Allergic Rhinitis Ebook
Allergic rhinitis (hay fever) is part of an inherited syndrome, which may also manifest as atopic eczema and asthma. In allergic rhinitis, airborne particles, such as grass pollens, moulds and animal allergens, are deposited on the nasal mucosa giving rise to acute and chronic reactions. Allergens combine with the IgE antibodies produced by the plasma cells of the nasal mucosa, which are avidly bound to the Fc-epsilon receptors on mast cells. This triggers degranulation of mast cells and releases the inflammatory mediators of the type I hyper-sensitivity reaction, causing rhinorrhoea and nasal obstruction. Microscopically, the nasal mucosa shows numerous eosinophils, abundant plasma and in some cases an increased number of mast cells. There is goblet cell
Several early studies evaluated the role of IgE in patients with a variety of allergic diseases ( 29,30 and 31). Adults and children with allergic rhinitis and extrinsic asthma tend to have higher total serum IgE concentrations. About half of such patients have total IgE concentrations that are two standard deviations above the mean of a normal control group. Significant overlap of total serum IgE concentrations in normal subjects and in patients with allergic asthma and hay fever has been demonstrated (Fig 3.3). Therefore, the total serum IgE concentration is neither a specific nor sensitive diagnostic test for the presence of these disorders. Total serum IgE has been found to be markedly elevated in atopic dermatitis, with the serum IgE concentration correlating with the severity of the eczema and with the presence of allergic rhinitis, asthma, or both. Patients with atopic dermatitis without severe skin disease or accompanying asthma or hay fever may have normal IgE concentrations...
In type I, or immediate, hypersensitivity, allergen interacts with IgE antibody on the surface of mast cells and basophils, resulting in the cross-linking of IgE, FceRI receptor apposition, and mediator release from these cells. Only a few allergen molecules, interacting with cell-bound IgE, lead to the release of many mediator molecules, resulting in a major biologic amplification of the allergen-IgE antibody reaction. Clinical examples include anaphylaxis, allergic rhinitis, and allergic asthma.
Leukotrienes are potent and possess a broad spectrum of biologic activity (43). They induce wheal-and-flare responses that are long lived and are accompanied histologically by endothelial activation and dermal edema. In the airway, they enhance mucus production and cause bronchoconstriction, especially by affecting peripheral units. In humans, LTD4 is most active, LTC4 is intermediate, and LTE4 is the least potent. LTE4 has been implicated as an inducer of nonspecific bronchial hyperreactivity. It has been suggested that LTD4 augments airway remodeling (44), possibly by stimulating matrix metalloproteinase release or activity. All depress cardiac muscle performance and diminish coronary flow rates. LTC4 and LTD4 have been recovered from nasal washings and bronchial lavage fluids of patients with allergic rhinitis or asthma, whereas LTE4 has been recovered from the urine.
Amb a 1 consists of two fragments, named A and B. These fragments are not bound covalently and are dissociated readily, which results in a significant loss of allergenic activity. Recombination of these polypeptide chains does not restore allergenic activity, presumably because the steric conformation is not readily restored. Amb a 1 is resistant to enzymatic degradation, suggesting that readily accessible amino or carboxyl groups are not the principal immunologic determinants. Interestingly, 10-fold more Amb a 1 is extractable in vitro at the pH of nasal secretions from patients with allergic rhinitis (pH 7 to 8), than at the pH of nasal secretions from nonatopic individuals (pH 6.3) (13). In addition to the short ragweed allergens just described, an allergen from giant ragweed (A trifida), Amb t V (Ra 5G), has been identified (58). Other allergens that cause allergic rhinitis have been purified from additional weeds. These include Sal p 1 from S pestifer (Russian thistle) (59), Par...
The effects of ozone on lung function have been investigated extensively. Ozone is generated by the action of ultraviolet light on precursor pollutants from such sources as automobiles and power plants. Ozone causes decreased FEV-, and forced vital capacity as well as increases in bronchial hyperresponsiveness in both asthmatics and nonasthmatics at concentrations as low as the National Ambient Air Quality Standard of 0.12 ppm ( 277). A few studies have suggested that ozone increases allergen responsiveness associated with both asthma and allergic rhinitis. Subjects given 3 hours of exposure to 0.25 ppm of ozone required less allergen to have a significant decrease in FEV-, (279). A similar effect was noted after 7.6 hours of exposure to 0.16 ppm ozone (2.80). Nitrogen oxides from car emissions also may play a role, although the evidence in controlled exposures is less convincing than for ozone ( 2.8.1).
