by Dr Adrian Morris.
The problem with hay fever and Allergic Rhinitis is that it is considered to be a trivial and inconsequential disease. Symptoms such as runny nose, itchy eyes and nose with sneezing and blockage are obviously not life threatening, but affect up to 25% of the population and are the cause of significant disability and cost to society. Patients may also experience fatigue, irritability, as well as mood, cognitive and sleep disturbance in addition to the nasal, ocular and throat symptoms. Allergic rhinitis has important co-morbid associations such as chronic sinusitis, glue ear, asthmatic exacerbations, nasal polyps, sleep disturbance and dental malocclusion.
Chronic allergic Rhinitis sufferers often have typical facial features called the “allergic facies”. Nasal blockage and venous congestion predispose to the bluish discolouration of the lower eyelids called “allergic shiners”, the characteristic linear creases under the eyelid are referred to as “Dennes lines”. Constant nasal rubbing typifies the “allergic salute” and results in a prominent “nasal crease” across the nose. Continuous nasal blockage causes “nasal” speech and mouth breathing with disturbed sleep. This results in a high arched palate and the “long face syndrome” with dental crowding and malocclusion.
Allergic rhinitis may be either seasonal or perennial:
Seasonal allergic rhinitis is better known as “hay fever”.
Tree and grass pollens and some fungi trigger seasonal allergic rhino-conjunctivitis during Springtime and early Summer (March to June). Patients experience intense nasal itch with explosive sneezing, watery eyes and nose and itchy palate and ears with profuse nasal drip. These people do not develop the typical “allergic facies” but have seasonal puffiness of the eyes and eyelids with associated nasal swelling.
Perennial allergic rhinitis or a “permanent cold”.
Allergens such as house-dust mites, cat and dog dander, horsehair, cockroach and perhaps hamster or rabbit allergen result in perennial allergic rhinitis with symptoms all year round. These patients are often misdiagnosed as having a permanent cold and receive inappropriate treatment with antibiotics. Their symptoms can be very subtle and include constant nasal blockage, snoring, watery postnasal discharge, loss of taste and smell sensation and sneezing only on waking in the morning. Coexistent glue ear and chronic sinusitis with polyps is a common feature.
In 1999, the World Health Organisation introduced a new nomenclature for Allergic Rhinitis (ARIA Guidelines). The purpose was to try and create similar treatment guidelines for asthma and allergic rhinitis which often co-exist in the same patient (80% of asthma sufferers have concomitant allergic rhinitis). Instead of the traditional seasonal and perennial divisions, they introduced Intermittent Allergic Rhinitis and Persistent Allergic Rhinitis types. Intermittent would replace the Seasonal (Hayfever) type disease and Persistent would replace Perennial (but some overlap does take place). These are then further sub-divided into Mild and Moderate/Severe symptom complexes and treated accordingly.
Allergic rhinitis occurs in atopic youngsters usually with raised blood levels of the IgE antibody to the common inhalant allergens such as house dust mites, tree and grass pollen, animal dander, cockroach droppings and mould spores. Occasionally foods such as milk, egg, wheat and soya can cause sensitisation. Children are sensitised in early life but may only manifest their allergy symptoms later in life. Perennial allergic rhinitis usually manifests before the age of 10 years, while seasonal allergic rhinitis occurs more commonly in young adults. Primary sensitisation results in specific IgE antibodies, which later cross-link with allergens on mast cell in the tissues, releasing histamine the acute phase mediator. As the condition becomes more entrenched as in chronic perennial rhinitis, then other inflammatory mediators and cells become involved.
The allergic reaction in the nose involves a complex interaction between inhalant allergen and multiple effector cells. An allergen will attach to specific IgE bound to mast cells near the mucus membrane surface, resulting in histamine release. This is termed the Immediate Nasal Reaction. Other mast cell mediators include tryptase, kinins and prostaglandin D2. Histamine has a direct effect on blood vessel H1 and H2 receptors causing oedema and nasal obstruction. It also has a reflex effect via sensory parasympathetic nerve pathways causing sneezing, itching and hypersecretion. This triggers sequential sneezing followed by discharge and finally nasal blockage.
Subsequent nasal symptoms that develop between 3 and 10 hours after allergen exposure are due to the Late Phase Reaction. This is associated with further inflammatory mediator production in the mucous membranes of the nose (Prostaglandins and Leukotrienes) and eosinophil plus basophil infiltration with increased nasal blockage.
