Allergic Rhinitis

Seth, Divya; Kamat, Deepak

doi:10.1177/0009922806298703

Cited by 15 publications

(27 citation statements)

References 28 publications

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“…Recent studies indicate that the prevalence is increasing [4,5]. Typically, seasonal allergic rhinitis follows repeated exposure to potentially sensitizing molecules and does not usually develop until the patient has been sensitized by two or more pollen seasons [1,6]. Both sexes are equally affected [1].…”

Section: Epidemiologymentioning

confidence: 99%

“…Children with food allergy by four years of age are at increased risk for allergic rhinitis [9]. Other risk factors include maternal smoking, formula feeding, early introduction of solid food, and a personal or family history of atopy [6,10,11].…”

Section: Epidemiologymentioning

confidence: 99%

“…This process causes degranulation of these cells with immediate release of preformed chemical mediators including histamine, tryptase, chymase, and cytokines such as IL-4, IL-5, IL-8, IL-13 and tumor necrosis factor- [6,9]. In addition, activated mast cells generate de novo several inflammatory mediators such as prostaglandins, cysteinyl leukotrienes, and platelet-activating factors from the phospholipid cell membrane [15].…”

Section: Pathogenesismentioning

confidence: 99%

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Seasonal Allergic Rhinitis

Leung

Hon²

2008

IAD

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Seasonal allergic rhinitis is characterized by seasonal rhinorrhea, nasal congestion/stuffiness, nasal and ocular pruritus, and paroxysmal sneezing. Symptomatic relief and improved quality of life can be achieved in the majority of patients by using pharmacotherapy appropriately. Mild cases can be managed with either an oral antihistamine or a nasal corticosteroid alone. More severe cases may require a nasal corticosteroid in combination with various agents. Immunotherapy is reserved for a selected group of patients. While all other interventions provide symptomatic relief, specific immunotherapy may have long-term effects. This review article also discuss recent patents related to the field.

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Section: Epidemiologymentioning

confidence: 99%

Section: Epidemiologymentioning

confidence: 99%

Section: Pathogenesismentioning

confidence: 99%

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Seasonal Allergic Rhinitis

Leung

Hon²

2008

IAD

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“…On nasal exposure to the same antigen, the antigen bridges two adjacent IgE molecules attached to the surface of mast cells in the nasal mucosa. This causes degranulation of the mast cells with rapid release of preformed chemical mediators (e.g., histamine), enzymes (e.g., tryptase and chymases), and cytokines [e.g., IL-4, IL-5, IL-8, IL-13, and tumor necrosis factor (TNF)-α ] (8,9). In addition, activated mast cells generate de novo several inflammatory mediators such as prostaglandins, cysteinyl leukotrienes, and platelet-activating factors (10).…”

Section: Introductionmentioning

confidence: 99%

“…These acute-phase mediators, histamine in particular, cause vasodilation, increase vascular permeability and mucus secretion, and stimulate sensory nerves. All these processes result in symptoms such as nasal itching, sneezing, rhinorrhea, and nasal congestion (8,10). These acute-phase responses typically subside within 30 -60 min.…”

Section: Introductionmentioning

confidence: 99%

Pharmacological Profile of the Novel Anti-inflammatory Corticosteroid NS-126, a Therapeutic Agent for Allergic Rhinitis

et al. 2010

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Abstract. NS-126 (9-fluoro-11 β ,17,21-trihydroxy-16 α -methylpregna-1,4-diene-3,20-dione 21-cyclohexanecarboxylate 17-cyclopropanecarboxylate) is a novel, highly lipophilic anti-inflammatory corticosteroid. We compared NS-126 and the widely used intranasal corticosteroid fluticasone propionate (FP) in a guinea-pig model of allergic rhinitis and a rat model of airway eosinophilia.In the allergic rhinitis model, NS-126 and FP reduced sneezing and nasal obstruction to similar extents. In the airway eosinophilia model, both compounds inhibited the infiltration of eosinophils into the bronchoalveolar lavage fluid, but the effect of NS-126 was longer-lasting than that of FP. In vitro, NS-126 showed lower affinity than FP for the glucocorticoid receptor and was a weaker inhibitor of Th 2 cytokine and chemokine production and mast-cell secretory responses. We also investigated DX-17-CPC, a metabolite of NS-126 generated in nasal tissue by carboxylesterasecatalyzed hydrolysis at the 17-position. DX-17-CPC showed greater affinity than NS-126 for the glucocorticoid receptor and was a stronger inhibitor of Th 2 cytokine and chemokine production and mast-cell secretory responses. The long duration of the anti-allergic effects of NS-126 may be explained by its high lipophilicity, while the strength of its anti-allergic effects may be explained by the generation of the active metabolite DX-17-CPC. NS-126 is a long-acting intranasal corticosteroid and a promising therapeutic agent for allergic rhinitis.

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