BSACI guideline for the diagnosis and management of allergic and non-allergic rhinitis (Revised Edition 2017; First edition 2007)

2.1 Classification of Allergic Rhinitis (AR)

The WHO ARIA workshop “Allergic Rhinitis and its impact on Asthma” classification[14] of AR based on frequency and severity of symptoms has been validated.[15] Additionally clinical classification into seasonal and perennial rhinitis is useful in UK practice for diagnosis and allergen-specific therapy.

2.2 Infective rhinitis

Any cause of congestion of the nasal mucosa can lead to occlusion of the sinus ostia, predisposing to acute rhinosinusitis and/or Eustachian tube dysfunction.

2.3 Non-allergic rhinitis (NAR)

The numerous diagnoses in this category need to be borne in mind for patients with negative skin prick tests (SPTs). Table 1 summarizes the causes and disease patterns of NAR.

5.1 Pathophysiology

The basic mechanisms of AR are illustrated in Figure 1.

Co-morbid associations of rhinitis (Table 2).

AR-associated comorbid disorders can be subdivided into:

• other allergic diseases, particularly asthma
• problems related anatomically to the nose: conjunctivitis, rhinosinusitis, hyposmia, middle ear problems, throat and laryngeal effects
• Sleep problems and secondary effects of symptoms on concentration, mood and behaviour

The most important co-morbidity is asthma: not only is rhinitis a risk factor for subsequent asthma but 80% of asthma sufferers according to ARIA have concomitant rhinitis, poor control of which is a risk factor for asthma exacerbations.[10, 11, 103, 104, 106]

6.1 Pathophysiology

At least two subgroups exist: one with nasal inflammation on histology,[107] the other without inflammation or local IgE production.[108] The former includes local allergic rhinitis[109] and non-allergic rhinitis with eosinophilia (NARES). A proportion of patients within this latter group are aspirin/NSAID sensitive.[110] There is evidence that some patients with apparently non-allergic rhinitis share similar histologic mucosal features as those with allergic rhinitis characterized by increased numbers of mast cells and eosinophils and produce local IgE,[107, 111, 112]

Patients with non-inflammatory type rhinitis are thought to suffer from dysfunction of the autonomic nerve supply to the nasal mucosa.[67, 113]

6.2 Occupational rhinitis

Occupational rhinitis, which can be allergic or non-allergic, describes abnormalities of the nasal mucosa mediated by airborne substances in the work environment. It is distinct from work-exacerbated rhinitis, which refers to individuals with pre-existing rhinitis who experience an exacerbation of symptoms due to workplace exposures. Over 300 agents can cause occupational rhinitis, and these are the same as those which can induce occupational asthma.[114]

HMW agents are protein allergens derived from plants or animals, for example, flour, latex, laboratory animals and evidence of sensitization are usually seen on skin testing or serum-specific IgE.[115] LMW agents cause mucosal inflammation either via airway immune sensitization, (e.g di-isocyanates and glutaraldehyde) or via irritant exposures (e.g chlorine and ammonia). Occupational rhinitis is three times more frequent than occupational asthma; the two conditions frequently occur together.[116, 117] The early identification of a causative occupational agent and the avoidance of exposure are important for the prevention of progression to occupational asthma [118-121] (Grade B).

Diagnosis is based on a detailed history, including symptom diary review, improvement of nasal symptoms during weekends and holidays, skin prick testing and measurement of specific IgE when appropriate.

Latex is a cause of both occupational rhinitis and asthma. Prevention of latex allergy by removing powdered gloves or substituting non-latex ones is essential. All healthcare environments should have a latex policy[119, 122] (Level of evidence=2+ and 4; Grade of recommendation=D, C for adults and children with perennial rhinitis or adults and children with latex allergy).

7.1 History

A detailed history is required, including seasonality (pollen, moulds), indoors/outdoors location (dust mite, the presence of house pets), work location (occupational), improvement of holidays and, relationship to potential triggers which can impact on the patient's quality of life. Symptoms of sneezing, nasal itching, itching of the palate are more likely to lead to allergic rhinitis.

