Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “NASAL POLYPS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1977

Nasal polyps, nasal polypectomy, asthma, and aspirin sensitivity. Their association in 445 cases of nasal polyps.

In a retrospective study of 445 patients with nasal polyps, 95 (21 per cent) had asthma. Forty-two (44 per cent) of the patients with asthma had been skin tested and 27 (60 per cent) had positive reactions. Nasal polyps were twice as common in men as women, though a woman with nasal polyps was twice as likely to have asthma as a man. The average age of onset of polyps was 39 years and of asthma was 38 years. No significant difference was found in the age of onset of polyps or asthma in various groups of patients. Two per cent of all the patients in the series had nasal polyps, asthma and hypersensitivity to aspirin (the ASA triad). Ten per cent of those with polyps and asthma were hypersensitive to aspirin and thus had the full triad. Overall, 6 per cent of all the patients in the series were recorded as being allergic to aspirin. Asthma developed more commonly before polypectomy than after in the ratio of 2.5:1. Around 1 per cent of first polypectomies and 0.5 per cent of all polypectomies were followed by the development of asthma within a few months. The onset of asthma was found to occur most frequently just before or just after the first polypectomy. Those who developed asthma after polypectomy had significantly more polypectomies than both non-asthmatics and those whose asthma preceded their polyps. Though it is possible polypectomy may on rare occasions precipitate asthma, it is felt that it does not cause it.

Adolescent↗
PubMed1998

Cytokine gene expression in nasal polyps.

Nasal polyps are the most common mass lesion of the nasal cavity. Various pathogenetic mechanisms have been proposed. However, the cause is still largely unknown, and treatment methods have not been changed for several hundred years. In order to investigate the role of cytokines in the pathogenesis of nasal polyps, expression of cytokine messenger RNAs (mRNAs) in nasal polyps was investigated. We performed reverse transcriptase-polymerase chain reaction and Southern blot to examine gene expression of the cytokines interleukin (IL)-1 beta, IL-6, IL-8, transforming growth factor (TGF)-beta, IL-4, IL-5, and interferon (IFN)-gamma and compared the results with the gene expressions of these cytokines in normal nasal mucosa. Nasal polyp tissues were obtained from 14 patients undergoing polypectomy for nasal obstruction. Among them, 4 patients suffered from associated perennial allergic rhinitis. The mRNAs of IL-4 and IL-5 (Th2 cytokines) as well as IFN-gamma (Th1 cytokine) were expressed in all of the nasal polyps obtained from the 14 patients, irrespective of the presence or absence of allergy, while 2, 0, and 4 of 6 normal turbinate mucosae expressed IL-4, IL-5, and IFN-gamma mRNAs, respectively. The mRNAs of IL-1 beta, IL-6, IL-8, and TGF-beta were expressed in 6, 1, 2, and 3 of 6 normal turbinate mucosae, respectively, while the mRNAs of these cytokines were expressed in all of the 14 polyp tissues except IL-6 mRNA, which was expressed in 13 nasal polyp tissues. There were no differences in the mean density ratios of each cytokine band on Southern blot between polyp tissues with allergy and those without allergy. These results suggest that many cytokines are produced in nasal polyps, that they may play important roles in the pathogenesis of nasal polyps, and that allergy per se may not play a fundamental role in the pathogenesis of nasal polyps.

Adult↗
PubMedDate not supplied

The cystic fibrosis conductance regulator gene exon sequence is normal in a patient with edematous eosinophilic nasal polyps.

Nasal polyps are the most common mass lesions found in the nose and their etiology is unknown. Nasal polyps from cystic fibrosis (CF) patients are histologically distinct from nasal polyps from patients without CF. It has been suggested that a mutation (G551D) of the cystic fibrosis transmembrane conductance regulator (CFTR) gene may play a role in nasal polyp formation in patients without CF. To investigate the possibility that this or other CFTR gene exon mutations are required for nasal polyp formation, the CFTR gene exons were sequenced from peripheral blood DNA derived from an adult patient with edematous eosinophilic nasal polyps and no personal or family history of CF. No mutations or deletions were identified in any of the CFTR exons. A single polymorphism (A or G) was found in exon 10, base pair 1540, amino acid 470. This polymorphism was detected in 11 of 16 subjects (69%) with edematous eosinophilic nasal polyps and 10 of 21 normal subjects (48%) without nasal polyps and was not statistically significant (p = 0.316). These results demonstrate that mutations of the CFTR coding region are not a prerequisite for the formation of edematous eosinophilic nasal polyps.

