CHAPTER 12

Nonallergic Rhinitis

Perhaps the most frequent question encountered by the authors during decades of courses and lectures has been, “What do I do when the allergy test results are negative?” Although there is no single answer to the question, the possibilities are by no means infinite (Table 12-1). In this chapter, we present our thoughts on how to handle this perplexing situation. Here are some of the questions to be addressed.

DIAGNOSTIC QUESTIONS TO BE ANSWERED

Has Inhalant Allergy Really Been Ruled Out?

When one says, “The allergy test results are negative,” the usual implication is that inhalant testing has been performed, with negative results. As has been emphasized in earlier chapters, the diagnosis of allergy is initially made by history, and then confirmed by testing to identify antigenic triggers. To avoid needless expenditure of time and money, the “screening” concept was introduced. Testing with a limited number of inhalant antigens (generally from nine to 15) gives a specificity and sensitivity well over 90%, but not 100%. Therefore, even though a patient s history is strongly suggestive of (for example) fall weed symptoms, if results of testing for the index antigen (in this case, ragweed) are negative, additional testing may be justified, based on strong clinical suspicion. In the example cited, this might include marsh elder, lamb’s quarters, pigweed, or other significant fall weeds in the local area. Results of tests for these will not always be positive, but in a few instances these additional tests will uncover allergies missed in a screening evaluation. It should be strongly emphasized that this is not a carte blanche to perform numerous other tests on every patient with a negative allergy screen result. Only if the history is strongly suggestive is such further testing justified.

A related situation occurs when the patient has allergic symptoms triggered by unusual antigens that are not routinely included in the screening panel, and that do not cross-react significantly with antigens in that group. Again, the history is all-important in this case, and the allergy team members are called upon to be detectives. The culprit may be an animal (e.g., rabbit, horse), an unusual pollen (e.g., Malaleuca in certain regions of Florida), or a perennial allergen not generally tested for (e.g., cockroach). If the history is strongly suggestive of atopy to such an antigen, additional testing is justified, although again, this will not be necessary or appropriate in every case. A strong historical suggestion of sensitivity to the unusual antigen should be present.

Not all allergy that affects the ear, nose, and throat is caused by inhalants. Foods may play either a primary or secondary role in producing such symptoms. Thus, a negative evaluation for inhalants does not mean that food allergy has been ruled out. The simplest means of doing this is through an assessment of a patient’s dietary habits, followed by omission of suspected foods and a challenge refeeding of the individual foods in question. Although this technique requires cooperation on the part of patients, it is fairly simple and is nonetheless probably the most accurate means of diagnosing food allergy Furthermore, the experience serves to demonstrate forcefully to patients the relationship of their symptoms (as produced by the challenge refeeding) to food ingestion. Dietary modification requires effort by patients, and those who will not attempt diagnostic manipulation will probably not be cooperative in efforts to alleviate symptoms by omission of foods. Most of these patients are instead looking for a “quick fix” that is effortless (on their part) and permanent. Details of evaluating and treating for food allergy are found in Chapter 13.

Are Nonallergic Triggers at Work?

Although debate continues, as it has for decades, as to whether chemicals cause a true “allergic” reaction or simply act as irritants, there is no doubt that these substances do produce symptoms that may include nasal congestion, rhinorrhea, drainage, and headache. Most, if not all, chemicals are not primarily antigens, but some may act as haptens. These are small molecules that, although not antigenic in themselves, bind to a protein carrier to form an immunologically active conjugate. The question of whether “immunotherapy” for chemicals is appropriate is beyond the scope of this book. What is indisputable, however, is that exposure to tobacco smoke, perfumes, hair-sprays, colognes, soaps, dyes, paints, inks, and numerous other chemicals produces undesirable upper respiratory symptoms in a significant number of patients. Important nonallergic, irritant causes of nasal symptoms are ozone and air pollution, which are products of high temperatures and calm winds. It behooves the members of the allergy team to frequently monitor the air quality readings for their location, as well as pollen counts, to assist them in their diagnostic efforts. Patients should also be taught to follow these markers. A good history, in which the patient is involved as a partner in detecting such exposure, is the best method for making the diagnosis of rhinitis caused by chemicals and irritants. Avoidance, if possible, remains the best treatment.

Does the Patient Have Idiopathic (Vasomotor) Rhinitis?

