Chapter 80: Allergic disorders including hay fever

Allergic disorders affect approximately 20% of the population. The clinical spectrum of allergic disorders includes asthma, rhinitis, atopic dermatitis, drug allergy, food allergy, insect sting allergy and anaphylaxis.¹ The most common allergies are those associated with IgE-mediated (immediate or type 1) hypersensitivity, such as allergic rhinoconjunctivitis (hay fever), atopic dermatitis (eczema) and allergic asthma.²

Less commonly encountered but of increasing clinical importance in the community are IgE-mediated allergies to foods such as peanuts and/or other nuts and seafoods (crustaceans or molluscs), which may cause urticaria, angioedema, anaphylaxis and even death. Peanuts are one of the most common causes of food-induced anaphylaxis in adults. A clinically significant cross-reactivity between peanuts and other legumes is uncommon, but allergy to tree nuts such as almonds and walnuts may occur in up to 50% of those with peanut allergy.¹ Another special case is the oral allergy syndrome, in which people with some degree of seasonal allergy to grass pollens or birch pollen suffer oral itch and swelling when they come into contact with certain fruits. This problem may be alleviated by desensitisation to pollens.¹

Natural rubber latex allergy is an increasingly important cause of type 1 hypersensitivity, affecting particularly medical and paramedical personnel, and patients who have had multiple operations or procedures. Diagnosis is suggested by history and confirmed by specific skin tests or the detection of serum-specific IgE. The development of urticaria on contact with latex is highly suggestive of underlying type 1 hypersensitivity. An interesting association between latex allergy and sensitivity to fruit occurs most commonly with banana, kiwifruit or avocado.¹

Atopy occurs in those 45% of the population who have an inherited tendency for an exaggerated IgE antibody response to common environmental antigens.² It is not a disease. There will be a positive response to one or more allergen skin-prick tests and usually a family history of allergic disorders. Of those who are atopic, one-half to one-third manifest an allergic disorder, most commonly allergic rhinitis, asthma, atopic dermatitis or allergic gastroenteropathy.

It is helpful to consider important allergen exposure during history taking. TABLE 80.1 lists sources of common allergens.

Inhalant allergies

Allergic rhinoconjunctivitis and asthma are the main manifestations. The history provides a strong pointer to the causative allergen. If symptoms are seasonal, pollen allergy is most likely; perennial symptoms may indicate an allergy to dust mites, household pets or moulds. Certain activities that precipitate symptoms may also provide a clue—these include mowing lawns, dusting and vacuuming.

Food allergy usually manifests in infancy and childhood, with symptoms ranging from severe urticarial-type reactions to gastrointestinal symptoms such as anorexia, nausea, vomiting and spitting up of food, colic, diarrhoea and failure to thrive.

Commonly implicated foods include milk and other dairy products, eggs and peanuts. Other foods include oranges, soy beans, nuts, chocolate, fish, shellfish and wheat.

The allergic reactions are not to be confused with non-immunological food intolerances such as lactose intolerance.

A food intolerance is an adverse reaction to a specific food or food ingredient. It is regarded as a food allergy if the reaction is immune based. Food allergies can be simply classified as:

• immediate reactions—occurring within 2 hours

• delayed reactions—occur up to 24 hours after ingestion

IgE-mediated food reactions³

These are immediate immune-mediated responses to a foreign glycoprotein which are relatively easy to diagnose.

Clinical features

• Typically in infants and toddlers

• Usually occur within 30–60 minutes

• Due to release of mast cell mediators

• Produce flushing or blotchiness/pallor (if severe)

• Itchy oropharynx

• Itchy, runny nose and eyes

• Wheeze

• Dizziness and confusion

• Urticaria—facial or generalised (see FIG. 80.1)

• Feeling of intense fear (angor animi)

• Angioedema of face and airway

• Vomiting, diarrhoea and abdominal colic (immediate or soon after)

• ± Anaphylaxis with wheezing, etc.

