ALLERGIC RHINITIS IN HIV-INFECTED PATIENTS - 09/09/11
Riassunto |
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 ⍺ interleukin (IL)-1 in mononuclear cells obtained from allergic rhinitis patients have been demonstrated in the laboratory of these authors. Nasal ⍺IL-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
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| Address reprint requests to Marianne Frieri, MD, PhD, Director of the Allergy Immunology Program, Nassau County Medical Center, 2201 Hempstead Turnpike, East Meadow, NY 11554 |
Vol 17 - N° 2
P. 291-301 - maggio 1997 Ritorno al numeroBenvenuto su EM|consulte, il riferimento dei professionisti della salute.
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