Watson WTA, Simons KJ, Chen XY, et al. Cetirizine a pharmacokinetic and pharmacodynamic evaluation in children with seasonal allergic rhinitis. J Allergy Clin Immunol 1989 84 457. 46. Chu TJ, Yamate M, Biedermann AA, et al. One versus twice daily dosing of terfenadine in the treatment of seasonal allergic rhinitis US and European studies. Ann Allergy 1989 63 12. 67. Wong L, Hendeles L, Weinberger M. Pharmacologic prophylaxis of allergic rhinitis relative efficacy of hydroxyzine and chlorpheniramine. J Allergy Clin Immunol 1981 67 223. 68. Schaaf L, Hendeles L, Weinberger M. Suppression of seasonal allergic rhinitis symptoms with daily hydroxyzine. J Allergy Clin Immunol 1979 3 129. 69. Empey DW, Bye C, Hodder M, et al. A double-blind crossover trial of pseudoephedrine and triprolidine alone and in combination, for the treatment of allergic rhinitis. Ann Allergy 1975 34 41. 70. Diamond L, Gerson K, Cato A, et al. An evaluation of triprolidine and pseudoephedrine in the treatment of...
Extensive evidence has accumulated that may define the underlying immunologic basis for the atopic phenotype, that is, individuals with allergic asthma, allergic rhinitis, and atopic eczema (24). The atopic condition can be viewed as a TH2 lymphocyte-driven response to allergens of complex genetic and environmental origins (36). The reciprocal action of IL-4 and IFN-g on IgE production led to several studies on the T-cell origin of these cytokines. Mosmann and Coffman ( 37) described two distinct types of helper T cells in murine systems and defined them as TH1 or TH2 cells by the pattern of cytokine secretion. TH1 cells produced IL-2, IFN-g, and lymphotoxin. TH2 cells produced IL-4, IL-5, IL-6, and IL-10.
Second-generation antihistamines are available only as oral formulations. They all have convenient once- or twice-daily dosing ( 10,1.7) (Iab e.,5.,4). Studies have reported that a single dose of terfenadine (120 mg) or fexofenadine (180 mg) is equally effective as 60 mg given twice a day in improving allergic rhinitis symptom scores and suppressing histamine-induced wheal-and-flare responses (46,47). Astemizole and loratadine should be injected on an empty stomach to avoid problems with absorption. All three agents have comparable antihistaminic potency to each another and to first-generation antihistamines.
Tolerance to antihistamines is a common concern of patients taking these agents chronically. This phenomenon has been speculated to occur because of autoinduction of hepatic metabolism, resulting in an accelerated clearance rate of the antihistamine ( 103). However, studies have failed to confirm this hypothesis, and most reports of tolerance to antihistamines are now believed to be secondary to patient noncompliance because of intolerable drug side effects or breakthrough symptoms due to severity of disease (104,105,106 and 107). Short-term studies evaluating tolerance to second-generation agents have found no change in their therapeutic efficacy after 6 to 8 weeks of regular use (108,109). Studies up to 12 weeks found no evidence that second-generation agents cause autoinduction of hepatic metabolism leading to rapid excretion rates and drug tolerance (42). The clinical efficacy of these agents in the skin and treatment of allergic rhinitis does not decrease with chronic use.
The discovery of H-, receptor antagonists has proved to be a significant breakthrough in the treatment of allergic diseases. Chemical modifications of these early agents have yielded the second-generation antihistamines, which are of equal antagonistic efficacy but have fewer side effects because of their lipophobic structures. Newer nonsedating antihistamines, which are metabolites or isomers of existing agents, are now under development. H 2 receptor antagonists have been found extremely useful in the treatment of peptic ulcer disease. However, they have been disappointing in the treatment of allergic and immunologic disorders in humans. Newer selective nonsedating H-, antagonists and dual-action antihistamines, because of their lower side-effect profiles, have provided therapeutic advantages over first-generation agents for long-term management of allergic rhinitis.
