Seasonal and perennial rhinitis share many of the same symptoms; however, seasonal rhinitis often presents with less itching while perennial rhinitis presents more frequently with obstruction. Patients with both types of rhinitis primarily present with nasal symptoms of rhinorrhea, sneezing, and congestion. On physical examination edematous, blue-red nasal turbinates may be appreciated. Coughing and wheezing may accompany nasal symptoms, especially if the patient suffers from asthma. Nasal congestion can progress to chronic congestion, increasing the risk of otitis media in children. Additionally itching of the mouth and nose is common. Itchy eyes may be accompanied by injected conjunctiva and edematous eyelids. Sinus obstruction can progress to sinusitis and facial pain.

The only proven method of diagnosing allergic rhinitis is through skin prick testing or in vitro IgE evaluation. No other patterns, signs or symptoms reliably identify the condition. The absence of some findings does not exclude allergic rhinitis. Physical exam of the nose is recommended and will typically shows edematous, blue-red or pale nasal turbinates and clear nasal secretions. Nasal polyps in children are an indication of cystic fibrosis. Once allergic rhinitis is high on the differential then a trial of therapy is often recommended. Intranasal corticosteroids or oral antihistamines are often sufficient to relieve symptoms. The severity of allergic rhinitis is subjective. Patient reported reduction of symptoms or improved quality of life is sufficient to determine the success of treatment. If symptoms do not respond to treatment or if the symptoms are too aggressive then allergy testing is recommended. There are two methods of allergic testing, IgE analysis in vivo or skin prick testing. In vivo IgE testing is more expensive but also more readily available and less invasive than the skin prick testing which is more specific and sensitive. In vivo IgE testing is recommended for patients with eczema or with patients taking medications with antihistamine properties (tricyclic antidepressants). A test panel usually includes common antigens (dust mite feces, pollen, molds, and certain foods) and geographically significant allergens. Test results can be used to direct environmental modifications and medical treatment.

There are two types of treatments: environmental and medical. Environmental treatment includes removal or avoidance of the allergen. This can entail elimination of dust mites and the use of special bed covers, pillow covers, avoidance of certain foods, first and second hand smoke, incense, and removal of cockroaches or unfortunately, pets. Special equipment and techniques can be used while house cleaning or performing yard work to prevent exposure including HVAC filters and face masks. There are several medications available to treat rhinitis, both oral and topical. Intranasal topical corticosteroids, oral and topical antihistamines, and a1-adrenergic receptor agonists are all very effective at treating symptoms. A-1 adrenergic agonists act as decongestants but when used for prolonged periods of time they can damage the mucous membranes and increase inflammation in what is called the rebound effect. The anticholinergic symptoms of antihistamines can be mitigated by taking them at night, before bed. Often a combination of these medications is most effective at providing relief. Intranasal administration is the preferred method of administration because there are fewer systemic side effects. Additional treatments are under review for the treatment of allergic rhinitis including medications that bind immune modulators (montelukast blocks leukotriene) or IgE directly (omalizumab). Intranasal saline spray and neti pots may relieve some symptoms and mobilize thick nasal secretions. Kits are available over the counter, but solutions can be formulated at home as well. Any water used for these therapies should be boiled to neutralize bacterial contaminants. Desensitization immunotherapy is a long term therapy that attempts to slowly introduce specific antigens to the body in higher and higher concentrations over time. In theory this will reduce the IgE response that is responsible for allergic rhinitis and enhance the IgG response. This is an invasive therapy requiring several injections administered annually over the course of several years. Other treatments may be more effective and less expensive.

The symptoms of allergic rhinitis are treatable with few side effects; however, they will reappear after every antigen exposure. Patients suffering from seasonal allergic rhinitis may be asymptomatic for several months and only have symptoms a few months out of the year, especially in the summer or spring when allergens such as pollen and molds are prolific. Perennial sufferers will have symptoms most days of the year.