7.2 Rhinorrhoea

Rhinorrhoea is either anterior, posterior or both.

• Clear—infection unlikely if continuously clear, although secretions are clear early in viral rhinitis
• Unilateral—is uncommon and cerebrospinal fluid (CSF) leak should be excluded[123]
• Coloured
  1. yellow—allergy or infection; green—usually infection; blood tinged
  2. unilateral—tumour, foreign body, nose picking or misapplication of nasal spray
  3. bilateral—misapplication of nasal spray, granulomatous disorder, bleeding diathesis, infection, nose picking.

7.3 Nasal obstruction

• Can be partial or complete; severity often correlates with systemic manifestations
• Bilateral—most likely rhinitis or nasal polyps but maybe septal (sigmoid) deviation
• Unilateral—usually septal deviation but also consider foreign body, antrochoanal polyp and tumours
• Alternating—due to rhinitis exposing the nasal cycle[124]

7.4 Nasal crusting

Severe crusting especially high inside the nose is an unusual symptom in rhinitis and requires further investigation. Consider: chronic rhinosinusitis,[125] nose picking, granulomatous polyangiitis, sarcoidosis or other vasculitides, (particularly if crusting is associated with bleeding), cocaine abuse, ozaena (wasting away of the bony ridges and mucous membranes inside the nose), non-invasive ventilation. Topical steroids rarely cause crusting.

7.5 Eye symptoms

Include intense itching, redness and swelling of the white of the eye, watering, Lid swelling and (in severe cases) periorbital oedema, which can be aggravated by eye rubbing.

7.6 Lower respiratory tract symptoms

• Cough, wheeze, shortness of breath—can occur with rhinitis alone since bronchial hyper-reactivity can be induced by upper airway inflammation.[126-128]

Disorders of the upper and lower respiratory tract often coexist:

• 80% of asthmatics have rhinitis—see section on rhinitis and asthma

7.7 Other symptoms

• Snoring, sleep problems, repeated sniffing, nasal intonation of the voice
• Pollen-food syndrome is triggered by ingestion of cross-reacting antigens in some fruits, vegetables and nuts[129]
• A proportion of patients suffering from allergic (mainly seasonal) rhinitis have an associated nasal hyper-reactivity which is generally not recognized/treated

7.8 Family history

A diagnosis of allergic rhinitis is more likely when rhinitis is seasonal, or with a family history of AR. However, it can arise de novo.

7.9 Social history

Consider pets or other contact with animals, occupation or schooling.

7.10 Drugs

A number of drugs can cause or aggravate rhinitis symptoms, and therefore, a drug history should include details of the use of alpha- and beta-blockers and other anti-hypertensives, aspirin and other non-steroidal anti-inflammatory drugs, oral contraceptives as well as topical sympathomimetics (see Table 1). It is also important to enquire about the efficacy of previous treatments for rhinitis and details of how they were used and for how long.

8.1 Visual assessment

• Allergic salute and/or horizontal nasal crease across dorsum of nose and/or eye involvement supports a diagnosis of allergic rhinitis
• Chronic mouth breathing
• Allergic shiners
• An assessment of nasal airflow—(e.g metal spatula misting in young children)
• Depressed nasal bridge—post surgery, granulomatous polyangiitis or cocaine misuse
• Widened bridge; polyps (see also BSACI guideline on rhinosinusitis and nasal polyposis[130];
• Purple nasal tip due to sarcoidosis

8.2 Anterior rhinoscopy

• Hypertrophic, pale and boggy inferior or middle turbinates suggest inflammation, but nasal appearance may be normal in AR
• The presence or absence of clear, coloured or purulent secretions
• A deviated septum does not usually cause rhinitis
• The presence or absence of nasal polyps, but it may not be possible to see small ones or if they are confined to the sinuses. Larger polyps can be seen in the nasal vestibule sometimes extending as low as the nares and can be distinguished from the inferior turbinate by their lack of sensitivity, yellow/grey colour and the ability to get between them and the side wall of the nose.
• Yellow submucosal nodules with a cobblestone appearance suggest sarcoidosis.[131]
• Crusting and granulations raise the possibility of vasculitis
• Septal perforation may occur after septal surgery or due to chronic vasoconstriction (cocaine, alpha agonists), granulomatous polyangiitis, anti-phospholipid antibody syndrome and nose picking
• Throat examination-cobblestoned lymphoid hyperplasia, post-nasal drip

