What Is Hay Fever (Allergic Rhinitis);Diagnosis And Treatment

Hay fever (Allergic Rhinitis) is the common name applied to allergic rhinitis which recurs each year at a specific season-usually spring or fall. It is characterized by rhinorrhea, sneezing, itching of the eyes, nose, ears, and palate, and edema of the nasal mucous membranes Non-scasonal allergens, such as feathers and animal danders, may produce year-round disease called perennial allergic rhinitis; vasomotor rhinitis is a “wastebasket” term which designates perennial rhinitis without an identifiable allergic basis.

What Is Hay Fever (Allergic Rhinitis);Diagnosis And Treatment

Etiology and Epidemiology of Hay Fever

Susceptible persons exposed each year to airborne pollen of many varieties of plants, particularly trees, grasses, and weeds, develop a “wheal and flare” type of immediate hypersensitivity to protein components of the pollen grains calk’d allergens The exact hervditable basis of hay fever is still unclear, but clustering of a variety of diseases which involve “wheal and flare” hypersensitivity in certain individuals. and in families, strongly supports the view that such a basis exists Recent evidence su^tM’sts that sensitivity to a particular allergen, such as ragweed, may be dependent upon transmission of a specific immune response gene and therefore might be predictable in an individual before development of the disease.

Drab, colorless plants, unattractive to birds and bee, must depend upon the wind for pollination and release of huge amounts of airborne pollen In contrast, colorful blossoms and odoriferous plants generally release smaller amounts of heavier, stickier pollen which is not widely disseminated. “Rose fever.” a form of allergic rhinitis prevalent in early summer, is a misnomer; while roses are visually in full bloom, it is the pollen from grasses such as timothy. June, and orchard grass which produces the disease.

Ragweed and grass pollen are the most common causes of allergic rhinitis in the United States. Ragweed abounds in the midwestern states, and is prevalent in the eastern and southeastern part of the country. West of the Rocky Mountains and in the dry Southwest, very little ragweed appears. Each area has a distinctive potentially sensitizing flora, and sufferers fleeing from one part of the country to another are often disappointed when symptoms rapidly reappear in their new location. In the northern United States early spring hay fever i April and May) is usually due to tree pollen; the grasses pollinate and produce symptoms in early summer (June and early July I and the ragweed in late summer and early fall. Spores of ubiquitous molds are present throughout the year but increase in numbers at different times because of increased mold growth on decaying vegetation. Spores of Homodcndrum peak in number in July, whereas spores of Alternaria increase in the fall, overlapping the ragwet-d season, and may be the basis of an erroneous diagnosis of ragweed hay fever.

The trees are a varied and an important group; ash, beech, birch. cedar. hickory, maple. oak. sycamore, and puplar all produce important windborne pollen, whereas the less antigenic pollens of the firs and pines are not usual sources of disease. Each species of tree produces an antigenicallv distinct pollen with a relatively short period of pollination lasting two to four weeks. Hypersensitivity to multiple species of trees with overlapping pollinating periods, and to grasses, molds, and ragweed, may blur the seasonal aspects of the patient’s problem and suggest a perennial allergic rhinitis. Unlike the trees, grasses such as timothy, fescue, orchard, redtop. and June ‘Kentucky bluegrass) share important antigenic determinants and in the extreme South and West may produce year-round symptoms.

A careful account of seasonal variations in symptoms coupled with a knowledge of the flora of the patient’s locality and the pollinating periods of the indigenous plants is vital to the specific diagnosis and management of this group of diseases. In the British Isles and the European continent, trees and grasses are important causes of pollinosis; allergic travelers would do well to check the season of their proposed trip. Europe has little or no ragweed, so American sufferers may doubly enjoy a late summer European vacation.

Pollen grains are about 20 to  m in diameter, and each species has a distinctive appearance. By collecting grains on a glass slide with a simple timed exposure or with more sophisticated air-sampling devices, pollen* may be identified and enumerated. The severity of symptoms of an allergic population will vary with the pollen numbers in an approximate way. but the use of daily radio broadcast pollen numbers as a diagnostic or predictive aid is of little value. The “counts” are derived from samples obtained the previous day. and at different locations and altitude-^ Often the patient will ask why he doesn’t feel better tor worse) liecause of the low (or high) pollen count’

Allergic rhinitis may be caused by any inhaled antigen. those often implicated, in addition to plant pollen, are house dust, feathers, fungus spores, and animal danders Food allergy is often suggested as a basis for inhalant symptoms, but manifestations in the skin such as urticaria or angioneurotic edema (see Ch. 75 and 76) are the rule, and the respiratory tract is an unlikely target organ for this type of hypersensitivity.

