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Nasal polyposis

There are few definitive data to substantiate the efficacy of LTRA therapy in refractory asthma, except for patients with aspirin-sensitive asthma. This is a fairly uncommon form of asthma that occurs generally in adults who often have no prior (i.e., childhood) history of asthma or atopy, may have nasal polyposis, and who often are dependent upon oral corticosteroids for control of their asthma. This syndrome is not specific to aspirin but is provoked by any inhibitors of the cycloxygenase-1 (COX-1) pathway. These patients have been shown to have a genetic defect that causes... [Pg.688]

The term refers to a distinct clinical syndrome characterized by aggressive and continuous inflammatory disease of the airways with chronic eosinophilic rhinosinus-itis, asthma and often nasal polyposis [6-8]. Aspirin and other NSAIDs that inhibit COX-1 exacerbate the condition, precipitating violent asthmatics attacks. This is a hallmark of the syndrome. The prevalence of aspirin hypersensitivity in the general population ranges from 0.6 to 2.5%, but is much more frequent in adult asthmatic subjects where it reaches 10-15%, although it is often underdiagnosed. [Pg.173]

In general, treatment of the asthma underlying NSAlDs sensitivity should follow standard asthma guidelines. This type of asthma is often severe and frequently high doses of inhaled corticosteroids and daily doses of oral corticosteroids are necessary. A special treatment option is a chronic desensitization to aspirin [8]. Desensitization and aspirin maintenance is routinely used in some centers for treatment of chronic rhinusinusitis with nasal polyposis. It is the only available procedure which allows AIA patients with ischemic heart disease to use aspirin. During the state of desensitization to aspirin, not only aspirin but almost all strong NSAIDs are tolerated, so desensitization and NSAID maintenance could be used for treatment of rheumatic disease or chronic pain syndromes. [Pg.176]

Systemic corticosteroids, administered orally or by depot injection, are considered last-resort options when all other treatments for SAR are inadequate. Systemic steroids may be used to control rhinitis symptoms in patients with severe PAR or nasal polyposis. Data comparing oral and parenteral steroid therapy are lacking however, oral therapy is preferred due to its low cost... [Pg.931]

Assess the patient s symptoms to determine if selftreatment is appropriate or evaluation by a physician is necessary. Determine type of symptoms, frequency (seasonal or chronic), and precipitating triggers. Does the patient have any AR-related complications (e.g., nasal polyposis, sinusitis, or otitis media) ... [Pg.934]

Nasal polyposis Presence of several polyps (benign growths) in the... [Pg.1571]

Hypersensitivity to salicylates or nonsteroidal anti-inflammatory drugs (NSAIDs). Use extreme caution in patients with history of adverse reactions to salicylates. Cross-sensitivity may exist between aspirin and other NSAIDs that inhibit prostaglandin synthesis, and aspirin, and tartrazine. Aspirin cross-sensitivity does not appear to occur with sodium salicylate, salicylamide, or choline salicylate. Aspirin hypersensitivity is more prevalent in those with asthma, nasal polyposis, chronic urticaria. [Pg.913]

Patients were ineligible if they had skin prick tests or nasal provocation tests positive to more than one allergen significant diseases or malformations of the nasal cavities such as nasal polyposis, septal deviation, choanal atresia nasal swab positive for bacteria or mycetes, or immunotherapy in the preceding 5 years. [Pg.91]

The rate of mucociliary clearance can be affected by the pathophysiological condition of the nasal cavity and this will also affect the rate of clearance of administered drag. Such conditions include rhinitis, the common cold, hayfever, sinusitis, asthma, nasal polyposis, Sjogren s and Kartagener s syndromes. In addition, environmental factors such as humidity, temperature and pollution can also affect the rate of nasal clearance. [Pg.227]

Patients who are sensitive to aspirin shonld not be given any other NSAID becanse of possible cross-sensitivity reactions. Aspirin cross-sensitivity however, does not appear to occur with the nonacetylated salicylates such as sodium salicylate or choline salicylate. As mentioned previously, aspirin hypersensitivity is more prevalent in patients with asthma, rhinitis, or nasal polyposis. This syndrome has been termed the aspirin triad. ... [Pg.100]

Urticaria, severe rhinitis and asthma occur in susceptible individuals, e.g. with nasal polyposis, who are exposed to NSAIDs, notably aspirin the... [Pg.284]

A 20-year-old woman developed chronic rhinitis 1 month after the last dose of hepatitis B, followed about 1 year later by severe asthma, nasal polyposis, and petechial purpura in her fingernail beds and on her feet. A skin biopsy from the left leg showed infiltrates consistent with leukocytoclastic vasculitis. [Pg.1606]