8.3 Nasal endoscopy

Used in specialist centres to examine both the anterior and posterior parts of the nasal cavity this is more specific than rhinoscopy and alters the diagnosis in up to a fifth of patients with nasal disease.[132]

9.1 Skin prick tests (SPT)

• Should be carried out routinely to determine if the rhinitis is allergic or non-allergic, and have a high negative predictive value. They should be interpreted in the light of the clinical history
• At least 15% of people with a positive skin prick test do not develop symptoms on exposure to the relevant allergen[133]
• Prick to Prick tests with fresh food can be used to diagnose oral allergy syndrome

9.2 Serum total and specific IgE

Serum-specific IgE may be requested when skin tests are not possible or when the SPT together with the clinical history give equivocal results. Total IgE alone can be misleading but may aid interpretation of specific IgE. Currently available SPTs and allergen-specific IgE show similar sensitivity for house dust mite (HDM), but SPTs are more sensitive to other inhalant allergens such as cat epithelium, mould and grass pollen.[134]

9.3 Laboratory investigations

Usually unnecessary, their use is guided by the history, examination and results of skin prick tests. Examples include:

• Full blood count (FBC) and differential white cell count, C-reactive protein (CRP), immunoglobulin profile, microbiological examination of sputum and sinus swabs when chronic infection is suspected
• Thyroid function tests in unexplained nasal obstruction
• Nasal secretions-asialotransferrin for CSF identification
• Urine toxicology when cocaine abuse is suspected

9.4 Olfactory tests

The University of Pennsylvania Smell Identification Test (UPSIT) is well validated, and can be helpful when there is suspicion of malingering,[135] it is accepted for legal cases.

9.5 Cytology

The techniques for obtaining cells for cytology in secretions, lavage, scraping, cotton buds or brushings have not been standardized, nor have the criteria for evaluating cell counts.[136]

Nevertheless the presence of eosinophils implies inflammation and may be helpful in predicting response to corticosteroids.[137, 138]

9.6 Exhaled nitric oxide (eNO)

Exhaled nitric oxide (FeNO=fractional exhaled nitric oxide) measurement can be useful clinically in the diagnosis and monitoring of asthma. Normal levels are less than 20 ppb, but become elevated in eosinophilic lower respiratory tract inflammation.[139]

9.7 Nasal NO

Levels are complex as there are two sources of NO: sinuses and nasal epithelium. However, very low levels (<100 ppb) indicate the likelihood of primary ciliary dyskinesia, but can also be observed in cystic fibrosis and in sinus obstruction caused by large polyps. NO measurements are restricted to specialist centres.

9.8 Radiology

Radiology is not routinely recommended for simple rhinitis. However, when rhinosinusitis or nasal polyposis is suspected, especially non-responsive to medical therapy, CT scan is helpful.

9.9 Nasal challenge

It is not routinely available outside specialist centres; there is no standardized methodology and asthmatic reactions can occur. It may be useful to confirm aspirin sensitivity or in occupational allergic rhinitis, where there is discrepancy between history and when there are potentially important occupational implications.

9.10 Objective measures of nasal airway

Objective measurements of the nasal airway are not made in routine clinical practice but can be useful when allergen or aspirin challenges are undertaken and may be helpful when septal surgery or turbinate reduction are being contemplated.

9.11 Tests for asthma

Measurements of lung function should be considered in all patients with persistent rhinitis.

9.12 ENT referral

Patients with unilateral symptoms, heavily blood stained discharge or pain, require ENT referral. Those with nasal blockage unrelieved by pharmacotherapy or structural abnormalities, such as septal deviation, sufficient to render nasal therapy difficult should be seen by a surgeon.