Nasal hypersensitivity occurs when non-specific irritants such as dust, perfume, tobacco smoke, ozone, sulphur dioxide, nitrogen dioxide, cold air and other environmental pollutants result in increased nasal mucous membrane permeability, increased nerve ending excitability, eosinophil infiltrates and more superficial distribution of mast cells in the nasal membranes. These factors lead to enhanced nasal responsiveness to negligible aeroallergen and histamine challenge and amplify the nasal inflammatory reaction. Some older anti-hypertensive medications such as reserpine, methyldopa, ACE inhibitors and alpha-adrenoceptor blockers as well as hormone replacement therapy may in addition cause nasal obstruction. Even the last trimester of pregnancy is associated with worsening of rhinitis symptoms. While aspirin sensitive individuals will often present with rhinitis, sinusitis and nasal polyposis after aspirin re-exposure.
We try to initially identify the allergen involved by means of a good clinical history and a thorough examination of the nose. We then try to confirm the allergy with Skin Prick Testing or blood tests such as specific IgE levels using the Cap RAST testing system.
Simple rhinoscopy or nasal examination using an otoscope will demonstrate pale bluish swollen nasal turbinates and a mucoid discharge and occasionally evidence of polyps.
Skin Prick Tests for the common inhalant allergens are a very simple and cheap to perform with results being immediately available. Allergen test kits are available from ALK-Abello and Allergy Therapeutics. These include extracts of House-dust mite, Cat, Dog, Grass and Tree Pollen. They help to confirm the causative allergen and the “weal and flare” reaction is useful to demonstrate the inflammatory nature of allergic rhinitis to the patient. Blood specimens can be drawn and sent to a pathologist for RAST testing. The Phadiatop is an excellent screening test for the common inhalant allergens implicated in allergic rhinitis, if this test is positive, individual UniCAP RAST tests are performed to determine the exact inhalant allergen. If food allergy is strongly suspected in children, the Paediatric Food Mix fx5 food screen (cow’s milk, wheat, egg, peanut, fish, and soya) is a recommended. Total IgE may often not be elevated in allergic rhinitis, unless there is associated asthma or eczema. Parasitic infections and cigarette smoking may also confuse the issue by elevating serum IgE in both atopic and non-atopic individuals.
A useful side-room test in allergic rhinitis is to take a nasal mucus smear for eosinophil estimation using Hansel’s stain. If sheets of eosinophils are present, this confirms the diagnosis of allergic rhinitis.
Radiology (plane x-rays and CT scanning) does not assist in the diagnosis of allergic rhinitis, but will identify complications such as sinusitis, infections, polyps and sinus effusions.
Nitric oxide (NO) levels in exhaled air from the nasal passages tends to be raised in allergic inflammation. This test is a useful measure of the degree of allergic inflammation, particularly in persistent rhinitis.
Specialist ENT’s may make use of nasal endoscopes to assess the turbinates, septum and osteo-meatal complex of the paranasal sinuses. Rhinomanometry a measure of nasal expiratory flow, nasal provocation tests with histamine and microscopy of nasal mucus specimens is only really of use for research purposes.
In a minority of patients with all the symptoms of nasal allergy, all allergy tests prove negative. We refer to these sufferers at having Chronic Non-allergic Rhinitis or Idiopathic Rhinitis. They are treated in a similar fashion to Allergic Rhinitis using the ARIA Guidelines. Some have a profuse symptoms with eosinophil cells present in their nasal mucus and this condition is termed Non-allergic Rhinitis with Eosinophilia Syndrome (NARES).
Once the offending allergen is identified, then Allergen Avoidance measures can be instituted. Grass pollens can be avoided, pets removed from the home and mattresses, pillows and carpets treated to eradicate house dust mites. If a particular food is implicated in allergic rhinitis, then that food should be excluded from the diet. Cigarette smoking should be strongly discouraged in all allergic individuals, as it will only exacerbate symptoms. Where allergen avoidance fails or is impractical, it may be necessary to commence medication to control symptoms and inflammation.
In Perennial Allergic Rhinitis, treatment should to be taken continuously, whilst in Seasonal Allergic Rhinitis treatment only need be taken for symptom control during the peak pollen season.
Antihistamines are the mainstay treatment in seasonal allergic rhinitis. They control the itch, sneeze runny nose and itchy eyes. Older antihistamines such as chlorpheniramine (Piriton) control symptoms, are cheap but have significant sedating side effects. The newer non-sedating antihistamines are more expensive, cause much less psychomotor disturbance, can be taken once a day and give good symptom control. Loratidine (Clarityn), desloratidine (Neoclarityn), fexofenadine (Telfast), Mizolastine (Mizollen) and cetirizine (Zirtek), or levocetirizine (Zyzal) are recommended.