Cystic Fibrosis Transmembrane Conductance Regulato↗
PubMed1994

Expression of transforming growth factors-alpha and beta 1 messenger RNA and product by eosinophils in nasal polyps.

Nasal polyps are thought to develop as a manifestation of a chronic inflammatory process involving the upper airways. The eosinophil characteristically represents a prominent component of the inflammatory cell infiltrate of these lesions. However, the major clinical problem associated with nasal polyps, nasal obstruction, reflects the proliferation of the stromal and epithelial elements, which constitute the bulk of these lesions. We recently reported that blood eosinophils of patients with hypereosinophilia can produce the cytokines transforming growth factors-alpha (TGF-alpha) and beta 1 (TGF-beta 1). These cytokines have many biologic activities, which include the regulation of epithelial proliferation, the promotion of extracellular matrix formation, and the induction of angiogenesis. We therefore used in situ hybridization to determine whether the eosinophils that infiltrate nasal polyps express TGF-alpha and/or TGF-beta 1 messenger RNA and used immunohistochemistry to determine whether these eosinophils also express TGF-alpha and TGF-beta 1 proteins. We found that eosinophils represented a major source of both transforming growth factors in each case of nasal polyposis examined and that in most cases the majority of all eosinophils expressed both TGF-alpha and TGF-beta 1. These results suggest that production of TGF-alpha and TGF-beta 1 by the infiltrating eosinophils may contribute to some of the pathologic changes observed in nasal polyposis, such as thickening of the epithelial basement membrane, stromal fibrosis, angiogenesis, and epithelial and glandular hyperplasia.

Aniline Compounds↗
PubMed1996

[Histological and immunohistochemical study of nasal polyps].

Nasal polyps, in general, have been histologically classified as edematous, adenocystic and fibrous types. It has recently been pointed out that eosinophilic infiltration in nasal polyps has increased along with an increase in nasal allergy. The purpose of this study was to classify the nasal polyps histologically and to examine the mode of infiltration and activation of eosinophils by means of immunohistochemistry. The subjects were 101 patients who underwent surgery for nasal polyps. There were 66 males and 35 females ranging in age from 12 to 76 years. Resected polyps were fixed in formalin, embedded in paraffin, and sliced at a thickness of 4 microns. Hematoxylin-eosin staining and streptavidin- biotinyl peroxidase complex staining were used to detect eosinophils. The results were as follows: 1) The nasal polyps were, histologically, edematous in 88.1%, adenocystic in 47.5%, and fibrous in 19.8%. 2) The number and distribution of EG1-positive cells and EG2-positive cells were almost the same in the superficial layer of the lamina propria. This study suggests that eosinophilic infiltration into nasal polyps occurs mainly in edematous polyps and that the majority of the infiltrating eosinophils are activated.

Adolescent↗
PubMed2002

[Bacterial flora as a potential etiopathogenic factor for nasal polyps].

Nasal polyps develop in patients with disturbed local homeostasis of nasal mucosa. Research of Bernstein and Stoop showed the influence of inflammation of nasal mucosa on growth of nasal polyps. Bacterial and viral infections play significant role in development and intensification of inflammatory and immunological process. Many bacteria produce factors which damage cilia cells, cause dyskinesis of cilia and destroy respiratory epithelium. Disturbed muco-ciliar cleaning permits bacteria to penetrate through mucous layer and facilitate their adhesion and colonization on the cells of respiratory epithelium. Adhesion and successive colonization with bacteria multiplication can lead to inflammatory process. Nose swabs results were different in each examined group. The aim of this work was to define bacterial flora in patients with nasal polyps and in patients after polypectomia and to compare it to bacterial flora in healthy patients. Nose swabs were performed in 51 patients with nasal polyps before polypectomia and additional in 15 patients after polypectomia. 25 healthy medical students were a control group. The patients were divided into two groups: I. patients with nasal eosinophilic polyps, II. patients with nasal neutrophilic polyps. In the group of patients with both neutrophilic and eosinophilic polyps dominating bacterial flora included bacteria which usually are the cause of inflammation. In the group of patients after polypectomia bacterial flora was not different from that which was found in patients with polyps.

Adult↗
PubMedDate not supplied

Epidemiology of nasal polyps.

