Allergy
Clinical conditions

Essential facts about allergic rhinitis, allergic conjunctivitis, allergic bronchial asthma, anaphylactic shock, urticaria and angiooedema

Allergic rhinitis

Key clinical features of allergic rhinitis include sneezing, itching, nasal discharge and impaired nasal breathing. Depending on the time pattern of symptoms, and hence on the triggering allergen, a distinction is made between seasonal allergic rhinitis (pollinosis, hay fever) and perennial allergic rhinitis. Recent reports in the literature have also suggested a distinction between intermittent allergic rhinitis (symptoms less often than on 4 days/week or in less than consecutive 4 weeks) and persistent allergic rhinitis (>4 days/week and > consecutive 4 weeks) [1].

In seasonal allergic rhinitis, symptoms are limited to periods of pollination, but, in patients with multiple sensitisations, may be protracted over longer periods of time in spring and/or summer. Seasonal allergic rhinitis in particular may include eye reactions (conjunctivitis). The chief complaint in perennial rhinitis is impaired nasal breathing [2].

Allergic rhinitis is accompanied by general symptoms such as sleep disorders or difficulty concentrating and, especially in children, may also be accompanied by increased susceptibility to upper and lower respiratory tract infections. Quality of life is significantly impaired. In addition, the chronic inflammatory reaction in allergic rhinitis substantially increases the risk of asthma. Therefore, allergic rhinitis is a condition that should be taken seriously [1].

Allergic conjunctivitis

Usually associated with allergic rhinitis, conjunctivitis is triggered by mast cells located mainly in the eyelids and in the conjunctiva of the eye whose activation causes symptoms such as itching, burning, redness and increased tearing. Eye symptoms are frequent harbingers of an immediate-type allergic reaction of the airways. If allergen exposure persists, or in case of particularly intense allergen exposure, patients may develop chemosis (swelling of the bulbar conjunctiva), which may involve the cornea [2;3].

Allergic bronchial asthma

The cardinal symptom of bronchial asthma is sudden-onset breathlessness (dyspnoea) with expiratory stridor (wheezing) and a troublesome cough [3]. The attack often begins with a sensation of tightness and dry cough. Auscultation reveals characteristic rhonchi, wheezing and sonorous rales. The sputum, often copious and expectorated with difficulty, is typically viscous. Pulmonary function testing reveals obstructive impairment of ventilation with increased airway resistance and reduced forced expiratory volume in one second (FEV1).

Regardless of the cause or pathomechanism, bronchial asthma is characterised by increased airway reactivity (bronchial hyperresponsiveness) to various stimuli: many patients with bronchial asthma report increased airway sensitivity to non-specific stimuli such as fog, smoke, exhaust fumes or pungent odours. Bronchial asthma is now defined as a chronic inflammatory airway disease on the basis of bronchial hyperreactivity.

The underlying pathophysiology is highly complex, and a basic distinction is made between extrinsic allergic bronchial asthma (extrinsic = exogenously triggered asthma) and intrinsic bronchial asthma (post-infectious asthma).

Allergic bronchial asthma tends to be a disease of the first half of life, typically manifesting before age 30.

The most common triggers are airborne allergens such as pollen and house dust mites, as well as animal danders and mould spores. A specific form is occupational asthma, which is caused by allergens on the job and whose incidence is on the rise. Triggering allergens include plastics such as epoxy resins, rubber ingredients, latex, “baking additives”, flours or metal salts [2].

In allergic bronchial asthma, the allergic immediate reaction in the lower respiratory tract is accompanied by airway obstruction produced by mucosal oedema and contraction of airway smooth muscle (bronchospasm). Its onset is a few minutes after allergen exposure. Approximately 6–10 hours after allergen contact, a second episode of bronchoconstriction may occur as part of the late-phase reaction and be accompanied by infiltration, mainly of neutrophils and eosinophils, resulting in bronchial hyperresponsiveness for days or weeks.

Therefore, even brief allergen exposure may lead to sustained exacerbation of symptoms [2;3]. An elevated IgE level may suggest allergic asthma. The differential blood count shows an increased number of eosinophils, which can also be detected by cytology in sputum.

Anaphylactic shock

Anaphylaxis is the most severe form of an allergic immediate reaction and may involve the entire body. Classically, the term anaphylaxis is confined to denote the IgE-mediated immediate reaction. However, specific IgG and IgM antibodies may, via the formation of circulating immune complexes, also trigger similar, complement-dependent symptoms (immune complex anaphylaxis). The triggering molecule is usually taken up percutaneously or orally, but entry from the air is also possible.

Common triggers include:

• foods
• insect venoms
• drugs
• additives
• natural latex
• airborne allergens

Physical triggers like cold or exercise (exercise-induced anaphylaxis) or anaphylaxis of unknown origin have also been described. Moreover, allergen application during specific immunotherapy may rarely trigger severe systemic allergic reactions. In many cases, anaphylactic symptoms occur only in response to the combined exposure to different stimuli, such as allergen exposure in combination with physical exercise, additional emotional stress or acute infection. This phenomenon is referred to as augmentation or summation [2;4]. The use of beta-blockers and possibly also of ACE inhibitors may lead to exacerbation of anaphylactic symptoms [4].

Symptoms include:

• on the skin: itching, erythema (flushing), urticaria and angiooedema
• in the oral cavity: itching of the palate and tingling in the throat; these are often the initial symptoms of anaphylaxis
• in the respiratory tract: rhinorrhea, hoarseness and bronchospasm to the point of respiratory arrest
• in the gastrointestinal tract: nausea, vomiting, cramps and defecation
• in the cardiovascular system: tachycardia, blood pressure drop, occasionally also transient blood pressure increase, shock and arrhythmia to the point of circulatory arrest. Great fluctuations of central venous pressure are characteristic. Anaphylaxis is classified as grades I to IV based on the intensity of clinical symptoms (see Table below).