Nasal congestion results from histamine release acting as a vasodilator around the turbinates and from the effect of leukotrienes and prostaglandins around the nasal mucosa. patient ages, the likelihood of development of allergic rhinitis declines. You will find many reasons for the increasing prevalence of allergic rhinitis over the past 100 years. More recently, attention has been drawn to the role of diesel-exhaust particles inducing IgE production.77 Increased mRNA for many cytokines that stimulate IgE production, in addition to increased interleukin (IL)-4 protein found in nasal lavage after intranasal challenge with diesel particles,31 may be one reason. In children, possible risk factors for developing allergic rhinitis before age 6 years include maternal smoking (at least 1/2 pack per day), parental history of atopy, ingestion of food (other than formula or breast milk) before age 2 months, and the presence of dogs indoors.112 ECONOMIC IMPACT OF RHINITIS Estimated costs for allergic rhinitis exceed $1.2 billion per year for direct (medication and physician) and indirect (time off of work) costs.4 Allergic rhinitis alone accounted for 811,000 missed workdays, 824,000 missed school days, and 4,230,000 reduced activity days in 1987.61 According to physician audits and other database data, estimated 1994 prescription antihistamines accounted for $460 million, intranasal corticosteroids $211 million, and prescription chilly medicines $169 million.70 In consideration of the profound economic impact that rhinitis has on all patients, it is imperative that all clinicians consider the pathophysiology and differential diagnoses for rhinitis in choosing appropriate therapy. PATHOPHYSIOLOGY OF RHINITIS For patients with allergic rhinitis, sensitization occurs by processing foreign antigens by an antigen-presenting CB-839 cell and presentation to T-helper 2 (TH2) cells. These T cells produce cytokines, which promote activation of B cells to produce IgE CB-839 specific for the antigen (allergen). When two IgE antibodies are cross-linked by binding to specific epitopes of the allergen, degranulation of the attached (at the Fc receptor) mast cell occurs with resultant mediator release. The allergic reaction exhibits a biphasic response characterized Rabbit polyclonal to ZBTB49 by release of prostaglandin (PG) D2, tosyl-L-arginine methyl esterase (TAME-esterase), kinins, and histamine immediately from mast cells and the same mediators (except PGD2) from basophils 3 to 6 hours later.75 Cytokines IL-3, IL-5, IL-9, and IL-10 promote IgE and mast cell production.3 Additionally, IL-4 and IL-13 promote production of IgE, whereas gamma interferon and IL-12 oppose IgE production. 7 The mast cell also enhances CB-839 IgE production by generating IL-4, IL-5, and IL-6.11 Inflammatory cells are recruited into the area by cytokine release also. Monocyte chemotactic and activating factor (MCAF), monocyte chemoattractant protein-1 (MCP-1), a chemokine known as RANTES (regulated and normal T cell expressed and secreted), and macrophage inflammatory protein1 (MIP-1) activate basophils (MCAF/RANTES) and eosinophils (RANTES/MIP-1), whereas IL-8 inhibits MCAFinduced histamine release from basophils.55 Increases in CD T lymphocytes and CD-positive, IL-2-receptor-positive activated T cells are seen in the nasal mucosa.104 A priming effect results in increased mast-cell density during continued (seasonal) allergen challenge.59 As a result of histamine release, sneezing with nasal and ocular pruritus result. Pruritus may be felt in the soft palate also, as well as referred into the ear along the eustachian tube. Nasal congestion results from histamine release acting as a vasodilator around the turbinates and from the effect of leukotrienes and prostaglandins around the nasal mucosa. Other components of nasal secretions include antibodies (especially IgA), macroglobulin, lactoferrin, lysozyme, and mucus cell glycoproteins. Histamine also activates glandular hypersecretion via nocioceptive-parasympathetic reflexes to produce mucus.3 Nonallergic CB-839 activation of the afferent pathway from nasal sensory receptors results in cholinergic activation via the efferent pathway to the nasal goblet cells resulting in further rhinorrhea. The majority of the producing rhinorrhea is usually propelled backwards by cilia in the nasal cavity toward the pharynx (postnasal drip), with the excess secretions draining anteriorly. 60 DIFFERENTIAL DIAGNOSIS OF RHINITIS CB-839 Allergic Rhinitis Deciphering between allergic and nonallergic reasons for rhinitis can be difficult, especially when viral infections may occur during the height of an allergy season. Many elderly patients are convinced they have allergies because of pseudo-allergic responses (such as gustatory and vasomotor rhinitis). Compounding the confusion that many patients experience are evaluations by practitioners inadequately trained to properly test for immediate (IgE mediated) hypersensitivity that perpetuates the patient’s belief of allergies. The history.