Pathogenem Of Hay fever

Sensitization may occur at any time of ife but usually occurs in childhood or adolescence It is curious that an adult may become sensitized to a pollen to which he has been exposed each previous year of his life; this suggests that factors other than genetic proclivity and exposure are necessary. When pollens impinge upon the nasal mucous membrane, they release a variety of protein antigens called allergens which initiate the immune response The major allergens of grasses and ragweed have been partially purified and are low molecular weight protein of relatively low antigenicity. This means that for a given amount of antigen, the immune response in terms of amount and avidity of antibody produced is small.

The important point is that this type of antigen in low doses tends to elicit an unusual response characterized by production of reaginic antibody, which is largely or completely of the IgE class. Such antibodies are present in nanograni quantities in serum, and ‘‘fix” to the surface of cells so that passive administration will sensitize a particular skin site for weeks. Because of this quality, reaginic antibodies are sometimes called homocytotropic Contact with the specific allergen will cause “sensitized” cells to release potent vasoactive substances, largely histamine and slow reacting substance of anaphylaxis (SRS-A). These materials cause capillary vasodilatation with leakage of fluid and colloid into the tissues leading to the major symptoms of allergic disease.

Although the symptoms produced by inhalation of pollen are localized to the mucosa with which it comes in contact, the sensitization is systemic. When peripheral leukocytes of .sensitive individuals are exposed to allergen in vitro, they release histamine. This reaction affords a rapid measurement of sensitivity, usually expressed in terms of amount of allergen necessary to produce release of 50 per cent of the cellular histamine, it also provides an objective measurement of the efficacy and mechanism of treatment. Production of IgK antibody is not limited to allergic individuals; normal subjects or laboratory animals will develop this cluss of antibody response after subcutaneous injection of allergens The presence of extracts of roundworms such as ascaris facilitates production of IgK antibody in an unknown way Similarly, the nasal route of allergen exposure in an allergic individual facilitates development of IgK antibody.

Non immunologic factors also play a role in producing what may be called th«- inertia” of allergic disease; patient.s who are well tend to remain well, whereas tho*-who are sick tend to remain sick. Nonspecific irritants of all sorts can cause incapacitating sneezing and rhinor rhea in a patient suffering from allergic rhinitis; these might be tolerated without a sniffle at another time of year. Upper respiratory infections, particularly sinusitis. occur more frequently in the allergic patient owing to edema and obstruction of normal drainage. Similarly, the normal effects of emotional states upon the nasal mucosa are often exaggerated in the allergic patient.

Clinical Manifestations of Hay fever

The abrupt onset of morning gneezing. usually in paroxysms of several sneezes in rapid succession, accompanied by rhinorrhea, itchiness of eyeB, palate, and pharynx, are characteristic of allergic rhinitis Symptoms recur each year at approxi mutely the same time, corresponding to the appearance of the offending pollen in the air Increased exposure will intensify symptoms dry, windy duy.s, riding in an open car, and working in a garden are frequently reported to worsen the symptoms A hay fever sufferer notes that the

morning and evening hours are the- worst, with a relatively better period during the midday Mucosal congestion and edema often lead to total blockage of the airway, necessitating mouth breathing. Theconjunctivae are red and weepy, and the lids and periorbital tissues may be puffy.

Hay fever is not often accompanied by temperature elevations, und the name i» therefore misleading Fever should alert one to the common complications sinusitis, otitis, or mastoiditis. Cough, wheezing, and dyspnea are frequent companions of allergic rhinitis Because pollen grains are too large to affect the terminal bronchioles, it was thought that the allergic reaction in the upper respiratory tract could trigger lower airway obstruction, but recent studies indicate that pollen fragments small enough to reach the bronchioles are present in the inspired air.

Hay fever Diagnosis.

