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Fluocortin butyl (FCB) is a newly synthesized corticosteroid with a high ratio of topical to systemic activity. FCB was studied in a multi-center, double-blind, placebo-controlled trial of therapy of perennial rhinitis. The study was conducted between January and May 1981. Patients evaluated suffered from either chronic allergic or chronic nonallergic rhinitis or both. A total of 306 patients from 16 investigative centers were evaluated by comparing FCB to placebo. Three separate dosage regimens were employed. Patients received a total daily dose of 2, 4, or 8 mg. FCB was found to be an effective therapeutic agent. It reduced symptoms of nasal congestion, rhinorrhea, postnasal drainage, and sneezing. It also markedly reduced the use of concomitant medications (chlorpheniramine maleate and/or pseudoephedrine). Relief of symptoms was noted as early as the first week of therapy, and the degree of improvement increased progressively during the study. There was little difference between the relief produced by the 4 mg and 8 mg regimens. Both of these were superior to the 2 mg regimen. The drug was well tolerated; no significant side effects were noted.

Diagnostic nasal cytology has been advocated for use in distinguishing allergic from nonallergic rhinitis. We sought to determine prospectively the frequency of nasal eosinophilia (NE) in 100 patients in whom having allergic rhinitis (AR), nonallergic rhinitis, and other atopic conditions not involving the respiratory tract have been diagnosed. A nasal smear was obtained from consenting adults using the Rhino-Probe curette. Patients taking local or systemic corticosteroids, those with chronic rhinitis associated with aspirin sensitivity, and those with sinusitis were excluded. All cytograms were coded and read by a single "blinded" investigator. NE was considered significant if greater than 20% of sampled cells were eosinophils. Twenty-six of 61 (43%) patients with AR had NE. No NE was detected in the control population or in the skin test negative group of patients in whom having nonallergic rhinitis was diagnosed. One of 16 patients with allergic disease not involving the respiratory tract exhibited NE; this patient had atopic dermatitis with peripheral eosinophilia. No cases of eosinophilic nonallergic rhinitis were detected. There was no significant correlation of symptoms or the number of positive skin tests with NE. These data suggest that the nasal smear for eosinophils is an insensitive but specific test for the diagnosis of allergic rhinitis, when patients with nasal polyposis and aspirin sensitivity and/or negative skin tests are excluded.

The spontaneous nasal secretions from about 128 patients with the symptomatic triad of rhinorrhea, sneezing, and nasal obstruction were studied. The cytological examination consisted of a morphological evaluation and a semiquantitative evaluation. Noncellular and nonliving presences in the smears have been considered, including mucus, Charcot-Layden crystals, and pollen grains, as well as fungi and bacilli. We found a net increase in eosinophils, goblet cells, and cellular debris in secretions of atopic patients. Pollen grains and vegetative fragments were present in the nasal smears of pollinosis. The presence of fungi was observed in five cases of allergic rhinopathy. The exfoliative cytology represents a valuable means for the differential diagnosis of rhinitis. In particular, the presence of noncellular elements has value regarding rhinocytology.

Eosinophilic nonallergic rhinitis is one of the major forms of nonallergic rhinitis. It is characterized by the presence of many eosinophils in nasal secretions, a negative history for allergen exacerbation, and negative skin tests. It is often associated with nasal polyps and shares their exquisite sensitivity to corticosteroid therapy, both systemic with prednisone or topical with flunisolide. Patients with rhinitis can be separated into diagnostic categories and assigned scores on the basis of history of allergic reactions, status of nasal mucosa, response to skin tests, and IgE titer. Based on these criteria, in a study of 142 patients with rhinitis, those with allergic or probable allergic rhinitis could clearly be separated from those with nonallergic rhinitis. Thirty-four percent had allergic rhinitis (mean score 5.4), 15% had probable allergic rhinitis (mean score 3.8), 37% had vasomotor rhinitis (noneosinophilic, nonallergic rhinitis; mean score 0.75), and 15% had eosinophilic nonallergic rhinitis (mean score 0.71). Eighty-three percent of patients with eosinophilic nonallergic rhinitis responded to antihistamines and 93% responded to the topical corticosteroid flunisolide, making the total response 90%. The response of the latter patients to these medications was statistically better than the response of those patients with allergic rhinitis.