Topical antihistamines such as levocabastine (Livostin) and azelastine (Rhinolast) have been marketed and seem to be a useful adjunct when symptom control of nasal and ocular itching is intractable. They have no effect on nasal blockage and tend to have an unpleasant taste.
Local administration of corticosteroids to the nasal mucosa has revolutionised the treatment of allergic rhinitis -particularly the perennial type. They control the underlying chronic inflammatory process and therefore are the treatment of choice in most patients. These preparations are safe to use for prolonged periods of time at the recommended dosages. They act on various components of the inflammatory cascade, causing vasoconstriction, reducing vascular permeability and decreasing tissue macrophage and eosinophil numbers. Nasal steroids such as Flunisolide (Syntaris), Budesonide (Rhinocort Aqua) and Beclomethasone (Beconase) are particularly useful for their prophylactic effects and newer preparations such as Fluticasone (Flixonase), Triamcinolone (Nasacort) and Mometasone (Nasonex) can be used effectively on a once daily basis
Betamethasone (Betnesol) drops may have some systemic absorption and should not be used continuously for more than 10 days. Once symptom control is achieved, the daily dosage can be slowly reduced. Intranasal steroids also control non-allergic rhinitis and reduce the size of polypoidal lesions in the nose. Occasionally they may cause local nasal irritation and nose bleeds. They do not relieve palatal and ocular itch, so antihistamines may need to be co-prescribed. If significant nasal obstruction is present at commencement of treatment, then pre-treatment with topical decongestants will be necessary.
Decongestants may be used topically or orally for relief of nasal blockage and congestion. Topical decongestants relieve nasal congestion very rapidly but over-use of Ephedrine is associated with rebound nasal congestion and so-called “rhinitis medicamentosa”. The safest preparations are Oxymetazoline (Dristan) and Xylometazoline (Otrivine) but continuous use should be restricted to 7 – 10 days at a time.
Oral decongestants such as pseudoephedrine (Sudafed and Galpseud) also combat nasal blockage by constricting blood vessels in the nasal mucosa and throughout the body to some degree. They therefore may exacerbate hypertension, dry mucus membranes, cause bladder neck obstruction and glaucoma. Some people are also sensitive to them and experience insomnia, restlessness, headache and palpitations.
The decongestant often compensates for the sedative effect of the anti-histamine although this may result in the side effect of jitteriness and insomnia
Cromolyn in the form of sodium cromoglicate (Rynacrom) has anti-inflammatory activity and relieves nasal itch, sneezing, hypersecretion and congestion particularly in seasonal allergic rhinitis. It is a particularly safe product but must be applied 4 times a day, and is also very effective in the eyes for treating allergic conjunctivitis. Cromolyns are a useful option for patients who are resistant to or prefer not to use topical steroids on an ongoing basis. A new Mast cell stabiliser/antihistamine eye drop called olopatadine (Patanol) is proving very effective if used twice daily.
Ipratropium bromide (Atrovent and Rinatec) is an anticholinergic agent derived from atropine. It provides good relief from profuse watery rhinorrhoea including non-allergic or vasomotor rhinitis, a particular problem in older males with the so-called “old man’s drip”. Ipratropium is very safe to use, with rapid onset of action and minimal side effects. It has no effect on nasal blockage, itch or sneezing.
A systemic steroid such as prednisilone is particularly useful in controlling nasal symptoms in allergic rhinitis and gives rapid relief especially when blockage is severe and intractable. They have significant systemic side effects and should therefore only be used in severe disease for short periods of 5 to 14 days. Use of injectable depot steroid (Depot Medrone, Kenalog) should be discouraged as they can lead to osteoporosis, muscle atrophy, hypertension, diabetes mellitus, glaucoma, cataracts, gastric ulceration and chronic infections.
Injection Desensitisation Immunotherapy is an effective option in severe grass pollen and Birch allergic rhinitis, which are not controlled by medication. It should be restricted to those patients who are mono-sensitised to Grass and Birch pollen or house dust mite. Potential systemic reactions such as urticaria and anaphylaxis during treatment, restrict its use to specialist units with readily available resuscitation equipment. The course of injections should be commenced before the tree or grass pollen season and usually take 3 years to complete. For many years, ALK have marketed the highly standardised Alutard SQ range of desensitising products. At present only grass pollen desensitisation is undertaken in the UK. Sublingual Immunotherapy (SLIT) given as oral drops is currently undergoing evaluation and results so far are very promising (Stallergenes and ALK Abello vaccines).
