__________________________________________________ DCA02AR Allergic Reactions in Dental Patients
TYPE I REACTIONS Type I allergic reactions are immediate, with an onset of only a few minutes to a few hours. The most serious type I hyper- sensitivity reaction is anaphylaxis, the most serious degree of an allergic response. It is characterized by a set of symptoms that involves various organs and systems and occurs indepen- dently, simultaneously, or subsequently [6]. Initial symptoms often include widespread hives and progress rapidly to bron- chospasm, respiratory arrest, and ultimately, cardiac arrest. Whether the anaphylactic reaction is of immune or nonim- mune origin, the stimulation of mast cells and circulating baso- phils releases chemical mediators that begin the anaphylactic process. A rapidly escalating systemic reaction can occur only minutes after exposure to a specific antigen or onset may be delayed several hours [7]. In 1% to 20% of anaphylaxis cases, there will be a biphasic response, with recurrence of symptoms 8 to 12 hours later, after the individual had seemed to recover [8]. The interval between the initial reaction and the recurrence has ranged from 1 to 72 hours [9; 10]. Another type I hypersensitivity reaction is atopy. Atopy is a genetic predisposition to develop allergic rhinitis, asthma, and dermatitis [11]. Urticaria (hives) are the most common lesion associated with atopic reactions, although these lesions are not unique to atopy. An outbreak of urticaria can occur anywhere on the skin, and the classic presentation is a wheal—a raised area surrounded by an erythematous base. The cause of urticaria during an allergic reaction is the release of histamine from cutaneous mast cells coupled with other progenitors of inflammation. These substances cause the extravasation of fluids from surface capillaries, with subsequent swelling and redness. Urticarial lesions are intensely pruritic and blanch upon the application of direct pressure. Resolution of urticaria may take several weeks, during which the patient may experi- ence moderate itchiness and discomfort. TYPE II REACTIONS Type II hypersensitivity reactions are mediated by IgG or IgM and are predominantly directed against erythrocytes, leukocytes, platelets, and their progenitor cells in the bone marrow. Hypersensitivity reactions in this category are cytotoxic reactions, the classic example of which is hemolytic transfu- sion reactions that occur when the transfused blood type is incompatible with the patient’s blood type [12]. Although this is not a reaction that would occur in the dental office, it is important that normal laboratory values for the formed elements of human blood return to the normal range before any invasive dental procedure is performed.
PATHOPHYSIOLOGY AND CATEGORIZATION OF ALLERGIC REACTIONS
In 1975, Gell and Coombs developed a classification system to categorize the unique physiologic pathways of various hypersensitivity (allergic) reactions [3]. While this classification system has evolved, allergic reactions remain classified as type I through type IV. Allergic reactions are associated with the production of immu- noglobulin E (IgE) by specialized B-lymphocytes called plasma cells. Immunoglobulins, also known as antibodies, are proteins secreted against any of a myriad of antigens. This reaction is beneficial when the antibodies are directed against pathogenic micro-organisms (e.g., bacteria, fungi, viruses); however, this response becomes detrimental when IgE production is trig- gered against a nonpathogenic substance. In some cases, the immune response is strong enough to lead to serious morbidity or anaphylactic shock. Plasma cells are concentrated in the skin, tonsils, and mucosa of the respiratory and gastrointestinal systems [4]. When the immune system recognizes an antigen, IgE binds to mast cells and basophils, which are stimulated to release compounds such as histamines, proteases, and chemotactic factors. The production of other mediators of an allergic response (e.g., prostaglandins, leukotrienes) is also enhanced. The systemic release of these substances leads to an increase in capillary permeability, vasodilation, spasms of the smooth muscles, and excessive secretion of mucus [5]. The degree to which these events occur varies considerably among patients. Extensive capillary permeability can lead to accumulation of interstitial fluids and swelling of the affected tissues. When this occurs in the laryngeal and tracheal areas, airway compromise can lead to asphyxiation. Spasms of the bronchiolar smooth muscles and excessive secretion of mucus can further exacerbate this problem.
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