Natural Treatment of Perennial Allergic Rhinitis

Alternative Medicine Review, Oct, 2000 by Stacy M. Thornhill, Ann-Marie Kelly

Abstract

Perennial allergic rhinitis is an IgE-mediated inflammatory disorder of the nasal mucosa characterized by paroxysms of sneezing, nasal congestion, pruritis, and rhinorrhea. The condition may be caused by certain environmental agents, food sensitivities, structural abnormalities, metabolic conditions, or synthetic drugs. Recent health impairment outcome studies on allergic rhinitis sufferers reveal a measurable decline in physical and mental health status and the inability to perform daily activities. Antihistamines, decongestants, anticholinergic agents, and corticosteroid drug therapy, alone or in combination, are typically used in the treatment of allergic rhinitis. Reported adverse side effects include sedation, impaired learning/memory, and cardiac arrhythmias. Therapeutic strategies should seek to decrease the morbidity already associated with this condition. Urtica dioica, bromelain, quercetin, N-acetylcysteine, and vitamin C are safe, natural therapies that may be used as primary therapy or in conjunction with conventional methods.

(Altern Med Rev 2000;5(5)448-454)

Introduction

Allergic rhinitis is the most common allergic disorder in the United States, affecting 10-20 percent of the population.[1,2] The condition is characterized by continuous or periodic nasal congestion, rhinorrhea, sneezing, pruritis of the conjunctiva, nasal mucosa and oropharynx, allergic shiners, lacrimation, and fatigue. Predisposing factors are a positive family history of similar symptoms and a personal history of collateral allergy manifested as eczematous dermatitis, urticaria, and/or asthma. Clinical presentation may include nasal polyps, pale and boggy (sometimes reddened or excoriated) nasal passages, congested and edematous conjunctiva, injected pharynx, and swelling of the turbinates and membranes of the ear. Often, there is a temporal relationship between an allergen exposure and an acute episode of allergic rhinitis. Environmental agents that can cause this condition are dust mites, feathers, animal dander, mold, pollen, grass, and fungus spores. Many people with allergic rhinitis are also allergic to certain foods and may experience symptoms as a result of eating allergy-triggering substances in such foods as eggs, nuts, fish, shellfish, dairy products, or wheat.[3] In the absence of nonspecific stimuli in the history, structural abnormalities of the nasopharynx, exposure to irritants, upper respiratory infection, pregnancy with prominent nasal mucosal edema, prolonged use of alpha-adrenergic agents, or use of rauwolfia, beta-adrenergic antagonists, or estrogens should be excluded.

Pathophysiology

Most cases of allergic rhinitis are due to an indeterminate, yet specific, allergen-reagin reaction in the nasal mucosa. The immediate-response phase consists of an allergen binding to the IgE component of the mast cell. This initial pathophysiological event results in recruitment of numerous chemoattractants and inflammatory mediators, which signal eosinophil, basophil, neutrophil, and monocyte infiltration.[4] Usually 2-8 hours after exposure to the antigen (delayed-response phase), there is intense infiltration of tissues with inflammatory mediators as well as tissue destruction in the form of mucosal epithelial cell damage, as there exists a perpetual mediator response (Figure 1). This late or delayed inflammation is associated with an increased sensitivity to the allergen after repeated exposures and a hyper-responsiveness to irritants or certain pharmacologic agents.

[Figure 1 ILLUSTRATION OMITTED]

While mast cells are widely distributed throughout the human body, they are found in high concentrations in the blood vessels of the sub-epithelial connective tissue of the respiratory tract and conjunctiva. Mast cell degranulation accounts for approximately one-half the symptoms of allergic rhinitis. Histamine, the principal inflammatory mediator in allergic rhinitis, is released by mast cells in the immediate-response phase and by basophils in the delayed-response phase. Histamine binding to H1-receptors has several consequences; it increases vasodilation, capillary permeability, and smooth muscle contraction, manifesting as rapid fluid leakage into the tissues of the nose as well as swollen, secretory nasal linings.[2]

Discussion

Antihistamines comprise the largest group of drugs on the market. Their effect is based on the blockade of [H.sub.1] histamine receptors located on the nasal vasculature and nerve endings.[5] Structural differences between the various drugs account for the differences in the potential side effects. The first-generation antihistamines contain ethylamine moieties that make them highly lipophilic and readily able to cross the blood-brain barrier.[5] This characteristic partly explains the numerous adverse effects associated with sedating antihistamines, including dizziness, tinnitus, cardiac arrhythmias, gastrointestinal distress, lassitude, incoordination, blurred vision, diplopia, euphoria, and tremors. In fact, it has been reported the first-generation antihistamines cause discernible drowsiness in 25 percent of adults.[6] Even in the absence of sedation, they can substantially impair thought processes and the ability to drive or operate machinery.