who underwent endoscopic intranasal operations. CFTR showed a typical apical distribution in the normal turbinate mucosae whereas, in the nasal polyps, CFTR demonstrated a heterogenous pattern of localization comprising diffuse or scattered cytoplasmic labelling, very low to undetectable labelling, intense perinuclear staining and intermingled typical apical location. In postoperative polypoid mucosae, the pattern of CFTR localization was less heterogeneous than in the nasal polyp epithelial cells and showed a more prominent feature of diffuse cytoplasmic staining. These results suggest that an altered localization of the CFTR may have a role in the pathogenesis of nasal polyps and postoperative polypoid mucosa.

Adult↗
PubMed2003

[Effect of proinflammatory cytokines on human leucocyte antigen expression of epithelial cells of nasal polyps].

OBJECTIVE: To explore the effect of proinflammatory cytokines on the expression of human leucocyte antigen(HLA-DR) in epithelial cell of nasal polyps. METHODS: The samples were from 23 patients with nasal polyps and 11 cases of normal inferior turbinates. The samples were fixed, paraffin-embeded and sectioned for observing distribution of HLA-DR positive cells. Nasal epithelial cells were obtained after enzymatic digestion and cell culture was performed for observing influences of interleukin (IL)-1 beta and tumor necrosis factor (TNF-alpha) to expression of HLA-DR of epithelial cells and the effect of dexamethasone(10(-5) mol/L). RESULTS: The HLA-DR expression in epithelium was significantly stronger in nasal polyps than that in inferior turbinates. The expression of HLA-DR in cultured cells under stimulation of proinflammatory cytokines was increased compared with controls, but the expression was more intense in nasal polyps than that in inferior turbinates. Increased HLA-DR expression under stimulation of cytokines was reduced significantly by dexamethasone. CONCLUSION: The epithelium is in a key position to participate in inflammatory and immunologic events in the airways. Epithelial cells potentially contribute to airway inflammation by antigen presentation and the production of proinflammatory cytokines.

Adult↗
PubMed2005

[Relationship between the expression of tenascin C and TGF-beta1 in human nasal polyp tissues].

OBJECTIVE: To explore the mechanism underlying the increased expression of tenascin C (TNC) in human nasal polyp tissues. METHODS: The method of immunohistochemistry was used to detect the protein expression of TNC and transforming growth factor-beta1 (TGF-beta1) and their relationship in nasal polyp tissues. The cell culture, real-time RT-PCR and in situ ELISA techniques were employed to investigate the effect of TGF-beta1 and eosinophils on the TNC mRNA and protein expression in BEAS-2B immortalized human bronchial epithelial cells. RESULTS: (1) TNC and TGF-beta1 protein expression were up-regulated in nasal polyp tissues. TNC expression level was associated with the number of TGF-beta1 positive cells (r = -0.58, P < 0.01) and TGF-beta1 positive eosinophils (r = -0.61, P < 0.01); (2) 1 ng/ml and 10 ng/ml TGF-beta1 induced TNC mRNA expression by 7.20 +/- 3.43-fold and 22.48 +/- 5.35-fold (P < 0.01) in BEAS-2B cells after 4 h stimulation respectively. The fluorescence intensity of TNC protein expression was 129. 50 +/- 47.42 and 151.20 +/- 48.36 after 24 h stimulation respectively. The protein expression was significantly increased compared with that without stimulation (60.60 +/- 38.53, P < 0.05); (3) Coculture BEAS-2B cells and eosinophils at 2:1, 1:1 and 1:2 ratio, TNC mRNA expression was induced by 4.90 +/- 1.40-fold, 5.48 +/- 1.60-fold and 4.78 +/- 1.32-fold (P < 0.01) in BEAS-2B cells after 4 h coculture respectively. The fluorescence intensity of TNC protein expression was 128.75 +/- 44.15, 142.33 +/- 29.06 and 131.33 +/- 20.87 after 24 h coculture respectively. The protein expression was significantly increased compared with that without eosinophils coculture (59.40 +/- 10.14, P < 0.05). Treatment with neutralizing antibody to TGF-beta1 significantly inhibited eosinophil-induced BEAS-2B cells TNC expression in a dose-dependent manner (P < 0.05). CONCLUSION: TGF-beta1 and eosinophils can induce TNC expression in airway epithelial cells. The effect of eosinophils is partially mediated through TGF-beta1. Up-regulated expression of TNC in nasal polyp tissues is related to eosinophil-derived TGF-beta1.