10.1 Allergen avoidance

Allergen avoidance clearly works in seasonal allergic rhino-conjunctivitis: hayfever sufferers are symptom-free outside the pollen season. For patients with house dust mite-sensitive AR the situation is complicated by the difficulties of reducing exposure to mites in the home. A systematic review of trials of mite allergen avoidance in rhinitis concluded that trials are generally small and of poor methodological quality and meta-analysis could not be performed.[140] Large studies of a combination of strategies to reduce exposure to dust mites have not been conducted but should probably include measures to reduce mites in cars, at school and work (see Figure 2).

Evidence from randomized studies is summarized in Table 3. For occupational AR complete avoidance of exposure to the causal agent is recommended.[115] Irritants such as smoke, traffic pollution can worsen rhinitis symptoms and should be avoided, where possible.

In a DBRPC study, the application of a cellulose powder (Nasaleze™) three times daily resulted in significant reductions in severity scores for sneezing, runny nose, stuffy nose and symptoms from eyes and lower airways with no clinically significant adverse effects (Grade B).[141]

Interventions that may help to reduce symptoms during the pollen season include patients wearing sunglasses (Grade C),[142] nasal filters,[121] balms and ointments applied to the nose.[143] Other practical/common sense measures that may reduce exposure to pollen are summarized in Table 3 but have not been tested in studies.

10.2 Pet allergens

For patients with AR sensitized to and symptomatic on contact with pets such as cats, dogs and horses, avoidance of the animal should be advised. For those who wish to keep pets to which they are sensitized, there is limited information from randomized studies on which to base recommendations[144] HEPA filters alone do not seem useful for cat allergic patients with cats.[145] Cat allergen exposure can be reduced using temperature-controlled laminar airflow treatment,[145] and although this treatment has shown to improve asthma-related quality of life, this has not been tested for rhinitis.[147]

10.3 Saline irrigation

Isotonic saline irrigation in both adults and children with allergic rhinitis was well tolerated,[148] inexpensive, easy to use with no evidence of adverse effect to health with regular use.[149, 150] It has a small beneficial effect in symptom reduction and may reduce the amount of pharmacotherapy needed (Grade B).

10.4 Carbon dioxide washing

The use of a ten second burst of carbon dioxide from a pressurized container into the nasal airway, with the mouth open, reduces all the symptoms of rhinitis within minutes. It is now available over the counter for rescue treatment as Serenz.[151, 152]

11.1 Antihistamines

Antihistamines are available as oral, intranasal and ocular preparations.

All demonstrate clinical efficacy. It is important to use a drug with the least adverse effect and that is considered safe for the current situation (i.e such as pregnancy, breastfeeding).

Second-generation antihistamines are long acting and are largely non-sedating and have no clinically significant anti-cholinergic activity at therapeutic doses, although there is variation in individual susceptibility to such effects.[154]

11.2 Oral H1-antihistamines

Reduce mean daily rhinitis symptom scores (in absolute terms) by an estimated 7% versus placebo[155] and can significantly improve quality of life.[156, 157]

They act predominantly on neurally mediated symptoms of itch, sneeze and rhinorrhoea and have only a modest effect on nasal congestion.[158-164] Additionally, they reduce histamine driven symptoms such as itch[165] at sites other than just the nose such as conjunctiva, palate and skin.[166-168] They should be used regularly rather than “as needed” use in persistent rhinitis.[169, 170] Acrivastine has the fastest onset of action, but needs to be used 8 hourly; fexofenadine is the least sedating oral antihistamine with a wide therapeutic index.

11.3 Adverse effects

First-generation antihistamines are less useful due to sedation and cognitive impairment, which can worsen driving and examination results already impaired by rhinitis,[171, 172] Their use is not recommended. Antihistamines with an anticholinergic effect are associated with development of dementia.[173]

11.4 Place in therapy

• First-line therapy for mild=to-moderate intermittent and mild persistent rhinitis
• Addition to intranasal steroids for moderate/severe persistent rhinitis uncontrolled on topical intranasal corticosteroids alone, particularly when eye symptoms are present.[178-180] Evidence for this combination is less good than for the addition of intranasal antihistamine to topical intranasal corticosteroids in a guinea-pig model.[181]