It has been suggested, especially by specialists in the United Kingdom, that the term idiopathic rhinitis should replace the more time-honored designation of vasomotor rhinitis. At present, the terms are often (and sometimes erroneously) used interchangeably. Idiopathic rhinitis is generally taken to mean rhinitis that suggests an allergic origin, but with negative allergy tests. The entity of true vasomotor rhinitis implies an autonomic instability, in which the normal balance of sympathetic and parasympathetic innervation to the nose is disturbed, resulting in an excess of cholinergic stimulation. This in turn produces nasal congestion and/or profuse rhinorrhea and postnasal drainage. The classic example of this problem is the “skiers nose,” represented by profuse rhinorrhea on exposure to cold weather.

It has been long recognized that emotional stress can produce nasal congestion and obstruction.¹ This is an altogether too common cause of nasal symptoms in patients with negative allergy test results. Rhinorrhea is less often associated with this problem, but postnasal drainage and chronic throat clearing may frequently be seen in association with stress-induced rhinitis.

The question of the nonallergic rhinitis with eosinophilia syndrome (NARES) generally is raised when patients are encountered who have symptoms of rhinitis, negative allergy test results, and large numbers of eosinophils in their nasal secretions. The original description of this syndrome² included a very small group of patients with symptoms of sporadic episodes of sneezing, watery rhinorrhea, and itching ocular and pharyngeal mucosa. None had nasal obstruction, nor did they experience the consequences of sinusitis, otitis media, or lower respiratory tract symptoms, which often accompany allergic rhinitis. Although they had high numbers of eosinophils in their nasal secretions during periods of symptoms, this level decreased when they were symptom-free. Results of allergy tests, in the form of skin tests, allergen-specific radioallergosorbent testing (RAST), and determination of total immunoglobulin E (IgE), were all negative.

A meta-analysis of all reported series of NARES by Carney and Jones³ pointed out that the criteria for making this diagnosis have varied significantly with individual investigators, with a range of nasal eosinophilia of from 10 to 25% being considered abnormal. It is their opinion that NARES is probably not a single, clearly defined clinical entity. They further postulate that NARES may represent allergy limited to the mucosal tissue, without systemic IgE-mediated disease.

The most common form of rhinitis medicamentosa is rebound rhinitis, which follows the use of topical nasal decongestants for a period exceeding a week or more. This occurs as the initial decongestion with closure of blood-filled spaces in the turbinates is followed by a reactive vasodilation, resulting in recurrent congestion and the need for more decongestants, setting up a vicious cycle. This rebound congestion may follow treatment with any of the topical decongestants currently available, such as phenylephrine (Neo-Synephrine) and oxymetazoline (Afrin). The incidence of rebound rhinitis is higher than might be imagined. In one series of 100 consecutive patients seen for the first time in an otolaryngologist’s office with the chief complaint of nasal congestion (excluding only patients with infection), more than half had used decongesting drops or sprays for 14 days or more.⁴ Correction of rebound rhinitis begins with making the diagnosis, which in turn means that all patients with the complaint of nasal congestion must be specifically asked about their use of nose drops or nasal sprays. It may take some effort on the part of the clinician to differentiate between decongestant use and use of other nasal sprays, such as corticosteroids, anticholinergics, and cromolyn. It is an effort that will be well rewarded, however.

Although most cases of rhinitis medicamentosa are forms of rebound rhinitis, a variety of systemically administered medications may also produce the side effect of nasal stuffiness. The most common cause of this congestion was once a variety of antihypertensive medications, such as reserpine (Serpasil), hydralazine (Apresoline), guanethidine (Ismelin), methyldopa (Aldomet), and prazosin (Minipress). The more frequent cause in recent times has been a noncardioselective β-adrenergic blocker, such as propranolol (Inderal) or nadolol (Corgard). Finally, nasal congestion may be a side effect of some antidepressants and anxiolytic medications, such as thioridazine (Mellaril), chlordiazepoxide-amitriptyline (Limbitrol), perphenazine (Trilafon), and alprazolam (Xanax). The only way to rule out rhinitis medicamentosa effectively as a contributory (or primary) cause of a patient’s nasal symptoms is by obtaining a complete history detailing all systemic medications taken. If doubt exists as to the ability of any given drug to produce nasal congestion, one should examine the list of side effects for that drug as printed in the Physicians Desk Reference (Medical Economics Publishers, Montvale, NJ) or Drug Information for the Health Care Professional (U.S. Pharmacopeial Convention, Rockville, MD).