Scanning electron photomicrographs of early spring airborne hay fever-producing pollen grains 1, pine (Pinus) 2, oak (Quercus) 3, birch (Betula) 4, sycamore (Platanus) 5, elm (Ulmus) 6, hackberry (Celtis) 7, maple (Acer) 8, willow (Salix) 9, poplar (Populus). (Courtesy of Professor James W. Walker.) Most of these trees are dioecious and produce large quantities of round pollen grains 20 to 30 mm in diameter with a thick intine (internal membrane). The mountain cedar is an important cause of allergic rhinitis in certain parts of Texas and has proliferated where the ecosystem has been disturbed by overgrazing of the grasslands. The bald cypress may be a minor cause of allergic rhinitis in Florida. Trees Angiosperms These trees produce large amounts of highly allergenic pollen. Pecan trees in particular are important in the etiology of allergic rhinitis where they grow or are cultivated. The pollen grains are 40 to 50 pm in diameter and usually contain three germinal pores.
Early and late summer airborne hay fever-producing pollen grains 1, timothy (Phleum) 2, orchard grass (Dactylis) 3, lambs quarter's (Chenopodium) 4, plantain (Plantago) 5, goldenrod (Solidago) 6, ragweed (Ambrosia). (Courtesy of Professor James W. Walker.) Sweet vernal grass (Anthoxanthum odoratum) is an important cause of allergic rhinitis in areas where it is indigenous. In the total picture of grass allergy, however, it is not as important as the species previously mentioned. The pollen grains are 38 to 45 pm in diameter.
Was there trauma to the nose Allergic rhinitis can cause itching and subsequent rubbing of the nose, traumatizing mucosa. Prior trauma from a direct blow on the nose may cause septal injury and bleeding. A dry environment causes crusting, and young children may be prone to picking the nose, irritating septal mucosa. Unilateral foul or purulent nasal discharge suggests a foreign body. In hospitalized patients, indwelling nasal tubes or suction trauma may injure mucosa and promote bleeding.
Preventive measures are essential in order to avoid barotrauma of the external and middle ear, the labyrinth, and the sinus. Repetitive Valsalva and or Frenzel maneuvers help to keep open the Eustachian tube which equalizes middle-ear and ambient pressure. Individuals suffering from upper respiratory infections or allergic rhinitis, which cause dysfunction of the Eustachian tube and produce edema of the mucosa around the sinus orifices, should avoid scuba diving. Treatment involves the use of analgesics, antihistamines, and vasoconstrictors. Antibiotics should be used if the tympanic membrane is ruptured ( Kizer.1995).
Acute conjunctivitis should be distinguished from the group of allergic forms of conjunctivitis, which can be due to seasonal influences and often affect the nasal mucosa. Examples include allergic conjunctivitis (hay fever Fig.4.17) and vernal conjunctivitis. In giant papillary conjunctivitis, the inflammation is triggered by a foreign body (hard or soft contact lenses. There may also be an additional chronic microbial irritation such microbial contamination of contact lenses. Phlyctenular keratoconjunctivitis is a delayed allergic reaction to microbial proteins or toxins (staphylococcal inflammation). This disease occurs frequently in atopic individuals and is promoted by poor hygiene. The cardinal rule in allergic conjunctivitis is to avoid the causative agent. Desensitization should be performed as a prophylactic measure by a dermatologist or allergist. Long-term treatment includes cromoglycic acid eyedrops to prevent mast cell degranulation. Treatment of acute allergic con- Fig....
The most common cutaneous illness associated with abnormal processing of HPV is atopic dermatitis, although some studies have not supported an increased incidence. A recent study from the United Kingdom demonstrated that cervical cancer is more common in eczema patients and patients who acquire common warts. However, this study suggests that non-atopic eczemas, such as seborrheic dermatitis, may be the type associated with cervical cancers, as hay fever, an illness commonly co-morbid with atopic eczema, was not statistically correlated to cervical cancer 31 .