Nasal polyps are found in 36% of patients with aspirin intolerance, 7% of those with asthma, 0.1% in children, and about 20% in those with cystic fibrosis. Other conditions associated with nasal polyps are Churg-Strauss Syndrome, allergic fungal sinusitis, and cilia dyskinetic syndrome, (Kartagener's) and Young Syndrome. Nasal polyps are statistically more common in nonallergic asthma versus allergic asthma (13% vs 5%, P < 0.01). About 40% of patients with surgical polypectomies have recurrences. There appears to be a hereditary factor for developing nasal polyps. A classification system for staging nasal polyps is proposed in order to standardize treatment, consider differential diagnosis, and harvest meaningful comparative research information.

Aspirin↗
PubMed1986

Immunological and non-immunological release of leukotrienes and histamine from human nasal polyps.

Nasal polyps were obtained from 22 patients undergoing polyp surgery. They were chopped into fragments of approximately 2 mm2, washed free of blood, and passively sensitized with serum from timothy allergen sensitive patients (RAST 30-40%), then, challenged with timothy allergen. Analysis of the incubation medium after a 30 min challenge as assessed by reversed phase high performance liquid chromatography and bioassay revealed the presence of leukotriene (LT) LTB4, LTC4, LTD4 and LTE4 (29 +/- 9, 6.6 +/- 3, 62 +/- 13 & 86 +/- 23 pmol/g tissue wet weight, respectively). The human nasal polyps also released histamine which reached a maximum after approximately 5 min (2.8 +/- 1.28 nmol/g tissue), as measured by radioenzymatic assay. A similar profile of leukotrienes and histamine release was observed when the nasal polyps were stimulated with ionophore A23187. However, the ionophore stimulated release was greater than that observed for the antigen challenge. When human polyps were stimulated with a mixture of the ionophore and arachidonic acid, all the above products as well as 5-hydroxy-eicosatetraenoic acid (5-HETE), 12-HETE, and 15-HETE were detected in the medium. These data, taken together, demonstrate that human nasal polyps are able to release significant amounts of leukotrienes and histamine upon both immunological and non-immunological stimulations and that these responses might significantly contribute to the symptoms of allergic rhinitis.

Allergens↗
PubMedDate not supplied

Efficacy of an aqueous and a powder formulation of nasal budesonide compared in patients with nasal polyps.

Nasal polyps are commonly treated surgically. Intranasal administration of topical corticosteroids has gained increased acceptance as a treatment alternative. The aim of our study was to compare the efficacy of treatment of two formulations of budesonide with placebo on nasal polyps. At four Danish clinics 138 patients suffering from moderate or severe nasal polyps were randomized to a twice daily treatment with Rhinocort Aqua 128 micrograms, Rhinocort Turbuhaler 140 micrograms or placebo (Astra Draco, Sweden) for 6 weeks. Polyp size (primary efficacy variable), nasal symptoms, sense of smell, and patients' overall evaluation of treatment of efficacy were assessed by scores. Polyp size was reduced significantly in both budesonide treated groups compared with placebo, but there was no statistical difference between the two actively treated groups. Patients' nasal symptom scores was significantly more reduced in the Aqua compared to the Turbuhaler treated group, and both reduced symptom scores were significantly better compared to placebo. Sense of smell was significantly improved in the actively treated groups compared to placebo. The proportion of patients rating substantial or total control over symptoms after 6 weeks treatment was 60.9% and 48.2% in the Aqua and Turbuhaler-treated groups, respectively, which was significantly better compared with 29.8% in the placebo-treated group. Rhinocort Aqua and Rhinocort Turbuhaler were equally well tolerated.

Administration, Intranasal↗
PubMed1987

Sweat sodium levels in adults with nasal polyps.

Nasal polyps occur in 10% of children and 48% of adults with cystic fibrosis. The prevalence of abnormal sweat tests and cystic fibrosis in adults with nasal polyps has not been reported. We therefore performed sweat tests on 35 adults with nasal polyposis seen in two allergists' office practice. Sweat sodium levels ranged from 12 to 65 mEq/L (median = 34). These were considered within the normal range for adults. Abnormal sweat tests and cystic fibrosis were not found in this series of adults with nasal polyps.

Adult↗
PubMedDate not supplied

Azelastine reduces mediators of inflammation in patients with nasal polyps.

