Etiology Of Rhinitis Research Articles

Current Approaches to Diagnosis and Management of Rhinitis

Rhinitis affects >20% of the population and is a common reason patients visit their primary care physician. Proper therapeutic intervention initially requires differentiating rhinitis from acute and chronic rhinosinusitis. After establishing rhinitis as the etiology of a patient's symptoms, a careful, thoughtful history and physical examination aids the cause. Rhinitis can be allergic, nonallergic, or mixed (having features of both allergic and nonallergic rhinitis). Therapeutic interventions vary, depending on the etiology of rhinitis. Symptoms that are refractory to avoidance and pharmacotherapy warrant referral to an allergist or otolaryngologist for consideration of immunotherapy or surgical intervention. In many cases, adhering to an evidence-based therapeutic treatment algorithm will allow physicians to effectively manage rhinitis.

Factors Affecting Outcome of Inferior Turbinate Mucotomy in Treatment of Postnasal Drip Syndrome

Postnasal drip syndrome may result from isolated hyperplasia of nasal inferior turbinates due to chronic rhinitis. Mucotomy (conchotomy) performed in such patients is generally effective but in some individuals the problem persists after surgery. The aim of this study was to determine factors influencing outcome of the therapy. One hundred six patients aged 17-60 years (mean = 34, SD = 12) with hyperplasia of the inferior turbinates underwent bipolar diathermy mucotomy. Nonallergic noninfectious rhinitis was diagnosed in 18, neutrophilic in 58, allergic in 18 and NARES in 14 patients. The participants were questioned about postnasal drip (PND) intensity before and 2 months after surgery. Results of mucotomy significantly depended on the etiology of chronic rhinitis and were worst in patients with NARES (p < 0.05). Percent values of reduction of PND intensity after mucotomy and percent of daytime with PND persisting after surgery depended on Staphylococcus aureus colonization of the nose (the results were worse in patients with the colonization, p < 0.001). Satisfaction scores were also dependent on S. aureus nasal colonization (p < 0.001) and significantly correlated with percent values of subjective reduction of PND intensity after surgery (p < 0.001) and reduction of PND daily duration (p < 0.001). Results of mucotomy performed for postnasal drip depend on etiology of rhinitis and are worse in S. aureus nasal colonization.

International variation in prevalence of rhinitis and its relationship with sensitisation to perennial and seasonal allergens

The relative importance of atopy in the aetiology of rhinitis is largely unknown. The present study investigated the geographical variations in rhinitis in relation to atopy. The cross-sectional study involved 54,178 children (aged 8-12 yrs) from 30 study centres in 22 countries worldwide. Symptoms of rhinoconjunctivitis and rhinitis without conjunctivitis in the last 12 months were reported in parental questionnaires and children were skin-prick tested. The prevalence of rhinoconjunctivitis and rhinitis without conjunctivitis varied widely (1.5-24.5% and 1.4-45.2%, respectively). For rhinoconjunctivitis, the population attributable fraction (PAF) varied 0-71% for a positive skin-prick test to one or more seasonal allergens and 0-41% for perennial allergens. The PAF for sensitisation to seasonal and perennial allergens was higher in affluent countries (36 and 25%, respectively) than nonaffluent countries (1.3 and 12.6%, respectively). For rhinitis without conjunctivitis, the PAF for perennial allergens was 8 and 4% for affluent and nonaffluent countries, respectively. No significant PAF was found for seasonal allergens. Overall, atopy explained only a limited proportion of rhinitis symptoms, suggesting that the importance of other environmental factors has been under emphasised, particularly in less affluent countries. Atopy seems to be only marginally relevant for rhinitis without conjunctivitis, which seems mainly to reflect nonatopic rhinitis.

ALLERGIC RHINITIS IN HIV-INFECTED PATIENTS

Infection with the human immunodeficiency virus (HIV) has been known to render persons more susceptible to allergic, as well as infectious disorders. As the number of HIV-infected persons increases, it has been noted by many practitioners that chronic nasal symptoms, sinusitis, and otitis are quite common problems.16 It is a matter of debate which percentage of these nasal symptoms are truly allergic in nature. The etiology of rhinitis is broadly classified into allergic or nonallergic forms, including chronic infectious rhinitis, mucociliary disturbances such as cystic fibrosis,9 and immune deficiency, predisposing to chronic infection.23 Seasonal or perennial allergic rhinitis may be caused by different pollens, mold spores, animal dander, dust mite, and other allergens. The pathophysiology of allergic rhinitis results from the development of both humoral and cellular immune reactions to airborne allergens, with symptoms of sneezing, rhinorrhea, nasal blockage, and itching, owing to IgE-dependent mast cell activation in the nasal mucosa with the release of numerous inflammatory mediators.12 An increase in vascular permeability, glandular secretion, and secretion of cytokines results, leading to chronic inflammation.13 Additional mediators from an influx of inflammatory cells are chemoattractants for neutrophils, eosinophils, T lymphocytes, and basophils,12 which have been shown to induce the release of histamine from mononuclear cells from patients with allergic rhinitis.5 An increase in the basal levels of α interleukin (IL)-1 in mononuclear cells obtained from allergic rhinitis patients have been demonstrated in the laboratory of these authors. Nasal αIL-1 levels in allergic rhinitis patients following grass and ragweed in vivo nasal provocation were demonstrated to diminish during the late-phase inflammatory reaction after 1 month of antihistamine treatment.6 We have also reported the release of soluble intercellular adhesion molecules by cytokine-activated human tracheal epithelial cells.24 Activation of allergen-specific Th2 lymphocytes can induce a cascade of events with secretion of IL-4, IL-5, IL-13. An increase in nasal IL-8 levels during the late-phase inflammatory reaction after grass and ragweed nasal provocation has been reported in patients with allergic rhinitis from our center.14

Rhinitis as a mechanism of respiratory defense

The incidence of rhinitis is on the increase, especially in towns and cities with high levels of pollution from motor traffic and industry. There is a growing body of evidence which links this increased incidence of rhinitis to chronic nasal irritation from industrial pollution. Studies on the mechanisms of nasal inflammation and the nasal immune response are now providing insights into the etiology of rhinitis. This knowledge will help in the development of therapies aimed at alleviating the symptoms of rhinitis and controlling the development of rhinitis in susceptible individuals. This review discusses some of the factors that may explain the increased incidence of rhinitis and examines basic mechanisms involved in the nasal response to infection and allergy.