11.5 Topical H1-antihistamines

12.1 Intranasal corticosteroids (INS)

Topical corticosteroids are the mainstay of anti-inflammatory intervention in AR. Factors which need consideration are systemic drug bioavailability, safety and cost.[189] Ease of device use may influence concordance. INS reduces all symptoms of rhinitis by about 17% more than placebo, with a variable effect on associated allergic conjunctivitis.[190, 191] Meta-analysis shows that INS is superior to oral antihistamines or leukotriene receptor antagonist alone on all aspects of allergic rhinitis[155, 192] (Grade Ia).

Unlike other treatments, INS reduce nasal congestion.[192] Onset of action is 6-8 hours after the first dose, clinical improvement may not be apparent for a few days and maximal effect may not be apparent until after two weeks.[192] Starting treatment two weeks prior to a known allergen season improves efficacy.[193] Similar clinical efficacy for all INS, but bioavailability varies considerably (see Figure 3).

Systemic absorption negligible with mometasone furoate, fluticasone furoate and fluticasone propionate and these preparations are favoured for children. Systemic absorption is modest for the remainder, and high for betamethasone which should be used short-term only.[194, 195]

12.2 Adverse events

Local nasal irritation, sore throat and epistaxis affect around 10% of users. Benzalkonium chloride is used as a preservative in several topical corticosteroids, and may irritate the nose, but does not adversely affect mucociliary clearance.[196] In patients with nasal irritation symptoms such as burning, for example, a trial with a benzalkonium free preparation, for example rhinocort, flixonase nasules are suggested. Reduction of local adverse effects such as nasal crusting, bleeding and pain can be achieved in many cases by correct use of the intranasal device, see Figure 4a; (Grade of recommendation=D). Nasal drops are useful for severe obstruction and should be used in the “head upside down” position to reach the ostiomeatal complex (OMC), see Figure 4b.

Hypothalamic-pituitary axis suppression may occur when multiple sites are treated with topical corticosteroids in the same person (e.g skin, nose and chest).[197] If corticosteroids are used in multiple sites, then a low bioavailability preparation should be favoured.

Raised intra-ocular pressure has been described with INS[198] thus limiting its use in patients with predisposition to high ocular pressure/glaucoma is important.

12.3 Place in therapy

First-line therapy for moderate-to-severe persistent symptoms.[14] First line of therapy if presenting with severe nasal obstruction,[192] possibly combined with a short-term nasal decongestant. In severe nasal obstruction steroid drops or oral steroids should be used initially for up to one week. For oral or topical antihistamines in uncontrolled rhinitis—see below.

13.1 INS and oral preparations

INS demonstrate similar or greater efficacy to an oral antihistamine plus a leukotriene receptor antagonist[199, 200] (see Appendix A2).

13.2 INS and topical H1-antihistamine combination

Currently available as a combination spray containing azelastine and fluticasone propionate (FP), dymista leads to greater symptom improvement than using either agent alone in SAR (Grade A).[201] All symptoms of allergic rhinitis were significantly improved with onset of action by 30 minutes.[202] The combination approach leads to clinical improvement of symptoms days earlier than seen with azelastine or FP monotherapy.[201] Ocular symptoms of allergy were better treated with the combination spray rather than FP or azelastine alone.[202] Efficacy over FP is demonstrated in perennial allergic rhinitis.[203]

13.3 Adverse effects

The main side-effect is the bitter taste of azelastine, which is experienced by a small proportion of users.

13.4 Place in therapy

Combination of topical AH with INS should be used in patients when symptoms remain uncontrolled on AH or INS monotherapy or on a combination of oral AH plus INS.

