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Article Excerpt
Allergic rhinitis (AR) is an important disease for health care practitioners to understand because it is the most common chronic condition in adults and children. (1) Although AR is often undertreated, it has a broad impact on economics, quality of life, work performance, and education, and can lead to other health problems. This monograph will provide an overview of AR with respect to epidemiology, pathophysioiogy, pharmacotherapeutic management, and practical problems in delivering therapy.
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Allergic rhinitis (AR) is a condition in which allergens cause a constellation of symptoms, including paroxysms of sneezing, rhinorrhea, coughing, nasal obstruction, and pruritus of the eyes, nose, and palate. It is directly associated with fatigue, irritability, chronic cough with postnasal drip, memory deficits, and depression. Additionally, it may lead to chronic sinusitis, bad breath, sleep apnea, and snoring, and may also pose difficulty in controlling asthma.
There are many causes of rhinitis; however, allergy accounts for approximately 50% of all cases (Table 1). (2)
AR can be categorized as seasonal or perennial. The seasonal type provides a predictable pattern during a defined season, whereas perennial is most often defined by symptoms lasting nine months or longer. (2)
EPIDEMIOLOGY
The prevalence of AR is becoming more difficult to track. This is due to the increasing number of OTC medications for its treatment and people's ability to recognize and self-treat the disorder. Previously, most studies used physicians and institutions to identify AR frequency. The prevalence of AR is rising in the United States parallel to that of other immunoglobulin (Ig) E-mediated diseases, such as asthma. This increase has been persistent for the past three decades and is now estimated to be 20% in adults and close to 40% in children. (3,4) The economic impact is staggering, estimated to be between 6.3 and 7.9 billion dollars per year, when considering direct and indirect costs. Direct costs include medications, medical visits, and other physical items used for AR avoidance, whereas indirect costs are associated with lost productivity and absenteeism. (5)
The overall incidence of AR peaks in adolescence between the ages of 12 and 15. Risk factors are environmental and genetic in nature (Table 2). If there is a negative family history, the incidence is 13%, in comparison to 29% and 47% if one or both parents, respectively, have allergic disease. If both parents have the same type of allergic disease, the risk increases to nearly 72%. (1)
The environmental effects prove to be just as important. The reunification of Germany offered a unique opportunity to study the impact of environmental factors on the development of childhood respiratory and allergic disorders in ethnically similar populations. Prior to this reunification, allergic disease was much less common in East Germany. A team of investigators evaluated the prevalence of asthma, hay fever, atopy, and bronchial hyperresponsiveness in 9- to 11-year-old children in West Germany (n = 5,030) and East Germany (n = 2,623). (6) Atopic sensitization was considerably more frequent in West German children than in their peers in East Germany (36.7% vs 18.2%, respectively). The prevalence of asthma and hay fever was significantly higher in West German children than in East German children (5.9% vs 3.9% and 8.6% vs 2.7%, respectively). Bronchitis, however, was more prevalent in the East German group than in the western part of the country. Logistic regression showed that the West German study area was no longer a significant independent determinant of asthma once sensitization to mites, cats, and pollen was taken into account. The authors concluded that sensitization to aeroallergens was strikingly more frequent in West Germany than in East Germany, which explained the differences in the prevalence of asthma and hay fever between the two parts of the country.
Epidemiologic studies looking at intestinal flora have shown that predominance of certain bacteria may lead to an increase or decrease in both asthma
and allergies. (7) Children with three or more siblings have a lower incidence of allergic diseases. Therefore, patients with repeated immune stimulation may be protected against atopic diseases. (7) Asthma and AR are closely related and often overlap; however, they do not always coexist together. The prevalence of AR is 89% and 94% in asthmatic adults and adolescents, respectively. (3)
PATHOPHYSIOLOGY
The nasal mucosa is very efficient at filtering air and providing humidification. Everyone inhales different types of allergens on a daily basis. Typically, individuals have a low-grade immunologic response, producing IgG Ab and T-cell proliferation and differentiation with a predominance of type-1 helper T ([T.sub.H]1) cells. [T.sub.H]1 cells produce interferon-[gamma] as well as interleukins. However, when antigens are introduced to the patient with AR, the response is different. The antigen-presenting cell causes an IgE-mediated response with differentiation of T cells to [T.sub.H]2 cells, producing some of the same but also different interleukins such as interleukin (IL)-4, IL-5, and IL-9. This IgE-mediated [T.sub.H]2-Cell predominance is the main difference in the individual's response to various allergens. (7)
This immune response occurs in two phases. The early phase occurs within minutes and is responsible for sneezing, pruritus, rhinorrhea, and some congestion. This is due to IgE-sensitized mast cells that degranulate, releasing cysteinyl leukotrienes, prostaglandins, cytokines, and histamine. It is histamine that is primarily responsible for these early-phase symptoms.
Congestion is the symptom that predominates in the late phase. The nasal mucosa becomes infiltrated with inflammatory cells, ie, basophils, eosinophils, neutrophils, mast cells, and mononuclear cells. It is histamine's action on receptors [H.sub.1] to [H.sub.4] that is believed to be responsible for the increased pro-inflammatory release of cytokines that sustain the congestion. After repeated exposure to allergens, the nasal epithelium becomes hypertrophied, due to the increased number of mast cells and eosinophils migrating to the area. (8)
DIAGNOSIS
There is no gold standard test for securing a diagnosis of AR. The diagnostic tests most often used are skin prick testing (SPT), intradermal testing, and in vitro Ab assays (detecting specific serum antibodies and determining their concentration). SPT is the most commonly used, given that it is the least expensive and the most convenient. If SPT produces a negative result, but there is a high pretest probability of allergy, then going on to intradermal testing makes sense. The advantage to intradermal testing is its sensitivity, although its specificity is low. The main problem with in vitro Ab testing is its high false-positive rate, although it does have good sensitivity and specificity. (9)
The true test is the clinician's ability to recognize the signs and symptoms of AR. Given its high prevalence in the population, it is reasonable to treat empirically. Since many products to treat AR are available OTC, pharmacists can play a major role in identifying patients suspected of having AR. It is important for pharmacists to recognize the signs and symptoms of AR: allergic shiners (darkening of the lower eyelids): allergic salute (upward rubbing of the nose); allergic crease (transverse skin line below the bridge of the nose); sneezing; coughing; itching of the eves. nose. and palate; irritability; and poor appetite. (1) Although diagnostic testing is still utilized, patients today may commence treatment without undergoing any testing. Testing is only indicated if it will alter a practitioner's decision to treat or help to provide more specific treatment. In patients who are refractory to conventional treatment, testing is recommended to provide information for specific avoidance and to function as a guide during the production of immunotherapy serums for administration. (10) In general, a...
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