Nasal polyps affect approximately 4% of the population in the western world. The etiology of this disease is unknown, although inflammatory mechanisms may play an important role. In preceding studies we and others have shown that besides H1-antagonism, azelastine influences the immigration and activation of inflammatory cells. In this open label study in 16 patients with nasal polyps and perennial mite-allergic rhinitis, the effect of azelastine nasal spray twice daily 0.14 mg to each nostril on recurrence of nasal polyposis after endonasal surgery was evaluated. One patient dropped out after 3 months, unwilling to take further medication. Clinical and laboratory data of 15 patients were recorded over 25 weeks in a total of seven visits. Of these one patient needed nasal budesonide during the 4 weeks between visits 3 and 4. All other patients did not take any steroids before inclusion into the trial or during the 6-month observation period. Concentrations of eosinophil cationic protein (ECP) for eosinophils, myeloperoxidase (MPO) for neutrophils and tryptase for mast cells were determined in nasal secretions before and after eight and 25 weeks of treatment using double antibody radioimmunoassays, because these have been demonstrated to be good inflammatory markers in nasal diseases. Mean concentrations of MPO decreased from 2724 ng/mL to 1610 ng/mL (p = 0.0015) over the entire treatment period. ECP decreased from 458 ng/mL to 264 ng/mL (p = 0.0342). Tryptase decreased from 37.9 ng/mL to 22.4 ng/mL (p = 0.0574). These data were consistent with a significant decrease in clinical symptoms. Thus, azelastine seems to have an inhibitory effect on eosinophil and neutrophil activation in patients with nasal polyps and mite allergy.

Administration, Inhalation↗
PubMed1987

Prostaglandins, leukotrienes, and other arachidonic acid metabolites in nasal polyps and nasal mucosa.

Prostaglandins (PGs) and leukotrienes (LTs) are known to play an important role in allergic inflammatory reactions. The triad of aspirin sensitivity, nasal polyposis, and asthma led us to suspect that PGs, LTs and other arachidonic acid metabolites may be involved in the pathogenesis of nasal polyps. The purpose of this study was to determine arachidonic acid metabolites and to measure concentrations of PGs and LTs in nasal polyps and nasal mucosa. Samples of nasal polyps and nasal mucosa were obtained at the time of polypectomies and nasal procedures. Metabolites of arachidonic acid in tissue were determined by incubation of tissue-homogenates with 14C-arachidonic acid and analyses with thin-layer chromatography and high performance liquid chromatography (HPLC). Levels of PGE2, 6-keto-PGF1 alpha, thromboxane (Tx)B2, 15-hydroxyeicosatetraenoic acid (HETE), LTC4, LTB4 were measured by radioimmunoassay. The predominant arachidonic acid metabolite in both nasal polyps and mucosa with 15-HETE. The HPLC analysis showed that the predominant metabolite in nasal polyp was 15-HETE, especially in polyps from aspirin sensitive patients. Levels of 15-HETE and PGE2 were higher in polyps from patients with a history of allergy than from nonallergic patients. Levels of LTC4 and LTB4 in nasal polyps were determined. The findings of this study will help to explain biochemical basis of the pathogenesis of aspirin-sensitive nasal polyps and to develop better medical treatment for them.

6-Ketoprostaglandin F1 alpha↗
PubMed1997

Nasal polyposis: immunohistochemistry and bioelectrical findings (a hypothesis for the development of nasal polyps).

Nasal polyps and turbinates were obtained from individuals undergoing surgery for symptomatic nasal obstruction caused by nonatopic rhinosinusitis or allergic rhinosinusitis. One part of the tissue from each patient was fixed in neutral buffered formalin and prepared for study by histochemical and immunohistochemical methods. Monoclonal antibodies were used to identify macrophages, lymphocytes, and plasma cells. In most cases (12 of 16, 75%) the remainder of the polyp and turbinate samples was treated with protease to achieve disaggregation of the epithelial cells. Those cells were cultured on permeable collagen matrix supports. Transepithelial potential difference and resistance were measured daily. At the time of maximal transepithelial potential difference, the epithelial cells were mounted in modified. Ussing chambers and exposed to a sodium-positive channel blocker (amiloride hydrochloride) and to selected chloride-negative channel agonists (isoproterenol bitartrate and adenosine triphosphate). Middle turbinates and polyps were found to have more macrophages, lymphocytes, plasma cells, HLA-DR-positive cells, and eosinophils than the inferior turbinates. Epithelial cells obtained from polyps exhibited higher transepithelial potential differences and equivalent short-circuit currents than turbinate cell cultures. The responses to amiloride, isoproterenol, and adenosine triphosphate were also greater for polyp than for turbinate cultures. A theory for the pathogenesis of nasal polyps is proposed. Local release of inflammatory mediators could cause sodium absorption and chloride permeability to be higher in polyps than in turbinate epithelia. Increased sodium absorption is consistent with the hypothesis that epithelial fluid absorption contributes to the development of nasal polyps and is a result of the increased recruitment of inflammatory cells, which are present in nasal polyps.

