Helping your patients cope with hay fever
The hay fever season is approaching its grass-pollen peak in mid-June. Allergy expert Professor Barry Kay reveals the latest advances in treatment of this seasonal bugbear.
With a growing range of remedies available over the counter and more treatment options than ever, there has probably never been a better time for the 15 to 20 per cent of the UK population cursed with hay fever.
It (seasonal allergic conjunctivorhinitis) is caused by allergy to the soluble substances that leach out of grass pollen grains when they impact the mucous membrane of the nose and eyes.
About 25 per cent of sufferers are also allergic to tree pollens, especially birch.
In the UK 35 per cent of hay fever sufferers are 13- to 14-year-olds. Most sufferers have their 'really bad days' at the height of the summer when vast clouds of grass pollens become airborne (see chart of peak pollen counts from the National Pollen Research Unit).
Grass pollen counts are usually very high on warm, dry, sunny days and fall during cold and wet periods. Counts of 50 grains per cubic metre usually cause symptoms in susceptible people, and a few very unlucky people will respond to concentrations as low as a single grain per cubic metre.
The diagnosis of seasonal hay fever is usually straightforward and consists of a history of sneezing, rhinorrhoea (runny nose), nasal blockage, itching of the soft palate, nose and eyes, watering of the eyes and, in some subjects (especially when the pollen counts are very high), wheezy breathlessness with tightness of the chest (seasonal allergic asthma).
The diagnosis can be confirmed by 'skin-prick tests' using extracts of pollen allergens.
Treatment of hay fever
The principles of treatment of hay fever, as of all allergic diseases, are allergen avoidance, anti-allergic drugs and hyposensitisation (also called desensitisation or allergen-specific immunotherapy).
Avoidance of airborne pollen is clearly difficult but simple measures can help. These include staying indoors, wearing wrap-around sunglasses when outdoors and installing pollen filters in the car and/or the home.
Drug treatment of seasonal rhinoconjunctivitis should be managed in a stepwise fashion, depending on the severity of symptoms. The effect of different classes of drugs on the various symptoms of hay fever is shown in table 1. There have been no recent advances of note in drug treatment, although more preparations are available over the counter and these are listed in table 2. OTC medication now includes the more potent nasal corticosteroid fluticasone.
The so-called 'third-generation' antihistamines – such as levocetirizine, desloratidine and fexofenadine – are only available on prescription and do not have any particular advantages over the second-generation selective and non-sedating antihistamines. They do offer an alternative but 'head-to-head' comparisons with established second-generation drugs are lacking.
Sensible advice by pharmacists is probably all that is required for the vast majority of sufferers with mild intermittent, mild persistent and even moderate persistent symptoms.
Mild intermittent symptoms
Most patients experience only mild intermittent symptoms. For these, oral or topical antihistamines are the mainstay of treatment. It is difficult to justify use of the non-selective, first-generation antihistamines, such as chlorpheniramine, with their attendant unwanted effects.
The antihistamines of choice are the newer selective and non-sedative preparations, which do not have significant interactions with other drugs and are virtually free of side-effects when administered orally.
A small minority of individuals do, however, have some mild drowsiness even with the second-generation antihistamines.
Topical administration of antihistamines to the nose and eyes is an attractive alternative to orally administered therapy because of their rapid onset of action – about 15 minutes.
Chromones such as sodium cromoglycate applied nasally or to the eyes are particularly safe and moderately useful but have to be applied four times a day and have a slower onset of action than topical antihistamines.
Oral antihistamines take effect after one to three hours and relieve eye symptoms, runny nose and sneezing but have little effect on nasal blockage.
When nasal blockage is the predominant symptom, intermittent topical application of decongestants can be tried for a few days, although rebound symptoms are a problem if continued for too long.
If allergen avoidance and the intermittent use of antihistamines and decongestants are insufficient to control persisting symptoms, then anti-inflammatory therapy should be started. Topical nasal steroids are the single most effective treatment for allergic rhinitis. They improve all nasal symptoms including nasal blockage. They are of some use for ocular symptoms and in this respect are as good as oral H1-antihistamines.
Nasal steroids are usually effective after a few days and should be stepped up and down according to symptoms, which in turn are related to the pollen counts.
Adverse effects include transient sneezing, stinging (with flunisolide), haemorrhagic crusting and dryness. Retardation of growth in children remains an issue but is unlikely to be a problem when nasal steroids are used for only a few weeks a year.
Topically applied nedocromil sodium is another option for controlling symptoms of allergic conjunctivitis. The advantage of non-steroidal chromones is their lack of any significant unwanted effects, and therefore their safety in children and in pregnancy.
In general, topical corticosteroids should be reserved for patients who have not responded satisfactorily to either oral or nasal antihistamines or chromones, or topical antihistamines or chromones for eye symptoms.
Nasal steroids are valuable for the treatment of nasal blockage, which can be one of the most debilitating rhinitic symptom. As with other anti-inflammatory drugs, treatment is best given on a regular basis and the initial management of nasal blockage may require use of topical decongestants.
This ensures rapid relief of symptoms and enables the topically applied corticosteroids to reach the inflamed nasal mucosa. Patients who regularly suffer moderate to severe hay fever symptoms during the grass and/or tree pollen season greatly benefit from topical corticosteroid therapy started one to two weeks before the pollen season. This has been shown to prevent influx of inflammatory cells into the mucosa, thus abolishing nasal priming.
The use of once- or twice-daily topical corticosteroids seems to be remarkably free of significant unwanted effects but, as with all corticosteroid therapy, their use must be matched to the severity of the clinical symptoms.
Severe persistent hay fever is disabling and requires urgent and effective treatment. In the short-term the most useful therapy is oral prednisolone in a dose of 30mg daily for up to two weeks. Improvement can then usually be maintained with topical corticosteroids, administered two or even three times daily.
Depot preparations of corticosteroids are not recommended since this is more likely to cause adrenal suppression and doses cannot be tailored to meet individual requirements.
Immunotherapy is reserved for sufferers who have not responded to maximum pharmacotherapy. The treatment course consists of increasing doses of standardised pollen extract given once or twice a week for eight to 10 weeks (the induction course) followed by two-weekly and then monthly injections (the maintenance course) for up to three years.
Patients have to wait for at least 60 minutes after each injection. This form of treatment must be given in specialised centres by trained allergists and where resuscitative facilities are immediately on hand.
The common side-effect of desensitising injections is general anaphylaxis, but this complication is easily recognisable by the skilled person and immediately reverses after intramuscular adrenaline.
Oral medication should be avoided during pregnancy, particularly during the first trimester. In general only intranasal chromones or topical steroids should be used.
Barry Kay is head of the department of allergy and clinical immunology, Imperial College London, National Heart and Lung Institute