Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Allergic rhinosinusitis has three forms of therapy: pharmacotherapy, immunotherapy, and surgical therapy. Pharmacotherapeutically, there are six classes of drugs that give symptomatic relief: mucolytics, decongestants, anti-cholinergic agents, antihistamines, mast cell stabilizers, and corticosteroids. All six classes are discussed individually and in detail. For immunotherapeutic therapy of allergic rhinosinusitis, there are four types of skin testing in current use: scratch testing, prick testing, single intradermal testing, and skin end point titration testing. Only the latter is able to quantitate the antigenicity of each antigen, and thus the treatment vial made from only this type of skin testing can adequately treat all antigens to which the patient is sensitive. These differences in testing and vial mixing are explained. The last form of therapy is surgical therapy, which corrects the obstructive phenomenon caused by allergic rhinosinusitis. The procedures described are reduction inferior turbinectomies and endoscopic sinus surgery. It is felt by the authors that the specialist who is uniquely positioned to offer a patient suffering from allergic rhinosinusitis all three forms of therapy is the rhinologist.
Ear Nose Throat J 1993 Feb
PMID:Allergic rhinosinusitis: the total rhinologic disease. 834 84

Ovalbumin-induced guinea pig model of rhinitis was assessed for its utility in the studies of rhinitis. Systemic sensitization and challenge with ovalbumin-induced rhinitis symptoms and an increase in anti-OVA-IgE and IgG titers, positive skin reactions and nasal lavage IL-4 concentration. Histopathology of nasal mucosa showed infiltration of eosinophils and other inflammatory cells consistent with the symptoms. Topical sensitization of ovalbumin yielded inconsistent symptoms of rhinitis. In systemic sensitization model, repeated challenge of ovalbumin caused similar response for at least 3 consecutive challenges. The symptoms were affected by relative humidity in the air and dosing volume of topical drugs. Sneezing and lacrimation were reduced by acute oral administration of the H1 receptor antagonists and steroids or the prophylactic oral administration of cysteinyl leukotriene (CysLT1) receptor antagonist montelukast or acute topical antihistamines, mast cell stabilizer sodium cromoglycate and anticholinergic agent ipratropium bromide, but not by a topical steroid. Nose rubbing was reduced significantly by some oral and topical antihistamines. Oral steroids offered excellent protection against all symptoms. Dexamethasone and montelukast also inhibited nasal lavage IL-4 concentration and inflammatory cell infiltration. Treatment with topical steroid fluticasone for 2 weeks had no effect on sneezing or rubbing. However, it caused complete inhibition of congestion. The cyclooxygenase inhibitor indomethacin had no effect on symptoms of rhinitis. The adrenergic alpha receptor agonist-decongestant oxymetazoline caused reduction in congestion. These results suggest that differential responsiveness to symptoms of rhinitis by a new agent can be very well profiled in the model in congruence with the mediation pathways and mechanism of action of drugs. The model provides complete symptomatic characterization of rhinitis and is a good tool for its study.
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PMID:Validation of guinea pig model of allergic rhinitis by oral and topical drugs. 1862 97