Although cromolyn sodium (Intal) and nedocromil sodium (Tilade) are widely known for their ability to prevent the release of histamine and other inflammatory mediators by mast cells during the early response to antigen challenge, these drugs have a wide variety of inhibitory effects on many cell types, including eosinophils, neutrophils, monocytes, and neurons. Cromolyn sodium and nedocromil sodium are used as pulmonary inhalants in the treatment of asthma. Nasal (Nasalcrom) and ophthalmic (Opticrom) preparations of cromolyn sodium can be used to reduce the symptoms of allergic rhinitis and conjunctivitis. More detailed information on these compounds may be found in Chapter 39.
Nasal obstruction contributes to the worsening of sleep-disordered breathing, but the extent to which this might be related to allergic rhinitis is not known. One case-control study did show that sleep apnea patients had a higher rate of perennial allergic rhinitis and atopy than controls (104).
An allergic reaction is simply the overresponse of the immune system to a specific stimulus, usually environmental. This stimulus is called an antigen. There are 4 basic types of allergic reactions. We are all very familiar with the type 1 response. This reaction is seen as a result of hay fever, bee stings, cats, dogs, or even medications. It is the cause of the itchy, watery eyes, and runny nose many of us experience each spring when we cut the grass or stroll through the park. A brief look at the cause of this response will help us better understand the treatment of these conditions.
Pulmonary features in allergic angiitis and granulomatosis are related to underlying asthma which is present in all patients. A phasic pattern of allergic angiitis and granulomatosis syndrome has been described initial allergic rhinitis, evolving into asthma and followed by peripheral blood eosinophilia, eosinophilic tissue infiltrates, and ultimately vasculitis. A study of 154 patients with allergic angiitis and granulomatosis revealed the following 84 males, average age of 28 years at onset of allergic rhinitis, average age of 35 years at onset of asthma, and average age of 38 years when vasculitis was diagnosed. Other observations included a mean peak eosinophil count of 12.9 * 109 l, anemia in 83 per cent, granulomas in 40 per cent, tissue eosinophilia in 50 per cent, and vasculitis in more than 70 per cent. Chest radiograph abnormalities are present in over 60 per cent of patients and include patchy and occasionally diffuse alveolar-interstitial infiltrates in the perihilar area....
Individuals with a history of atopy, hay fever, rhinitis, asthma or eczema. In a number of reports examining latex allergy in various populations, atopy was one of the significant predisposing risk factors. In a study of latex sensitization in a low-risk pediatric population, Bernardini et al. reported that all the children with latex sensitization were atopic whereas only 29 percent of non-sensitized subjects had positive skin prick responses to environmental or food allergens.48 Liss et al. demonstrated a five-fold increase in positive skin tests among atopic health care workers compared to non-atopic workers.43
Allergen immunotherapy is effective in patients with allergic rhinitis. Allergy treatment begins with identification of allergens, institution of avoidance procedures and administration of medication. Immunotherapy may be considered if other measures fail.
Bacterial rhinosinusitis usually follows a viral infection or allergic rhinitis, and the most commonly involved agents are Streptococcus pneumoniae, Haemophilus influenzae and Moraxella catarrhalis 11, 34 . A dense inflammatory infiltrate mainly made of neutrophils occupies the lamina propria. Acute bacterial rhinosinusitis usually resolves with antibiotic therapy. Complications are rare and include contiguous infectious involvement of the orbit or central nervous system.
Nasal congestion is a common side effect of CPAP therapy (53). Although most patients experience initial self-limiting nasal congestion, at least 10 complain of persistent nasal stuffiness of some degree after six months of therapy (54). There appear to be many possible reasons for nasal symptoms. CPAP may provoke pressure-sensitive mucosal receptors, leading to vasodilation and increased mucus production. In some patients, it may unmask allergic rhinitis by restoring the nasal route of breathing after years of mouth breathing. In others, fixed nasal obstruction with polyps or a deviated septum may produce symptoms. Mouth leaks also cause increased nasal resistance (55).
Keys to locating an active source of anterior bleeding or intranasal foreign body are adequate light, appropriate instruments, cooperative patient, and skilled assistance. Assess color and texture of mucosa. Clear secretions, boggy turbinates, and bluish mucosa are seen in patients with allergic rhinitis.