• Death can occur (especially if asthma history)

• Big three foods—cow’s milk, egg, peanuts

• Also: soy beans; fish, especially shellfish; wheat; tree nuts; various fruits and vegetables

• Cow’s milk can cross-react with goat’s milk and soy protein

• Frequently resolves by 3–5 years

• In adults the foods are mainly peanuts, tree nuts, fish and shellfish

Management

• Document diet, symptoms, past history, family history

• Refer for specialist allergy advice

• Provide patient education sheet

• Advise avoidance of suspected food

• IgE reactions investigated with skin testing

• Consider provision of an adrenaline auto-injector

Non-IgE-mediated food reactions³

These are less common and are usually delayed, occurring within 24–48 hours of food ingestion—but some reactions may be immediate. The real explanation is not clear. This includes cow’s milk protein intolerance with both breast milk- and formula-fed infants. It affects 2% of infants under 2 years with most resolving by 2–3 years of age.

Clinical features

• Gastrointestinal symptoms (e.g. vomiting, diarrhoea, abdominal colic)

• May be malabsorption, weight loss, failure to thrive (rare)

• Aggravation of atopic dermatitis

• Severe reactions possible

• Main foods—cow’s milk, soy proteins

• Uncommon after 3 years of age

Management

• Elimination of suspected food, then formal food challenge

• For milk protein intolerance first-line treatment is a formula containing cow’s milk protein hydrolysate. Don’t use soy-based formulas under 6 months since many are also soy protein intolerant.

• Skin testing usually not helpful and may be risky

Food protein-induced enterocolitis syndrome (FPIES)

This is seen in young infants usually <6 months and is usually due to cow’s milk, soy or cereals. It can be seen in breastfed infants and older children. A typical reaction is delayed onset of projectile vomiting and protracted diarrhoea. The stool contains blood and eosinophils. Treatment is with substance elimination.

Food intolerances⁴

In general practice it is common to see a variety of food intolerances that are not immune (allergic) or psychologically based. The food constituents represent an important group. The intolerances can be grouped as:

• fructose intolerance from excessive ingestion of fruit juices and soft drinks

• lactase deficiency from milk

• histamine-related reactions from strawberries, tomatoes

• chemical triggers:

  • – aspirin, tartrazine, sodium metabisulphite—triggering rhinitis and asthma

  • – aspirin, tartrazine, benzoic acid—triggering chronic urticaria

• others—salicylates (manufactured or natural), amines, preservatives and colourings

Note:

• foods with high-content natural salicylate include: dried fruits, pineapple, apricots, oranges, cucumbers, grapes, honey, olives, tomato sauce, wines, tea, herbs

• foods likely to contain tartrazine (food colouring) include: bottled sauces, cakes (from shops), coloured fizzy drinks, fruit cordial, custard, coloured sweets, ice-cream and lollies, jam

Symptoms

There can be a variety of symptoms:

• irritability, behavioural problems

• gastrointestinal (e.g. infant colic, diarrhoea, irritable bowel syndrome)

• respiratory—rhinitis, asthma

• headache/migraine

Management

• Document diet, reactions, past/family history

• Elimination diet and controlled food challenge

• Referral for specialist allergy advice

• Radioallergosorbent (RAST) testing is indicated where skin testing contraindicated

Peanut allergy

Peanuts are one of the most common causes of food-induced allergy including anaphylaxis in adults. The diagnosis is confirmed by demonstration of peanut-specific IgE by either skin-prick tests with peanut extract or RAST testing. Reaction to peanuts usually begins within minutes of ingestion, the first symptoms being oropharyngeal itching or burning. Flushing, urticaria, wheeze, stridor, angioedema and collapse may follow.⁵ The combination of peanut allergy and asthma is dangerous, as evidenced by fatal or near-fatal reactions in young children.⁶ The key to management is avoidance of peanut-containing foods. Desensitisation is currently not recommended. Those at risk should carry an anaphylaxis kit (see TABLE 80.2).