13.5 Systemic glucocorticoids

There are no trials of oral steroid use and efficacy in AR, although there is grade A evidence in chronic rhinosinusitis with nasal polyposis where inflammation is more severe. Use is rarely indicated in the management of allergic rhinitis except for:

14.1 Injectable corticosteroids

Injected preparations are not recommended as compared to other available treatments the risk-benefit profile for intramuscular corticosteroids is poor.[204, 205]

14.2 Intranasal decongestants

Topical formulations allow relief of nasal congestion via vasoconstriction within minutes, faster and with greater impact than intranasal steroids.[206, 207] A decongestant spray may allow delivery of intranasal drugs beyond the inferior turbinates. For example, oxymetazoline and fluticasone furoate when used together further improved nasal congestion more than either alone.[207] There is no licensed INS plus decongestant combination preparation in the UK at present.

14.3 Adverse events

Only short-term use (generally fewer than 10 days) is recommended as a paradoxical increase in nasal congestion secondary to rebound vasodilatation (rhinitis medicamentosa) can occur.[208] The risk of this occurrence increases with duration of 3-5 days maximum.[209, 210] Intranasal decongestants are less likely to lead to rhinitis medicamentosa when used short-term and alongside an intranasal steroid.[210] They can also cause nasal irritation and may increase rhinitis.

14.4 Place in therapy

• Eustachian tube dysfunction when flying (evidence level D)
• To increase nasal patency before douching (Grade D) or intranasal administration of nasal steroids[211]

14.5 Oral decongestants (pseudoephedrine)

• Weakly effective in reducing nasal obstruction[212] and have many side-effects, so are not recommended.[213]

14.6 Anti-leukotrienes

These have a therapeutic profile similar to antihistamines, with efficacy comparable to loratadine in seasonal allergic rhinitis,[214] and are less effective than topical nasal corticosteroids.[214-217] The response is less consistent than that observed with antihistamines.[217-219] LTRAs reduce the mean daily rhinitis symptom scores by 5% more than placebo.[155]

Combination of anti-leukotriene plus antihistamine has no advantage over either drug used alone[221-224] and is not any more effective than topical corticosteroid alone.[198, 224] Anti-leukotrienes may have a place in asthma patients with seasonal allergic rhinitis.[226]

14.7 Adverse events

They are usually well tolerated; occasional headache, gastrointestinal symptoms or rashes. Neuropsychiatric manifestations have been reported in children, especially adolescents. There is a possible causal link between LTRA use and eosinophilic polyangiitis.[227, 228]

14.8 Place in therapy

Montelukast is licensed in the UK for those with seasonal allergic rhinitis who also have concomitant asthma (UK licence for age > 6 months; Zafirlukast UK licence>12 years).

15.1 Ipratropium bromide

Used three times daily it decreases rhinorrhoea (particularly if neurogenic rather than inflammatory origin) but has no effect on other nasal symptoms.[19, 229-231] Regular use may be effective as an “add-on” for allergic rhinitis when watery rhinorrhoea persists despite topical steroids and antihistamines[229, 232]

15.2 Adverse events

Dry nose and epistaxis,[145] systemic anti-cholinergic effects are unusual.[233, 234] Caution is advised in the elderly in whom periodic revisions of its requirement may have to be instigated.

15.3 Place in therapy

Patients with watery rhinorrhoea despite compliance with INS or INS plus antihistamine

16.1 Adverse events

Generally very well tolerated (including in pregnancy) but these include local irritation, taste disturbance and headache.

16.2 Place in therapy

• Children and adults with mild symptoms only and sporadic problems in season or on limited allergen exposure.[238] Useful for individuals unable to take other medications, for example pregnant females.
• Cromoglycate and nedocromil eye drops are useful in conjunctivitis as topical therapy.[236, 239]

18.1 Subcutaneous injection immunotherapy (SCIT)

SCIT is effective for both seasonal rhinitis due to pollens (Cochrane meta-analysis[244] evidence level 1++) and perennial rhinitis due to house dust mite,[245] evidence level 1+). There are few randomized controlled trials of immunotherapy for cat allergy,[246, 247] (level 1) SCIT requires weekly up-dosing regimens followed by 4-6 weekly maintenance injections for 3-5 yr. Pre-seasonal SCIT is effective for pollen allergy. In view of the risk of systemic side-effects SCIT should only be given in specialist clinics by trained personnel with immediate access to adrenaline and resuscitation facilities.[248]

18.2 Sublingual Immunotherapy (SLIT)

SLIT has emerged as an effective and safe alternative for the treatment of allergic rhinitis with/without seasonal asthma[242] due to grass pollen[249-255] ragweed,[256, 257] evidence level 1++) and house dust mite(evidence level 1).[249, 258]

Sublingual immunotherapy is well tolerated, with side-effects largely confined to local itching and swelling in the mouth and throat. After supervision of the first dose by the prescribing physician with a one-hour period of observation, SLIT is self-administered daily at home.

