World Allergy Forum: Non-Allergic Rhinitis and Polyposis

The Different Faces of Non-Allergic Rhinitis

Glenis K. Scadding

The most recent classification of rhinitis (rhinosinusitis)is in the WHO document: "Allergic Rhinitis and its Impact on Asthma"(ARIA) (1). Rhinitis is divisible into 3 parts: allergic, infectious and other causes. These are not mutually exclusive, for example allergic rhinosinusitis may predispose to nose and sinus infection.

Infectious Rhinitis
This can occur with a wide variety of organisms, the commonest being acute viral rhinosinusitis which affects millions annually (2). Approximately 0.5% to 2% of viral upper respiratory tract infections progress to an acute bacterial infection.

Chronic rhinosinusitis is one of the most common chronic conditions of man (3).Sinus abnormalities are seen in 30-45% of CT or MRI scans undertaken for other conditions.

The common responsible bacteria are shown in Slide 5. These are carbohydrate coated, rendering phagocytosis difficult. Most also exert deleterious effects upon muco ciliary clearance. Immunological dysfunction of the innate(primary ciliary dyskinesia,cystic fibrosis) or acquired (hypogammaglobulinaemia,IgG subclass abnormalities) systems predisposes to sinusitis,which may be the mode of presentation.

Fungi such as aspergillus or the Dermataceous fungi: alternaria, bipolaris or curvularia are found in allergic fungal sinusitis (4). Their role in chronic sinusitis/nasal polyposis is under review. With careful techniques fungi can be isolated from the nasal secretions of most individuals whether or not they have sinusitis. Ferguson (5) has pointed out several highly significant clinical differences between patients with eosinophilic mucin rhinosinusitis and allergic fungal sinusitis.

Drug-induced rhinitis
Many medications can cause nasal symptoms. These include aspirin and the other non-steroidal anti-inflammatory agents which can give rise to nasal polyps, eosinophilia, intrinsic asthma,usually with a good response to corticosteroids. Five percent of these patients are also sensitive to paracetamol. The recent introduction of Cox 2 antagonists has demonstrated that many such individuals are able to tolerate meloxicam.

Other drugs which can cause nasal blockage are anti-hypertensives, particularly beta-blockers. Alpha-agonists if overused can lead to vaso-motor rhinitis with a chronically blocked and reddened nasal mucosa which is unresponsive to intrinsic or extrinsic alpha stimulation. Exogenous oestrogen can cause rhinitis, as can chlorpromazine.

Hormonal rhinitis
This occurs most commonly with pregnancy, but is also seen sometimes at puberty and during the menstrual cycle. Hypo-thyroidism and acromegaly can also give rise to the chronically blocked nose.

Food-induced rhinitis
This is much rarer than is popularly supposed. Food allergy is an unusual cause of isolated rhinitis, although in anaphylaxis rhinitis is often seen. The oral allergy syndrome occurs when a patient sensitive to tree pollens ( e.g. birch) exhibits oral allergic reactions to fresh fruits and vegetables such as apples, carrots, celery due to cross-reactive epitopes. Food intolerance can cause nasal symptoms. This is seen with dyes, preservatives and alcohol in some non-allergic patients. The mechanisms are unknown. Spicy foods, such as peppers, cause rhinorrhoea probably via their capsaicin content which stimulates sensory nerve fibres inducing neuropeptide release(6).

Atrophic rhinitis
This is characterised by atrophy of the mucosa and underlying bone. The patient presents with a widely patent nose which is crusted and odoriferous. Infection with Klebsiellae ozaenae is found (7), but it is uncertain whether this is the primary problem. Secondary atrophy can occur follow excessive nasal surgery, radiation trauma or chronic granulomatous disease.

Other causes of rhinitis
Various physical and chemical stimuli cause rhinitis, these include: exposure to dry air, spices, air pollutants, occupational irritants. Emotions such as stress and sexual arousal also have a powerful effect on the nose via the autonomic system. Gastro-oesophageal reflux can result in rhinitis especially in small children.

The remaining patients with rhinitis can be divided into those with a nasal eosinophilia (variously characterised as over 5% ,10%,20% or 25%) and those without. The former group is called NARES (non-allergic rhinitis with eosinophilia), and may evolve into nasal polyposis, aspirin sensitivity and asthma. There appear to be a number of patients contained within this sub group in whom the nasal histology is similar to that of allergic rhinitis and who are positive on nasal allergen challenge. Local IgE synthesis has been demonstrated in the nose in previous papers (8,9). This has important implications for diagnosis.

Patients with non-allergic, non-eosinophilic rhinitis are termed "idiopathic". Many of these appear to have an autonomic dysfunction. Nasal histology and immunohistology are normal, however local nasal reflexes (such as the diving reflex, nasal resistance on standing and on putting a crutch under the arm), are abnormal as well as some cardiovascular reflexes,suggesting the problem may be more generalised. Local therapy with ipratropium (10) has proved successful. A double-blind, placebo-controlled study of capsacin has confirmed its effectiveness.(11)

Since various studies(12,13)report that 37% to 64% of patients presenting with rhinitis are allergic; between one and two-thirds of patients are non-allergic and will need to have their rhinitis dissected carefully by means of a careful history(14) thorough examination, investigations and possibly by means of a trial of therapy.

References

1. Bousquet J. et al Allergic Rhinitis and its impact on Asthma. 2000 WHO.
2. Gwaltney J Jr. Acute Community-acquired sinusitis. Clin. Infect Disease 1996;23:1209-1223.
3. Melen I. Chronic Sinusitis; Clinical and pathophysiological aspects. Actor Otolaryngol suppl 1994;515:45-48.
4. deShazo RD, Swane RE. Diagnostic criteria for allergic fungal sinusitis. Journal Allergy Clin. Immunol 1995;96:24-35.
5. Ferguson BJ. Eosinophilic mucin rhinosinusitis; a distinct clinicopathological entity. Laryngoscope 2000;110:799-813.
6. Lacroix JS, Buvelot JM, Polla BS, Lundberg JM. Improvement of symptoms of non-allergic chronic rhinitis by local treatment with capsaicin. Clin. Ex Allergy 1991;21:595-600.
7. Henriksen S, Gunderson W. The aetiology of azaena. Actor Pathol Microbiol Scan 1959;47:380-386.
8. Durham SR, Gould HJ, Hamid QA. Local IgE production in nasal allergy. Int Arch Allergy Immunol 1997;113:128-130.
9. Platts-Mills TA. Local production of IgG, IgA and IgE antibodies in grass pollen hayfever. Journal Immunol 1979;122:2218-2225.
10. Borum P, Mygind N, Schultz Larsen F. Intranasal ipratropium: a new treatment for perennial rhinitis. 1979;4:407-411.
11. Blom HM, Van Rijswijk JV, Garrelds IM, Mulder PGH, Timmermans T, Gerth Van Wijk R. Intranasal capsaicin is efficacious in non-allergic, non-infectious perennial rhinitis. A placebo-controlled study. Clinical and Exp Allergy 1997;27:796-801.
12. Mullarkey MF, Hill JS, Web DR. Allergic and non-allergic rhinitis; their characterisation with attention to the meaning of nasal eosinophilia. Journal Allergy Clin Immunol 1980;65:122-126.
13. Mygind N, Dirkasen A, Johnsen NJ, Weeke B. Perennial rhinitis; an analysis of skin testing, serum IgE and blood and smear eosinophilia in 201 patients. Clin Otolarygol 1978;3:189-196.
14. Togias A. Age relationships and clinical features of non-allergic rhinitis: Journal Allergy Clin. Immunol 1990;85:182.

 

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