Several reports have documented the high risk of ketorolac in patients with a history of asthma, nasal polyposis, and sensitivity to aspirin or any other NSAID (SEDA-18, 105). Exacerbation of chronic asthma has been reported after the use of ketorolac eye-drops (SEDA-21, 106). [Pg.1979]

Aspirin and other nonsteroidal anti-inflammatory drugs can precipitate an attack in up to 20% of adults with asthma. The mechanism is related to cyclooxygenase inhibition, and 5-hpoxygenase inhibition can prevent the symptoms. The prevalence increases with age. The greatest frequency occurs in severe corticosteroid-dependent asthmatics in their fourth and fifth decades who also have perennial rhinitis and nasal polyposis (presence of several polyps). Other drugs that do not precipitate bronchospasm but which prevent its reversal are the 8-blocking agents. ... [Pg.512]

The upper respiratory tract is also involved commonly in CF. Sinusitis and nasal polyposis occur in 90% and 50% of patients, respectively. Sinusitis is chronic in character, and acnte symptoms are unusual. Although its etiology is not entirely clear, sinusitis may result from obstruction of the sinus ducts, thus preventing drainage. The bacteria generally isolated in these cases include P. aeruginosa, H. influenzae, streptococci, and anaerobes. Usually, the same strain... [Pg.593]

In addition, the impact of allergic rhinitis goes well beyond these central nervous system issues. Allergic rhinitis is associated with several other serious medical conditions, including asthma, rhinosinusi-tis, otitis media, nasal polyposis, respiratory infections, and orthodontic malocclusions. ... [Pg.1729]

Van Zele T, Gevaert P, Watelet J-B, Claeys G, Holtappels G, Claaeys C, van Cauwenberge P, Bachert C Staphylococcus aureus colonization and IgE antibody formation to enterotoxins is increased in nasal polyposis. J Allergy Clin Immunol 2004 114 981-983. [Pg.131]

There is recent evidence that S. aureus enterotoxins also affect the airways, and modify diseases such as allergic rhinitis, nasal polyposis, severe late-onset asthma, chronic obstructive pulmonary disease (COPD) and early childhood persistent wheeze. We here summarize the current evidence for an active, at least modifying role of superantigens in upper and lower airway disease, and speculate on the possible clinical implications for the management of patients affected. [Pg.216]

Enhanced Immune Response to S. aureus in Nasal Polyposis... [Pg.217]

From the first study in patients with local IgE against SEs [10] it appeared that the highest IgE concentrations were obtained from samples of aspirin-sensitive subjects. We therefore extended our observations in a nonallergic, but severely inflamed subgroup of patients, who also suffered from asthma. Subjects with nasal polyposis from Poland were classified as aspirin-sensitive (ASNP) or aspirin-tolerant (ATNP) asthmatics, based on a bronchial aspirin challenge test [47], Homogenates prepared from NP tissue were analyzed for concentrations of eosinophilic markers, total IgE and IgE antibodies to enterotoxins (SEA, SEC, TSST-1) [22], and compared to inferior nasal turbinates from healthy subjects. [Pg.223]

Tripathi A, Conley DB, Grammer LC, et al Immunoglobulin E to staphylococcal and streptococcal toxins in patients with chronic sinusitis/nasal polyposis. Laryngoscope 2004 114 1822-1826. [Pg.233]

Bachert C, Gevaert P, Holtappels G, Cuvelier C, van Cauwenberge P Nasal polyposis from cytokines to growth. Am J Rhinol 2000 14 279-290. [Pg.234]

Perez-Novo CA, Kowalski ML, Kuna P, et al Aspirin sensitivity and IgE antibodies to Staphylococcus aureus enterotoxins in nasal polyposis studies on the relationship. Int Arch Allergy Immunol 2004 133 255-260. [Pg.235]

Suh YJ, Yoon SH, Sampson AP, et al Specific immunoglobulin E for staphylococcal enterotoxins in nasal polyps from patients with aspirin-intolerant asthma. Clin Exp Allergy 2004 34 1270-1275. Perez-Novo CA, Watelet JB, Claeys C, van Cauwenberge P, Bachert C Prostaglandin, leukotriene, and lipoxin balance in chronic rhinosinusitis with and without nasal polyposis. J Allergy Clin Immunol 2005 115 1189-1196. [Pg.235]


See other pages where Nasal polyposis is mentioned: [Pg.932]    [Pg.427]    [Pg.284]    [Pg.185]    [Pg.187]    [Pg.19]    [Pg.2680]    [Pg.594]    [Pg.215]    [Pg.217]    [Pg.224]    [Pg.230]    [Pg.232]    [Pg.233]   


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