Adolescent↗
PubMedDate not supplied

[Analysis of the cellular infiltrate and epithelial class I and II molecular expression in edematous type nasal polyps].

Although in the last few years histopathological, immunohistochemical and immunological studies on nasal polyps have been carried out by several Authors, the etiology of these formations still remains unknown. Nasal polyps have a very characteristic structure and have been classified in three histologic types: edematous, glandular and fibrous. In the present report, 11 nasal polyps of edematous type, representing 61% of total number of collected polyps, were studied employing immunohistochemical methods. All the examined polyps were similar in histology and positivity pattern for HLA molecule expression. The edematous core appeared infiltrated (149 cells/mm.2) mainly by eosinophils (> 90%), whereas the peripheral subepithelial connective tissue contained cellular clusters (416 cells/mm2.) made up of different subsets of hematic cells (30.8% were monocytes-macrophages and 48.6% were lymphocytes largely represented by CD4+ cells). On the contrary, mast cells were quite rare (on the average 1.7 cells/mm2.) and located near T cell clusters. The epithelial positivity for HLA-DR and HLA-A,B,C molecules showed a characteristic discontinuous pattern. In the same patient, controlateral nasal mucosa showed a histological structure very similar to that of polyps. The above data suggest that the presence of polyps is the result of an inflammatory process brought about by a complex array of cellular and humoral components.

Edema↗
PubMedDate not supplied

Intercellular adhesion molecule-1 expression in nasal polyps treated with corticosteroid.

PURPOSE: The aim of this study was to compare intracellular adhesion molecule-1 (ICAM-1) expression in nasal polyp cases who were administered topical corticosteroid and in middle turbinates. MATERIALS AND METHODS: Twenty-four patients with nasal polyps were included in the study group. These patients were treated with 100 microg budesonide in each nostril twice daily for 2 months before the surgery. Twenty-one nonatopic patients with concha bullosa were included in the control group. The specimens were taken from patients undergoing endoscopic surgery. RESULTS: In polyps, significantly higher mean ICAM-1 intensity scores were found by comparison with the control turbinates. CONCLUSIONS: Corticosteroid treatment in patients with nasal polyps does not diminish ICAM-1 to that of turbinate tissue. The initiating events in the formation of nasal polyps still occur in these patients despite treatment with the topical nasal steroid.

Administration, Intranasal↗
PubMed2005

[Examination expression of CD3 and CD69 in nasal polyps].

OBJECTIVE: To investigate the infiltration of T lymphocytes with CD3 expression as surface marker and the activation of T lymphocytes with CD69 expression as activation marker. METHODS: Nasal polyp tissue samples and peripheral blood were obtained from 21 patients. The normal inferior turbinate mucosa and peripheral blood were obtained as comparison. Flow cytometry was adopted to detect the expression of CD3 and CD69 of T lymphocytes. RESULTS: Nasal polyp tissue consisted of abundant T lymphocytes. Activation marker CD69 was expressed in T lymphocytes of nasal polyps (36.96 +/- 2.50)% and peripheral blood (4.66 +/- 0.18)% from the same patient. The expression rates of CD69 after a short-term stimulation (5 h) in response to PDB were (59.88 +/- 2.59)% and (92.76 +/- 0.55)% respectively. While T lymphocytes was rarely detected in normal inferior turbinate and the expression of CD69 was low in peripheral blood from normal human but almost all T lymphocytes were activated after stimulation. CONCLUSIONS: There were generous of T lymphocytes infiltrating in nasal polyps. The expression of CD69 in T lymphocytes was abnormally high, which indicated that T lymphocytes infiltrating in nasal polyps were in activated state immunologically.

Adolescent↗
PubMed2000

Relation of epidermal growth factor receptor expression to goblet cell hyperplasia in nasal polyps.