SLIT has an excellent safety record, although there are case reports of systemic reactions and of eosinophilic oesophagitis, but no deaths have been reported. Oral antihistamine given prior to SLIT initiation and for the first two weeks of the course of therapy can reduce local oral irritation (level D).

18.3 Long-term benefits

Immunotherapy is the only treatment that can modify the course of allergic rhinitis, with long-term remission following discontinuation.[259-261] Subcutaneous immunotherapy in children with seasonal rhinitis reduces progression to asthma, an effect that persisted for 10 years.[262] Immunotherapy may prevent development of new sensitizations.[263, 264]

18.4 Place in rhinitis therapy

Allergen immunotherapy within the United Kingdom is recommended in patients with a history of symptoms on allergen exposure and objective confirmation of IgE sensitivity (skin prick test positive and/or elevated allergen-specific IgE) in the following circumstances[265]:

1. Seasonal pollen induced rhinoconjunctivitis in patients whose symptoms persist despite maximal drug therapy (combinations of intranasal corticosteroid and antihistamine taken regularly) (Evidence level 1++, category A). The choice of SCIT or SLIT is based largely on patient preference as there are no adequately powered head-to-head comparative trials
2. Perennial allergic rhinoconjunctivitis in patients with an allergy to house dust mite who respond inadequately to anti-allergic drugs and where the allergen is not easily avoided (e.g veterinary surgeons and public sector workers)

20.1 Intranasal ipratropium

This is effective for watery rhinorrhoea (level 1b; Bronsky et al.[234]).[266-278]

20.2 Topical capsaicin

Desensitization reduced symptoms for several months in non-allergic, non-infectious rhinitis, NINAR.[279-281]

20.3 Topical corticosteroids

Topical corticosteroids have an effect in skin prick test-negative rhinitis patients (level 1b), probably on those with underlying inflammation, since studies give variable results,[282-286] and relief was limited in subjects with low levels of nasal eosinophils in a recent study.[287]

20.4 Topical nasal antihistamines

Azelastine and olopatadine[288-291] (level 1b) and a combination of azelastine with fluticasone (level 3) reduced symptoms in skin prick test-negative patients over one year.[203]

Decongestants and oral antihistamines are ineffective.

20.5 Montelukast

It has not been formally trialled in NAR but low quality studies[224] suggest a possible effect in SP-negative patients.

TRPV1 was considered a prime target for neurogenic rhinitis therapy, but a recent study proved negative when cold dry air challenges were used,[292] but antagonism did reduce the response to capsaicin.[293]

20.6 Aspirin desensitization

This may be effective in those with aspirin—sensitive NAR, but should be preceded by nasal or oral aspirin challenge to establish the diagnosis.[294-297] A suggestion for NAR therapy is given in Figure 5.

24.1 Frequent monitoring visits for SLIT

Paediatric patients who were reviewed at three monthly intervals were significantly more adherent than those reviewed twice or once a year.[308]

24.2 Enhanced patient education

A 3-hour educational programme together with written information achieved greater compliance than standard oral instruction.[309]

28.1 AR

• Prevention of AR development: for example environmental changes, use of synbiotics
• Adoption of single unified scheme for assessing rhinitis control
• Prevention of progression from AR to asthma: confirmation of effect of immunotherapy, investigation of AR well-controlled by pharmacotherapy
• Reduction of proportion of SCUAD sufferers by combination therapies

28.2 NAR

Prevalence—accurate figures needed

28.3 Endotypes

Trials of therapy in well-selected endotypes

Levels of evidence[12]

Evidence table—recent combination therapy for rhinitis