Originally published: October 2017

Key learning points

  • Seasonal allergic rhinitis is one of the commonest disorders seen in primary care
  • Allergic rhinitis is diagnosed by history and examination, supported by specific allergy tests
  • Topical nasal corticosteroids are the treatment of choice for moderate to severe disease
  • Combination therapy with intranasal corticosteroid plus intranasal antihistamine is more effective than either alone and provides second-line treatment for those with rhinitis poorly controlled with monotherapy

Introduction

Seasonal allergic rhinitis has a high prevalence and is often undiagnosed.1 One of the earliest descriptions is from the beginning of the 19th century.2

The latest British Society of Allergy and Clinical Immunology (BSACI) guideline for allergic rhinitis has just been published,3 making it appropriate to revisit this disease and illustrating some of the guideline facets with a case history.

Case study

Patient D is a 25-year-old, female, non-smoker who presented to the surgery on a bright, breezy, sunny April day. She looked unwell. Her eyes were full of tears, there were dark shadows under them and she was constantly sniffing.

Her symptoms started three or four days previously. She commenced her antihistamine tablets, as she recognised the symptoms from previous years, when they had provided some relief of her symptoms. She had not been sleeping, was feeling tired and was unable to drag herself to work that day. She has one sibling with asthma and another with atopic dermatitis.

She had noticed that she was more breathless than usual with some wheezing from her chest, similar to her sister. On enquiries after any disturbances in eating, she admitted that when she eats apple or celery her tongue tingles and her lips swell for about 15 minutes. She also volunteered that throughout the year she had brief attacks of blocked and runny nose after drinking some wines and eating curries.

Examination revealed Morgan-Dennie lines with deep shadowing. She had a transverse nasal crease. Looking up her nostrils, she had oedema of the inferior turbinates and a fair amount of clear nasal secretion. Her eyes were both pink with conjunctival oedema. Chest examination was clear but her peak flow registered 300l/min against an expected of 450l/min. Two puffs of salbutamol were administered via a spacer device: four minutes later her peak flow reading was 400l/min indicating significant reversal of bronchial obstruction.

The diagnosis was severe intermittent allergic rhinitis with (probable) seasonal asthma. She also had oral allergy syndrome and an element of non-allergic rhinitis.

Treatment options were discussed. The oral antihistamine was obviously not working effectively and she required fairly rapid relief of symptoms. Dymista (MP-AzeFlu) (azelastine hydrochloride and fluticasone propionate), a new treatment that provides rapid onset of action with a high level of symptom relief over a few days, was discussed with her. The possibility of a transient unpleasant taste, which occurs in some users, was also discussed.4,5

Dymista was prescribed and use of the nasal spray was demonstrated. There was specific emphasis on blowing the nose to clear it prior to use, and use of her contralateral hand to insert into the nostril, which directs the tip of the nozzle away from the nasal septum to the lateral nasal wall, which should obviate damage to the septum.

Her eye symptoms were so severe that it was felt that she would benefit from specific topical treatment and she was prescribed olopatidine eye drops, twice daily.

She appeared to have accompanying asthma. Watchful waiting will tell whether this is seasonal. She requested a metered dose inhaler like her sisters. Inhaler technique was demonstrated and checked. This was good and she was prescribed Qvar (beclometasone) inhaler 100mcg two puffs bd with a salbutamol inhaler alongside.6

She was also given a peak flow meter and chart for use over the next couple of weeks, with a clear indication of when she should seek urgent treatment.

It was explained that the likely pollen causing her symptoms is birch because of the effects she has in her mouth when eating raw apples and celery. This is known as the oral allergy or pollen food syndrome and is caused by cross-reacting plant allergens.7

She was also advised not to drink alcohol or eat curries until her symptoms have come under control, as her history suggests that her current problems will be made worse by her elements of non-allergic rhinitis.

She enquired about a course of oral steroids for a few days as she is familiar with this as a treatment option. This is also suggested in the BSACI guideline. However there were concerns about the immediate side-effects that even a short course could bring,8 so it was agreed on the strategy above. She was requested to come back in a week if symptoms were not resolving, but sooner if they deteriorated (especially her asthma symptoms) and in any case to return in two weeks.

She returned in two weeks, looking much improved. She said that her medication was really effective and that she had started to feel human in about three days, when she started to have uninterrupted sleep. She had stopped taking her eye drops as her eye symptoms had resolved, but she was sure to take her Dymista twice daily. Her peak flow had improved dramatically over the course of the first week and was now 475l/min with little diurnal variation.

It was agreed that she would continue with the medications until the end of May when the birch pollen season would be over and at which time, stepping down or off her asthma medication would be considered.

Treatment Options: Simplified

Mild allergic rhinitis (AR)
(symptoms not impacting quality of life)
Oral 2nd generation antihistamine or topical nasal steroidNB: sedating antihistamines eg chlorphenamine, should not be used
Moderate/severe AR
(symptoms impairing sleep, daily activities, work or school performance)
Preferred: fluticasone/azelastineAlternative: topical intranasal steroid (INS) + 2nd generation antihistamine
Eye symptomsOlopatadineAlternative: cromoglycate or nedocromil eye drops
Emergency useShort course of oral steroids

A small number of patients achieve good relief of symtoms with leukotriene receptor antagonists and may be worth consideration.

For those with grass pollen allergy, allergen immunotherapy is an option.

Patients who remain uncontrolled should be referred for specialist assessment.

Common cross reactivities in the UK

Birch pollenApples, celery, cherries, almonds, avocados, bananas
Alder pollenApples, celery, cherries, peaches, raspberries, strawberries
Grass pollenMelons, tomatoes, oranges, peaches
Mugworth pollenCarrots, celery, coriander, pepper

This list is by no means exhaustive. Many of the foods mentioned above can be consumed without symptoms after cooking or processing as the responsible allergens become denatured. Specific IgE tests help little in making a diagnosis. If the symptoms are troublesome a specialist opinion should be sought.

Dr Dermot Ryan is a recently retired GP. He is the immediate past Chairman of the Primary Care Interest Group of the European Academy of Allergy and Clinical Immunology. He is an Honorary Clinical Research Fellow at the University of Edinburgh.

This project was initiated and funded by Teva Respiratory. Teva have had no influence over content. Topics and content have been selected and written by independent experts.

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