BACKGROUND: Because the epidermal growth factor receptor (EGFR) system regulates mucin production in airway epithelium, we hypothesized a role for this system in mucus hypersecretion that occurs in nasal polyposis. OBJECTIVE: We examined the relationship between goblet cell hyperplasia, EGFR expression, and inflammatory mediators produced by eosinophils and neutrophils in nasal polyp tissues. METHODS: Nasal polyp tissue samples from 8 patients and nasal turbinate biopsy specimens from 6 normal control subjects were examined for alcian blue/PAS staining, mucin MUC5AC (MUC5AC), and EGFR immunoreactivity and EGFR gene expression (in situ hybridization). We also examined the role of eosinophils and neutrophils in goblet cell hyperplasia. RESULTS: In control nasal mucosa alcian blue/periodic acid-Schiff- and MUC5AC-stained areas were 18.40% +/- 1.31% and 21.89% +/- 1.43%, respectively. In polyps the alcian blue/periodic acid-Schiff- and MUC5AC-stained areas were 51.30% +/- 5.85% and 52.07% +/- 6.58%, which was significantly larger than that found in control subjects (each comparison, P <.01). Four of 6 control specimens expressed EGFR messenger RNA and protein weakly in the epithelium. In polyps 4 of 8 specimens expressed EGFR gene and EGFR protein strongly; the EGFR-stained area was greater in hyperplastic than in pseudostratified epithelium. TNF-alpha immunoreactivity, expressed in eosinophils, was increased in EGFR-positive polyps compared with EGFR-negative polyps, suggesting a role for TNF-alpha in EGFR expression. Neutrophils were increased in the epithelium of EGFR-positive compared with EGFR-negative polyps, suggesting a role for these cells in mucin expression and in goblet cell degranulation. CONCLUSION: These data suggest a role for EGFR cascade in the regulation of goblet cell mucins in nasal polyps. Proof of concept will require clinical studies using selective EGFR inhibitors.

Cell Movement↗
PubMedDate not supplied

A macrolide antibiotic, roxithromycin, inhibits the growth of nasal polyp fibroblasts.

Recently, the efficacy of macrolide antibiotics in cystic fibrosis and bleomycin-induced lung injury was reported. Nasal polyposis is a chronic inflammatory disease of the upper airway characterized by structural abnormalities including stromal fibrosis. Fibroblasts are resident cells thought to play an important role in the development of fibrosis. Although the effect of Roxithromycin (RXM) on inflammatory cells is well known, there is no evidence on the effect of RXM on fibroblasts. The purpose of the present study was two-fold: to examine the effect of RXM on the growth of fibroblasts in vitro and to examine the effect of RXM on the proliferation of fibroblasts in vivo. Nasal polyp fibroblast lines were generated from untreated patients, and those who were treated with RXM (300 mg/day) for one month before biopsy. Nasal polyp fibroblast lines from untreated patients were cultured for 72 hours with or without RXM, and the direct effect of RXM on fibroblast growth in vitro was examined by cell counting and 3H thymidine uptake. Next, we examined the in vivo effect of RXM on nasal polyp fibroblasts (NPFs) by comparing the growth characteristics of NPF lines from RXM treated and untreated patients. Finally, we examined the proliferating rate of NPF lines from the same patient before and after treatment with RXM. NPF lines that were treated with RXM exhibited a lower proliferating rate in vitro as compared to those that were not treated with RXM. Treatment of NPF lines with RXM suppressed the proliferation of fibroblasts in a dose-dependent manner. In addition, NPF lines from patients treated with RXM exhibited a lower proliferating rate in vitro as compared to NPF lines from the same patient taken before RXM treatment. We demonstrated that RXM directly suppressed nasal polyp fibroblast proliferation, and that this effect of RXM on fibroblast growth was persistent, indicating that RXM may prevent the progression of nasal polyposis by inhibiting the development of fibrosis.

Adult↗
PubMed2003

[Expression and significance of vascular permeability factor (VPF) in inflammatory cells of nasal polyps].

OBJECTIVE: To study the expression and significance of vascular permeability factor (VPF) in eosinophil, macrophage and plasma cell in nasal polyps. METHOD: VPF in 12 nasal polyps was studied by immunohistochemistry, double immune-enzymatic staining technique and double MGG staining technique. Each section was observed under optical microscope. RESULT: Immunohistochemistry result: VPF was detected in the cells showing morphological feature of plasma cells. Double immune-enzymatic staining result: CD68 positive cells in the second staining conformed to VPF positive cells in the first staining. MGG and immune-enzymatic double staining result: eosinophils in MGG staining were in conformity with some VPF positive cells. CONCLUSION: Positive expression of VPF in eosinophils, macrophages and plasma cells indicates that VPF may play a role in the formation of heavy edema of nasal polyps.

Adolescent↗
PubMed2006

Expression of cyclooxygenase-2 and 5-lipoxygenase in nasal polyps associated with interleukin-4 promoter polymorphism -590.