Risk-minimisation strategies for food anaphylaxis¹

• Achieve optimal asthma control (unstable asthma is the major risk factor)

• Notify others: school, homes, restaurants

• Carry treatment: action plan and adrenaline

• ‘Touch test’ food on external lip before consumption

• Avoid skin preparations containing natural foods

Egg allergy

Previous advice was to avoid introducing potentially allergenic foods to babies. The evidence now shows that babies who are given foods such as peanuts, eggs and seafoods in the first year of life develop fewer allergies than babies where these foods are strictly avoided. The Australian Society of Clinical Immunology and Allergy (ASCIA) has detailed information about introducing foods on its website.⁷

Current vaccinations do not include egg; it is present in only minute amounts in the MMR vaccine.

Latex allergy

The clinical manifestations of type 1 hypersensitivity reactions to latex protein are wide-ranging, from urticaria to life-threatening anaphylaxis and death. It is believed that some episodes of intra-operative anaphylaxis are due to the patient—who has been sensitised to latex—reacting after mucosal contact with gloves worn by operating staff. Some institutions now provide latex-free operating suites in response to this serious problem.⁸

Latex allergy is thus a significant problem for at-risk people, including health care workers, patients with spina bifida or other spinal cord abnormalities, and those who have had multiple operations. The greatest risk is contact with ‘dipped’ rubber products (e.g. gloves, condoms, balloons). Some hard rubber products may not pose a risk.

Symptoms

• Contact dermatitis (type 4 hypersensitivity), urticaria, worsening atopic dermatitis, allergic rhinoconjunctivitis, asthma, allergy to multiple fruits and possibly anaphylaxis

Diagnosis

Skin-prick tests (dangerous and best left to experts) are more sensitive than blood tests at this stage but carry a risk of anaphylaxis. Measurement of serum specific IgE is safe although less sensitive. Contact allergy (type 4) is identified by patch testing.

Management

Health care workers who are allergic can never again wear latex gloves.⁹

Skin-prick tests

This is the preferred method as results can be read at the first consultation, provided high-quality allergen preparations are used. A positive test alone may be of no diagnostic significance if the patient is asymptomatic to the specific allergens. A negative test is very useful for excluding IgE-mediated allergy.

Detection of serum-specific IgE

A number of tests, including RAST tests¹ and ELISA tests, measure allergen-specific IgE in the serum. They are no more accurate than skin testing, are expensive and do not provide an immediate result.

Indications include: history and skin tests not matching, extensive eczema, dermographism, infants and very young children, immunotherapy work-up, antihistamine use in past 48 hours.

Allergen avoidance

If relevant from history and skin-prick testing, special attention should be paid to reducing exposure to house dust mites and mould, to pet selection and specific food avoidance. Change of occupation and environment may be necessary for some people.

Pharmacotherapy

Drugs are used to alleviate symptoms where avoidance methods have failed or are impractical. Examples include antihistamines (H₁-receptor and H₂-receptor antagonists), adrenaline (emergency use), sodium cromoglycate, corticosteroids, some anticholinergics and sympathomimetics.

Immunotherapy (desensitisation)

This involves repeated administration of small, increasing doses of allergen by subcutaneous injection. This is the treatment of choice for severe wasp or bee venom allergy and for resistant allergic rhinoconjunctivitis where a single causative allergen can be identified. Patients should be observed for at least 45 minutes after each injection and adequate resuscitation facilities are essential.

Management of specific allergic disorders

• Asthma—see CHAPTER 82

• Atopic dermatitis—see CHAPTER 121

• Urticaria—see CHAPTER 120

• Anaphylaxis and angioedema—see CHAPTER 128

Refer to CHAPTER 59.