Hypersensitivity reactions are immunological reactions that cause tissue damage. Type I hypersensitivity reactions mediated by cell-bound IgE antibodies occur immediately after exposure to antigen. The reactions are caused by the release of mediators from mast cell granules. Localized anaphylactic reactions include hives, hay fever, and asthma generalized reactions lead to anaphylactic shock. Immunotherapy is directed toward
Tens of millions of people suffer from pollen allergies, one cause of hay fever. Hay fever is an allergic reaction that results in sneezing, a runny nose, and watering eyes. Pollen allergies occur at three seasons. In early spring, deciduous trees, such as oak, ash, birch, and sycamore release pollen. In late spring or early summer, it is mainly wild and pasture grasses that cause allergy problems. Of the cereal crops, only rye pollen seems to be an important cause of allergies. In late summer and fall, the highly allergenic pollen of ragweeds, shown in Figure 27-11, affects many people. Contrary to popular belief, large, colorful flowers do not cause hay fever. Pollen that causes allergies comes from small, drab flowers that are wind-pollinated.
There are two types of histamine receptors H1 and H2. H2 receptors cause an increase in gastric secretions and are not involved in this response. The differences are illustrated in the charts. (See Antihistamine (H1 blocker) chart and Antihistamine Use to Treat Allergic Rhinitis chart.) Antihistamine Used to Treat Allergic Rhinitis Antihistamine Used to Treat Allergic Rhinitis (continued)
Sinus problems, hay fever, bronchial asthma, hives, eczema, contact dermatitis, food allergies, and reactions to drugs are all allergic reactions associated with the release of histamine and other autocoids, such as serotonin, leukotrienes, and prostaglandins. Histamine release is frequently associated with various inflammatory states and may be increased in urticarial reactions, mas-tocytosis, and basophilia. Histamine also acts as a neu-rotransmitter in the central nervous system (CNS). Upon release from its storage sites, histamine exerts effects ranging from mild irritation and itching to ana-phylactic shock and eventual death.
By promoting the formation of T lymphocytes, thymic factors are used to enhance T-lymphocytic functions. Thymic factors have been used with some success in clinical trials in patients with severe combined immunodeficiency, DiGeorge's or Nezelof's syndrome, and viral disorders. Studies with thymodulin show promise in treating symptoms in asthmatics and patients with allergic rhinitis. The primary consideration in the use of thymic factors for immunodeficiency states is the presence of T-lymphocyte precursors.
Atopy is an underlying disease syndrome which has been consistently connected with dermatophytosis. A high proportion of chronically infected individuals, over 40 in some surveys, have hay fever, asthma, or atopic eczema either on personal or family history (Hay, 1982 Jones et al., 1973). In addition a high proportion of individuals seen in dermatological clinics with peripheral dermatophyte infection either have negative or immediate-type hypersensitivity to dermatophyte antigens on intradermal testing. Increased prevalence of immediate-type responses to intra-dermally injected antigens is also a feature of atopic subjects. There is also evidence that some individuals with persistent dermatophytosis may also have sensitivity to environmental moulds suggesting a modified (atopic) immunological response to a family of antigens.
An allergy is the body's reaction to a substance that may be harmless in itself but the immune system misidentifies and treats it as a pathogen. Antibodies, called immunoglobulin E or IgE, react by attacking the substance and in the process histamine is released by the surrounding cells which causes an allergic reaction. The allergic reaction may include itchy nose and throat, nausea, vomiting, diarrhea, skin irritations, hay fever, hives, asthma, high blood pressure, abnormal fatigue, constipation, or hyperactivity. A severe reaction called anaphylactic .shock will swell the larynx, obstruct the airway, and may be fatal. This is an emergency situation and remedied by an injection of adrenalin. Ephedra 20 mg capsules, relieves symptoms of hayfever. Stinging nettle 1 to 2 freeze dried capsules every 2 to 4 hours, relieves symptoms of hayfever, hives, and itching. Khella relieves spasms in smooth muscle of the bronchi in hayfever, do not use on skin.