Early in the* course, the differentiation of allergic rhinitis from that caused by irritants or infections is difficult, but in retrospect the patient will usually remember similar but milder symptoms at the same time in previous years. The seasonal bistory ih the 11111*1 important of all clues to correct diagnosis. Allergic rhinitis may be differentiated from viral upper respiratory’ infections when pruritus of eyes. nose, and pharynx is present, and by the absence of fever, sore throat, and malaise. The nasal mucous membranes appear swollen, pale, and boggy in allergic rhinitis, and red and “angry” in viral infections; but inflammation secondary to sneezing and frequent blowing to clear the nose may blur these differences. Nasal secretions may be obtained by asking the patient to blow his nose into a piece of ordinary wax paper; smears stained with Wright’s or Giemsa stains show an abundance of eosinophils in allergic rhinitis, whereas in infectious rhinitis smears reveal polymorphonuclear leukocytes.

Environmental allergens other than pollen are more difficult to diagnose as the basis of allergic rhinitis, but a careful history will often elicit them Inquiry should be made into the home: Mow old is it? What is the heating system? What are the floor, wall, and window coverings? What types of pillows, matt reuses, quills, and comforters are used by the patient and bv his or her spouse? Frequently the nonnllergic marriage partner will sleep on a feather pillow not five inches from the allergic one sleeping on a nonallorgenic pillow. The question of what makes symptoms worse or better has a special significance in the allergic history. Often patients can specify a place or activity associated with symptoms which when avoided keeps them symptom-free.

Hay Fever Treatment

Treatment is directed toward avoiding the allergen, modifying the state of hypersensitivity, and ameliorating the symptoms. By far the most effective means is strict avoidance of the offending allergen. When this is due to an increased sensitivity to an animal dander such as that of horse or cat, merely identifying the cause will help greatly in avoidance. Often patients will “hide” their pets from the physician’s inquiry- because they have a strong suspicion of the offender but hope that something else will be found. Effective filtration of the air within the patient’s house is now possible with a variety of electrostatic and barrier-type filters. Dust control and attention to bedding and furniture filling will be rewarding in selected rases.

Treatment with repeated injections of specific allergens has been in vogue for 70 years, and recent studies have confirmed the efficacy of this mode of therapy and given insight to its mechanism. Preseasonnl, coseasonal. and perennial administration of allergens all have their proponents, but perennial administration avoids the necessity of building up the dosage each year and results in the tame number of patient visits. Increasing amounts of allergen are irejected subcutaneously once or twice weekly, starting with a dose shown to be tolerated by skin tests. The goals of hyposensitization are two: production of a nonreaginic ‘blocking) antibody which can effectively compete with reaginic antibody for allergen, and reduction of the amount of reaginic antibody produced ‘tolerance induction), thereby decreasing cellular sensitivity to allergen. Addition of serum from a treated individual to sensitized leukocytes in vitro may increase by 100-fold the amounts of allergen necessary for 50 per cent histamine release from these leukocytes.

The increment of allergen injected at each visit is determined by the patient’s skin reaction to the previous injection. If redness and swelling exceed the size of a 50-cent piece, the dose should be repeated or lowered until it is better tolerated. Often an increase in sensitivity occurs early in treatment; this may lead to a worsening in symptoms if it coincides with the patient’s season. Usually patients are treated for two or more years after maximal benefit has been achieved, at which time hyposensitization is stopped.

A proportion of patients will maintain their improvement whereas, in many, a slow return of symptoms during the following year or 18 months is common Patients should always be advised to remain in the office for 30 minutes after the injection, because the allergen may provoke a constitutional reaction This is often herald<-d by reddening of the conjunc-tivae, nasal swelling, red ears and nose, and a feeling of faintness Tourniquets should be applied above the injection sites and 0.2 toO 5 ml of aqueous epinephrine 1:1000 injected above the tourniquet Such reactions are uncommon They are usually easily managed in the office or clinic; but if the patient leaves the office immediately after an allergen injection, the reaction at best will be very frightening and might possibly be fatal.

A variety of repository allergen preparations, including mineral oil emulsions. and alum-precipitated allergens. have generated interest because of a putative ability to administer more allergen in fewer injections with less likelihood of systemic reactions. The efficacy and safety of these preparations are still to be determined.

Symptomatic Treatment.

Antihistamines ure often lelpful in ameliorating symptoms of allergic rhinitis. In general they are only partially effective, and patients romplain of the soponfic side effects. Brompheniramine Dimetane) and chlorpheniramine (Chlor-Trimetonl areboth available in 4 mj; tablets and in long-acting preparations containing 8 or 12 mg. Both these preparation* seem to have less soporific effects than Benadryl, which should be used only at bedtime.

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