OBJECTIVE: To evaluate expression of cyclooxygenase (COX)-2 and 5-lipoxygenase (5-LO) associated with interleukin (IL)-4 promoter polymorphism -590 in nasal polyp tissues. STUDY DESIGN AND SETTING: A prospective controlled study. A venous blood sample was taken to determine the genotype in 61 nasal polyp subjects. The C-590T variant was determined by the polymerase chain reaction-restriction fragment length polymorphism method. The expression of 5-LO and COX-2 was determined with immunohistochemical staining in 37 nasal polyp tissues associated with genotype. RESULTS: The genotype frequencies at position -590 of the IL-4 gene in the patients with nasal polyp were C/C (8.20%), C/T (40.98%), and T/T (50.82%). There was no significantly increased expression of COX-2 among genotypes. The 5-LO expression was significantly increased in C/C compared with C/T and T/T. CONCLUSION: We suggested that the IL-4 promoter polymorphism -590 C/C is associated with the expression of 5-LO in the patients with nasal polyp.

Arachidonate 5-Lipoxygenase↗
PubMed2001

Matrix metalloproteinase-1 and tissue inhibitor of metalloproteinase-1 gene expressions and their differential regulation by proinflammatory cytokines and prostaglandin in nasal polyp fibroblasts.

Chronic inflammation of the paranasal sinus leads to nasal polyp (NP) formation. In this study, we investigated the effect of stimulation of the proinflammatory cytokines interleukin-1alpha (IL-1alpha) and tumor necrosis factor-alpha (TNF-alpha) and prostaglandin (PG) E2 on the production of messenger RNA (mRNA) of matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of metalloproteinase-I (TIMP-1) in nasal polyp fibroblasts (NPFs) and nasal mucosa fibroblasts (NFs). The mRNAs of IL-1alpha, TNF-alpha, MMP-1, and TIMP-1 in 40 surgical specimens of NPs were studied by in situ hybridization to corroborate the in vitro findings. The results indicated a significant amount of constitutive MMP-1 mRNA in NPFs and cytokine-induced MMP-1 steady-state mRNAs in NFs. The effect of stimulation of cytokines on TIMP-1 mRNA synthesis was unremarkable in NPFs and NFs. Exogenous PGE2 enhanced cytokine-stimulated MMP-1 mRNA synthesis in NPFs. In situ hybridization revealed that cells expressing MMP-1 and TIMP-1 mRNAs (primarily plasma cells, fibroblasts, and endothelial cells) gathered around areas with loose stroma, suggestive of rapid extracellular matrix degradation. These data suggest that the pathogenesis of nasal polyposis could be related to production of MMP-1 and consequent promotion of matrix collagenolysis.

Cytokines↗
PubMedDate not supplied

Aeroallergen hypersensitivity: comparing patients with nasal polyps to those with allergic rhinitis.

Immunoglobulin E-mediated allergy generally has not been considered to be important in the pathogenesis of nasal polyps, despite elevated immunoglobulin E in polyp exudates, tissue eosinophilia, and degranulated mast cells. In previous reports, patients with nasal polyps were more likely to have positive skin tests to perennial than to seasonal allergens. It is postulated that nasal polyps result from the constant nature of perennial allergen exposure. The objective of this report is to compare the prevalence of sensitization to six aeroallergens in a group of nasal polyp (NP) patients, a group of allergic rhinitis (AR) patients, and those subjects with positive skin tests in the National Health and Nutrition Examination Survey (NHANES) II. Twenty-five consecutive NP patients evaluated over a 3-month period of time at Northwestern Allergy and Immunology Outpatient Center, in addition to 50 of the allergic rhinitis patients evaluated over the same time, were chosen randomly. All were skin tested with the following antigens: dog, cat, dust mite, grass, tree, and ragweed. Published skin test data from the NHANES II study of 14,367 individuals was obtained also. The percent of NP patients, AR patients, and NHANES II subjects with sensitization to perennial allergens was 72, 96, and 7.6%, respectively. The difference between the AR and NP patients was statistically significant (p = 0.006). The percent of NP, AR, and NHANES II subjects sensitized to seasonal allergens was 84, 86, and 17.7%, respectively. No statistical significance existed between the AR and NP patients, regarding seasonal allergens. Although the AR and NP had similar levels of reactivity to perennial and seasonal allergens, the NHANES II group was more than twice as likely to be sensitized to a seasonal allergen. The NP and AR groups were similar in prevalence of reactivity to seasonal allergens, but the NP patients in our population actually were less likely to be sensitized to perennial allergens than individuals with AR.

Air Pollution↗