The classification of rhinitis can be summarised as:

• seasonal allergic rhinoconjunctivitis = hay fever

• perennial rhinitis:

  • – allergic (often due to house dust mites)

  • – non-allergic = vasomotor: eosinophilic, non-eosinophilic

The severity of symptoms is classified as either mild (normal function including sleep and only slightly troublesome symptoms) or moderate/severe (troublesome symptoms with impairment of activities).⁹ Its prevalence has increased worldwide, affecting 20% of the adult population and up to 40% in children; 60% have a family history. It varies from 5–20% with a peak prevalence in children and young adults up to 20%.¹¹ The symptoms are caused by release of powerful chemical mediators such as histamine, serotonin, prostaglandins and leukotrienes from sensitised mast cells.¹¹

Seasonal allergic rhinoconjunctivitis (hay fever)

This is the most common type of allergic rhinitis and is due to a specific allergic reaction of the nasal mucosa, principally to pollens. The allergens responsible for perennial allergic rhinitis include inhaled dust, dust mite, animal dander and fungal spores.

Most cases of hay fever begin in childhood with one-half of eventual cases having the problem by the age of 15 and 90% by the age of 30.¹² Approximately 20% suffer from asthma.

While patients with hay fever tend to have widespread itching (nose, throat and eyes), those with perennial rhinitis rarely have eye or throat symptoms but mainly sneezing and watery rhinorrhoea. Nasal polyps are associated with this disorder (refer to CHAPTER 59).

Management

Management consists of four main areas:

1. appropriate explanation and reassurance

2. allergen avoidance

3. pharmacological treatment

4. immunotherapy

Intranasal corticosteroids which reduce inflammation and nasal secretions are first-line treatment for moderate to severe cases.¹⁴

Advice to patients

• Keep healthy, eat a well-balanced diet, avoid ‘junk food’ and live sensibly with balanced exercise, rest and recreation. If your eyes give you problems, try not to rub them, avoid contact lenses and wear sunglasses.

• Avoid using decongestant nose drops and sprays: although they soothe at first, a worse effect occurs on the rebound.

• Avoidance therapy: avoid the allergen, if you know what it is (consider pets, feather pillows and eiderdowns).

• Sources of the house dust mite are bedding, upholstered furniture, fluffy toys and carpets. Seek advice about significantly reducing the dust in your bedroom or home, especially if you have perennial rhinitis.

• Pets, especially cats, should be kept outside.

• Avoid chemical irritants such as aspirin, smoke, cosmetics, paints and sprays.

Allergen avoidance

This is difficult during the spring pollen season, particularly where patients are living in high-pollen (e.g. country farming) areas, or spending considerable time outdoors in the course of work or sporting and recreational activities.

Treatment (pharmacological)⁹

Therapy can be chosen from:

1. antihistamines:

   • oral (not so effective for vasomotor rhinitis)

   • intranasal spray (rapid action)

   • ophthalmic drops

2. decongestants (oral or topical)

3. sodium cromoglycate

   • intranasal: powder insufflation or spray

   • ophthalmic drops for associated conjunctivitis

4. corticosteroids

   • intranasal (not so effective for non-eosinophilic vasomotor rhinitis)

   • oral (very effective if other methods fail)

   • ophthalmic drops for allergic conjunctivitis

Immunotherapy

Consider hyposensitisation/immunotherapy when specific allergens are known (very important) and conventional response is inadequate. Immunotherapy to grass pollen is generally very effective and should be considered in moderate to severe springtime hay fever. Immunotherapy by injection or oral administration can be labour-intensive, often taking years.

Antihistamines

Oral antihistamines are the first line of treatment for seasonal hay fever and are generally effective where symptoms are intermittent, or when used prophylactically before periods of high pollen exposure. The newer ‘non-sedating’ antihistamines that do not cross the blood–brain barrier are used in preference to the first-generation drugs, although some degree of sedation may occur even with these. A list of non-sedating antihistamines is presented in TABLE 80.3. It is claimed by some that the newer topical preparations, levocabastine and azelastine, as intranasal sprays, are rapidly effective for an exacerbation of symptoms. If sedation is desirable (e.g. overnight), a sedating antihistamine can be used.