Normal saline douching with a touch of bicarbonate of soda added is a useful non-drug treatment for clearing the nasal passages in allergic rhinitis. It is important to use “physiological” saline for if the solution is hyper- or hypotonic, nasal mucosal damage may occur. The solution is sniffed up using a tea saucer and then expelled from the nose. Commercially available saline nasal sprays include “Sterimar” Menthol nasal preparations also give some symptom relief while steam inhalations using Eucalyptus extract will help decongest the nasal passages. Application of a small amount of Petroleum Jelly (Vaseline) to the nasal membranes with a cotton bud also helps to relieve symptoms
There is a growing demand by the general public for alternative therapies to conventional medication. These treatments are much less effective than conventional medication, but certain compounds may have some beneficial effects in allergic rhinitis. More recently the herb Butterbur was shown to have some beneficial effects. It must be stressed that these preparations give minimal therapeutic benefit and should only be offered as second line treatment to conventional rhinitis medication.
Antioxidants are particularly popular in the lay press and are aggressively marketed by manufacturers as “cure all’s”. Vitamin C, Vitamin E, Beta-Carotene, Selenium and Zinc are included in this category. There is no good evidence that these products have any beneficial effect in treating allergic rhinitis. N-acetyl cysteine (Solmucol) also a mucolytic with respiratory antioxidant activity may be of some limited benefit when used in combination with conventional treatment. Other mucolytic medication such as carbocisteine, which is used in Cystic Fibrosis, is often co-prescribed in allergic rhinitis, where it has little or no therapeutic value.
The leukotriene antagonists Zafirlukast (Accolate) and Montelukast (Singulair) seem to be useful additions in treating allergic rhinitis, especially in aspirin-sensitive people. These products also seem to have beneficial effects in treating patients with asthma and co-existent allergic rhinitis as they also block the inflammatory action of Leukotrienes in the nasal mucosa. Olopatadine (Patanol) is very effective for ocular allergies associated with hay fever. This eye drop has both antihistaminic and Mast Cell stabilising properties and has a simple twice daily dosage.
Role of dietary restriction
Some people will benefit from empirical dietary exclusion of common food allergens such as cow’s milk, hen’s egg, citrus, alcohol and wheat in their diet. This is often tried in patients who have intractable symptoms and don’t respond to other measures. The offending food should be excluded for a 4-week period to adequately evaluate any beneficial response. The advice of a qualified dietician should be sought if a prolonged exclusion diet is instituted. Food additive such as sodium benzoate, tartrazine and nitrites have also been implicated as triggers for chronic non-allergic rhinitis and avoidance may benefit up to 8% of rhinitis sufferers.
Probably the greatest hurdle facing those entrusted with treating perennial allergic rhinitis, is that of non-compliance. Unfortunately most people will automatically stop treatment as soon as they experience some relief, only for the symptoms to return. It is particularly difficult to persuade patients to continue to take medication as a preventative measure in controlling hay fever and allergic rhinitis. Remember that Enzyme Potentiated Desensitisation (EPD) is ineffective and not recommended for hay fever treatment.
Finally our top 11 simple measures to combat your hay fever!
- Remain indoors when pollen levels peak and when the grass in being cut.
- Take antihistamines starting two weeks before the pollen season starts.
- Apply a little Vaseline to the lower nostrils to protect and trap pollen grains from entering the upper nose.
- Wash or douche the nasal passages with a dilute salt water solution or use commercial saline sprays available from all chemists (Sterimar).
- When travelling, make sure the car windows are closed and switch on the air con which will filter out pollen grains.
- Wear protective “wrap around” sunglasses to prevent allergic eyes.
- Keep the bedroom windows closed during the day to keep pollen grains out.
- Rather tumble dry washing and do not hang washing outdoors during the day (it acts as a pollen trap).
- Shower and wash your hair in the evening as soon as you return home from work or college to remove all pollen.
- Change into fresh clothes as soon as you return home from work (pollen will have become trapped in your clothes).
- Consider taking a teaspoonful of local honey everyday starting a few months before the pollen season starts – this may act as a form of oral desensitisation (the honey will have been contaminated with pollen)
Copyright Dr Adrian Morris
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