Though perennial allergic rhinitis is not considered a serious condition, its symptoms can reduce the quality of life. Symptom severity may wax and wane depending on the type of antigen, amount of antigen, and state of the immune system. There are documented cases of patients outgrowing the condition entirely. Especially severe symptoms may result in missing work or school time. A severe outbreak may trigger other autoimmune conditions such as asthma, eczema, and sinusitis. Additionally, this may lower the threshold to upper respiratory tract infection.
A major consideration of medical treatment, especially first and second generation anti-histamines, is anticholinergic side effects, such as drowsiness. Hives and rash occasionally accompany other methods of treatment including immunotherapy or allergy shots. These treatments may improve symptoms in about two-thirds of patients but they also require years of treatment before results are noticed.

At this time, the cause of allergic rhinitis is not known. Research is currently underway to determine if the etiology has a genetic component or a developmental component or if it is a combination of both. While studying the genetic component of rhinitis researchers are analyzing similar conditions, such as atopic disease, and family histories. Atopic diseases demonstrate characteristics similar to allergic rhinitis and have been linked to genes on many different chromosomes. The signs and symptoms are likely the result of these genes working in combination with environmental variables. Also multiple generations often have atopic disease, implying a significant genetic component. Additionally, the risk of development of atopic disease in the absence of parental history is 13%, but that risk increases to 29% if one sibling has a history of atopic disease, and 47% if both parents have a history of atopic disease [7]. The “hygiene hypothesis” describes the developmental component of allergic rhinitis. This hypothesis implies that the cleanliness of the developed world, especially in the vicinity of the very young, prevents interaction with antigens from animals, microorganisms, and other antigens in the environment during key times of development [8].

The Australian National Health Survey of 2004-2005 showed approximately 16.1% of the population (3.2 million people) self-reported symptoms of seasonal and perennial allergic rhinitis. The age group most affected was found to be between 25-34 years with a slightly higher prevalence in females (1.7 million) compared to males (1.5 million). However, the exact prevalence of the disorder is difficult to calculate because most people do not seek treatment and the condition is under reported.

Allergic reactions, or hypersensitivity reactions, are classified into four groups. Allergic rhinitis is a type 1 hypersensitivity reaction, meaning the response is primarily mediated by antibodies and mast cells.

Before an allergic reaction can occur the body must be sensitized. In hypersensitivity type 1 reaction an antigen must first enter the body and interact with the receptors on the outside of a mature inactivated B cell. This first reaction is slow as cells mature, undergo somatic hyper mutation, and start upregulating antibody production. Under the right conditions a B cell will become activated and form antibodies to a very specific epitope of the antigen. Subsequently IgM antibodies will switch class to produce many IgE antibodies. These IgE antibodies become attached to mast cells by their Fc region leading to sensitization. If the immune system interacts with that antigen again the adaptive immune response will be rapid, taking moments to release immune modulators [9] [10].

The time course of an allergic reaction is divided into two parts: early-phase and late phase. The early-phase involves the rapid release of preformed mediators that are stored in mast cells. Mast cells are found in the skin and mucous membranes with higher concentrations around nerves and blood vessels. Histamine is the main inflammatory signal molecule. Other molecules include heparin, tryptases, kinins, and chymases [10]. These molecules are held in an inert granular form. They are rapidly released during the process of degranulation which occurs when the membrane bound IgE antibodies bind to an antigen, crosslink, and send a signal to the cell. IgE binds both exogenous peptides and carbohydrates [9]. Other molecules are then synthesized by the mast cells including prostaglandin D2 and leukotrienes. The result of the rapid release of these immune modulators are the symptoms associated with allergic rhinitis. They stimulate mucous glands to increase secretion, increase vascular permeability which results in localized edema, and stimulate dilatation of the vasculature leading to congestion. Certain nasal nerves are also stimulated which results in sneezing and itching sensations. A majority of these signaling molecules are focused on the nasal mucosa. However, as the molecules circulate throughout the body systemic symptoms are also possible and include fatigue, malaise, and sleepiness.