Oral decongestants

Oral sympathomimetics, either used alone or in combination with antihistamines (where they may help reduce drowsiness), may be of some value, particularly where nasal discharge and stuffiness are major symptoms. Side effects include nervousness and insomnia. They should be used cautiously in patients with hypertension, heart disease, hyperthyroidism, glaucoma and prostatic hypertrophy.

Examples:

• pseudoephedrine HCl 60 mg (o) tds (max. 240 mg/day), or 120 mg controlled release (o) bd

Intranasal therapy^9,10

Intranasal decongestants should be used for limited periods only (i.e. less than a week) or intermittently (3–4 doses per week) because of the potential problems with rebound congestion and rhinitis medicamentosa. They are often of particular value during the first week of treatment with intranasal corticosteroids (where the onset of action is delayed several days), improving nasal patency and allowing more complete insufflation of the corticosteroids. Adverse reactions similar to those of oral decongestants may occur.

Intranasal sodium cromoglycate acts by preventing mast cell degranulation and is effective without serious side effects. The capsule variety must be used (the spray form requires 1–2 hourly dosage to be effective); it is useful in perennial allergic rhinitis but is not as effective as intranasal corticosteroids for springtime hay fever.

Intranasal corticosteroid sprays are the most effective agents for treating seasonal allergic rhinitis. Side effects are minimal and adrenal suppression is not a problem with normal usage. Patients should be informed that these medications will not give immediate relief (often taking 10–14 days to have peak effect) and must be used continuously throughout the hay fever season for at least 6–8 weeks. Local side effects include dryness and mild epistaxis.

Intranasal antihistamines group—includes azelastine and levocabastine—are effective at relieving itching and sneezing.

TABLE 80.4 lists intranasal preparations for rhinitis.

Ophthalmic preparations

Sodium cromoglycate eyedrops are usually very effective for springtime conjunctivitis. They can be used as necessary (no dosage limit) and are most helpful when used prophylactically before periods of high pollen exposure. Decongestant eyedrops may also be helpful (care with narrow angle glaucoma), while corticosteroid eyedrops are reserved for resistant allergic conjunctivitis and should be used with care to exclude infection and glaucoma. Antihistamine eyedrops antazoline and levocabastine are yet another option.

Other treatments

Corticosteroids (oral)

These can be very effective where other treatments or methods have failed. A 6–10 day short course can be used. An example of a 6-day ‘rescue course’ is prednisolone 25, 25, 20, 15, 10, 5 mg daily doses.

Ipratropium bromide (Atrovent)¹³

The nasal preparation of this topical anti-cholinergic is often very effective when rhinorrhoea is the major problem.

Leukotriene receptor antagonist

Regarded as equivalent to oral antihistamines, they have a place in the management of children with concurrent asthma and hay fever (e.g. montelukast).

Surgery

Inferior turbinate reduction aims to reduce the size of turbinates and so reduce nasal obstruction when congested.

Guidelines from elite task force¹⁵

1. For initial treatment of seasonal allergic rhinitis in people aged 12 or older, routinely prescribe monotherapy with an intranasal corticosteroid rather than an intranasal corticosteroid in combination with an oral antihistamine.

2. For initial treatment of seasonal allergic rhinitis in those aged 15 or more, recommend an intranasal corticosteroid over a leukotriene receptor antagonist.

3. For treatment of moderate to severe seasonal allergic rhinitis in people 12 or older, you may recommend the combination of an intranasal corticosteroid and an intranasal antihistamine initially.

TABLE 80.5 summarises recommended steps in management.

• Where surgical intervention is required, such as with nasal obstruction from polyps, bulky nasal turbinates and deviated septum

• For immunotherapy

Australasian Society of Clinical Immunology and Allergy <www.allergy.org.au>