Adenosine Triphosphate↗
PubMed1988

Insulinlike growth factor I immunoreactivity in nasal polyps.

Nasal polyps from 15 patients were all found to express increased insulinlike growth factor I immunoreactivity. A hypothesis for the formation of nasal polyps is described: macrophages, seen in allergic and infectious reactions, produce and release growth factors, tentatively including insulinlike growth factor I. In enclosed paranasal sinuses this results in an accumulation of insulinlike growth factor I stimulating the growth of both epithelium and blood vessels in the sinuses. The mucosa increasingly bulges out through the ostium after having filled out the sinusity. Continuing growth stimulation is supplied by the inflammatory reaction, endothelial cells in the polyp, and activated macrophages inside or outside the polyp.

Adolescent↗
PubMed2000

[The role of chemokines in nasal polyps].

Nasal polyposis is an inflammatory condition of the nose and the sinuses characterised by a marked infiltration of eosinophils in addition to lymphocytes, mast cells and macrophages. The selective recruitment of eosinophils to inflammatory sites is mediated by CC chemokines such as Eotaxin and Eotaxin-2. In the present study histology, immunohistochemistry and ELISA were performed. The levels of Eotaxin and Eotaxin-2 and for comparison other chemokines RANTES and IL-8 were measured in nasal polyp tissue and in control nasal tissue. On histological examination 6 polyps showed an oedematous structure, one was glandular and one had a fibromatous pattern, while all showed a marked eosinophil infiltration. Immunohistochemistry of the polyps showed that epithelial cells were strongly positive for Eotaxin and IL-8, whereas endothelial cells stained positive for Eotaxin-2. Significantly higher amounts of Eotaxin, Eotaxin-2 and IL-8 were detected in polyp tissue when compared with control middle turbinates. The increased levels of eosinophil-stimulating chemokines, such as Eotaxin and Eotaxin-2 in nasal polyps suggest that they may be important regulators of eosinophil recruitment in this inflammatory disease.

Chemokine CCL11↗
PubMed1985

Innervation of human nasal polyps.

Nasal polyps from 12 patients were studied by means of transmission electron microscopy. Nerve fibers in the polyp could be recognized in 4 out of the 12 polyps. Both myelinated and nonmyelinated nerve fibers were observed. The endings of the nonmyelinated nerve were adrenergic and observed in the area close to the smooth muscle cells of the artery. The secretory cells in the form of acini did not accompany nerve endings although these acini contained myoepithelial cells. Some nerves had normal features but others had a degenerated form in the pedicle of the nasal polyp. No cholinergic fibers were observed in these polyps.

Adrenergic Fibers↗
PubMed1993

Eosinophils in nasal polyps and nasal mucosa: an immunohistochemical study.

Immunohistochemical staining was performed at the time of endoscopic sinus surgery (ESS), after 6 months, and after 1 year on nasal polyps and biopsy specimens of the macroscopically unaffected mucosa of the middle and inferior turbinate bones of 46 patients with nasal polyps. During the follow-up period the patients were treated with topical corticosteroids. At time of ESS significantly more BMK13+ and EG1+ (pan eosinophil markers) and EG2+ (activation marker) eosinophils were found in the polyps than in the macroscopically unaffected mucosa of the middle and inferior turbinate bones of the patients. In the middle and inferior turbinate bones of 10 healthy subjects no EG2+ (activated) eosinophils were detected, whereas low-to-moderate numbers of BMK13+ and EG1+ eosinophils were seen in these specimens. This emphasizes that eosinophils play a role in the pathogenesis of nasal polyps. Compared with numbers at ESS, after 6 months and 1 year of follow-up, lower numbers of BMK13+, EG1+, and especially of EG2+ eosinophils were found in recurrences of polyps and in the macroscopically unaffected mucosa of the middle and inferior turbinate bones of the patients. The decrease in number of EG2+ (activated) eosinophils is an indication of a reduced local inflammatory reaction, and could be an important factor in postponement of recurrences of nasal polyps.

Adolescent↗