The late-phase immune response forms over several hours. Inflammatory cells are drawn to the nasal and nasopharyngeal mucosa by chemo attractants and cytokines released as part of the allergic chemical cascade. Eosinophils, lymphocytes, and neutrophils accumulate in the mucosa and continue to release immune modulators. Whereas an early-phase response is characterized by sneezing and itching, the late-phase response is characterized by congestion and mucous production and can last from hours to days.

Once a patient is sensitized to an antigen the most effective strategy to prevent symptoms is to minimize exposure. Prophylactic medication such as antihistamines is also effective when taken as a single dose before bedtime prior to antigen exposure. This method may prevent an exacerbation before it starts. Patients with perennial allergic rhinitis should limit their exposure outdoors during the heavy pollen season, especially during the early morning and just before sunset, when the pollen count is usually highest. House cleaning should be completed in a way so as to prevent excessive airborne dust. It should also be performed regularly to minimize buildup. Dust is composed of a variety of antigens such as human skin, dust mite feces, animal dander, cockroach feces, etc. Any one of these antigens can result in allergy symptoms and must be removed regularly.

Rhinitis is an inflammatory response of the mucous membranes in the nose and nasopharynx. The most common type is allergic rhinitis. It affects about 20% of the population worldwide. In allergic rhinitis the immune system over responds to an environmental trigger. House dust,animal dander, dust mite fecal matter, industrial particulate matter and fumes may trigger this response. It is primarily characterized by congestion and itching of the nose, sneezing, watery nasal discharge (rhinorrhea), and watery itchy eyes [1] [2]. Other mucous membranes lining the ears, Eustachian tubes, conjunctiva and sclera of the eyes, sinus cavities, and throat may also be inflamed. These symptoms are also associated with hay fever and seasonal rhinitis. While hay fever is seasonal, perennial rhinitis lasts all year round. Complications are rare but have the potential to significantly impair quality of life [3] [4]. It is estimated that allergic rhinitis costs 5.3 billion annually [5]. A retrospective analysis of allergic rhinitis has indicated that the condition increased individual health care costs by $1500, increased the number of prescriptions by an average of nine and increased office visits by an average of three [6].

What is perennial allergic rhinitis?
Perennial allergic rhinitis is an autoimmune hypersensitivity reaction to an otherwise benign compound. It is similar to hay fever. While hay fever is a seasonal disorder perennial symptoms last all year round. Symptoms usually consist of a combination of nasal congestion, runny nose, itchy and watery eyes, sneezing and sinus pressure. An exacerbation can be minimal or can greatly affect quality of life, leading to missed work or school. Other symptoms include cough, decreased sense of smell.

What causes allergic rhinitis?
People occasionally become hypersensitive to benign compounds found in the environment. Special cells called mast cells, are covered with receptors. Many of these mast cells line the tissue of the nose and release chemicals, such as histamine, when they are activated. Materials such as dust, tree pollen, and animal dander are the most common compounds. When the body interacts with these compounds symptoms develop and can stay active for hours even after the offending compound is removed. Most hypersensitivity reactions have a genetic component and the condition affects multiple generations.

How is allergic rhinitis diagnosed?
This condition can be diagnosed clinically followed by a treatment of medication and evaluation of symptoms. Definitive diagnosis is made with a blood test to evaluate antibodies or by a skin prick test. In the skin prick test a patient is pricked with a small dose of allergen and monitored for a response, usually swelling and redness. Many allergens can be tested at the same time.

What is the treatment for this condition?
There are many treatments available for perennial allergic rhinitis. Removal of the offending material is effective, but sometimes that is impossible. When considering treatment, topical treatment is preferred over oral medications. Topical treatment has fewer side effects. Medications can treat the symptoms associated with allergic rhinitis. Antihistamines treat most symptoms but are associated with drowsiness. Decongestants are useful to improve airway circulation and relieve sinus pressure. Eye drops can reduce eye itching and redness. Occasionally, patients grow out of this condition and do not require treatment or medications. Allergy shots are an alternative treatment and involve periodic injections of allergens to knockdown the allergic immune response.

How can rhinitis be prevented?
Unfortunately there is no way to prevent allergic rhinitis. Symptoms can be mitigated with the use of modifications to the environment, medication, or allergy shots.

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