The pathogenesis of nasal polyps has been debated for many years. The lymphocytes that infiltrate nasal polyps have been identified as predominantly memory T cells in an activated state, and these cells produce a mixed cytokine pattern of T1 helper (Th1) and T2 helper (Th2) cells. We conducted a prospective study to compare the expression levels of some Th1 and Th2 cytokines in atopic and nonatopic patients. Our study population consisted of 75 adults—42 men and 33 women (mean age: 38 yr)—with nasal polyposis. Patients with an allergy were distinguished from those without an allergy on the basis of the history, the results of skin-prick testing, and measurement of total IgE serum concentrations. Based on these criteria, patients were divided into two groups: atopic (n = 38) and nonatopic (n = 37). Levels of cytokine gene expression in the atopic patients were compared with those of the nonatopic patients by real-time polymerase chain reaction. Statistical analysis found no significant differences in the rate of interleukin (IL) 10 and IL-12 gene expression between the allergic and nonallergic patients. On the other hand, rates of interferon gamma and IL-4 gene expression were significantly higher in the atopic patients (p = 0.03 and p = 0.02, respectively). Our research suggests that an imbalance of Th1 and Th2 cells plays an important role in the pathophysiology of nasal polyps. Although nasal polyposis is a multifactorial disease associated with several different etiologic factors, chronic persistent inflammation is undoubtedly a major factor, regardless of the specific etiology.

Patients with nasal eosinophilia and no evidence of systemic allergy have recently been described.’ The paper by Jacobs et al. in this issue of the JOURNAL (p. 253) extends these findings by clearly indicating that local allergy is not present in such individuals. What is unclear in this paper is how these patients are distinguished historically from patients with allergic rhinitis who also have rhinoconjunctivitis, pruritus, and nasal congestion. There is also a question of nomenclature raised by the title of this article, “NARES Syndrome. ” Is nasal eosinophilia in association with nonallergic rhinitis a syndrome? And do we wish to restrict this association with an eponym? In the classification of rhinitis, let us follow the admonitions of Dr. Richard Asher, who warned

At the April meeting of the American Rhinologic Society, Palm Beach, Fla, Murray Sacks, MD, Rochester, Minn, presented his work on the use of topical and systemic steroids in the treatment of nasal disorders. Sacks classified rhinitis into three types: allergic, nonallergic with eosinophilia, and nonallergic without eosinophilia (vasomotor rhinitis). Earlier double-blind cross-over studies from The Johns Hopkins University, Baltimore, demonstrated the efficacy of both topical beclomethasone and flunisolide in the treatment of allergic rhinitis. The prolonged use of topical nasal steroid therapy appears to be safe. The primary local complication is burning, a problem more frequent with flunisolide. Other local complications, such as epistaxis, may be seen occasionally, but other complications are rare when the medications are used at the recommended doses. Systemic effects have not been observed. A previous study of nonallergic rhinitis with eosinophilia demonstrated that 52% of these patients have sinusitis and 33% have nasal polyps.

In the common practice of respiratory allergy, the confirmation by IgE tests of the relationship between the occurrence and duration of symptoms and the exposure to specific inhalant allergens allows an aetiological diagnosis. However, to see patients with suggestive history but negative IgE tests is not rare, and this generally leads to a diagnosis of nonallergic rhinitis or asthma. In many cases, such diagnosis is wrong, because the patient may be revealed as allergic by using additional testing. This is true for local allergic rhinitis, characterized by an exclusive IgE production in the nasal mucosa, that may be correctly diagnosed by performing a nasal IgE measurement or a nasal provocation test with the suspected allergen (s). Another misleading issue is the role of T cell-mediated, delayed hypersensitivity in the pathophysiology of rhinitis and asthma. Recent studies showed that in patients with rhinitis or asthma and negative IgE tests, especially when there is a positive history for current or past atopic dermatitis, the clinical symptoms are actually driven by such mechanism, that may be detected by performing an atopy patch test (APT). The allergen source most frequently responsible for this kind of allergy is the house dust mite, but other allergens may also be involved. Thus, before delivering a diagnosis of nonallergic rhinitis or asthma in patients with negative result to common allergy testing, further tests are needed. To miss the diagnosis of allergy has obvious consequences in terms of management, including allergen avoidance, patient’s education, and specific immunotherapy. Keywords: Rhinitis, Asthma, LgE tests, Nonallergic, Local allergic rhinitis, T-cell mediated hypersensitivity, Atopy patch test