IgE-mediated Anaphylactic Reactions Research Articles

Immunochemical particularities of anaphylactic reactions to compounds used in anaesthesia

The main compounds causing anaphylactic reactions in anaesthesia are myorelaxants, opiate or barbiturate derivatives or natural allergens (latex). While the latex-derived allergens are of sizeable molecular weight and behave as regular complete allergens, most of the other compounds are low molecular weight molecules behaving as incomplete allergens or haptens. For these, the sensitization process usually encompasses direct reaction (conjugation) with cellular surface proteins (e.g. histocompatibility antigens) of an antigen-presenting cells and ensuing formation of hapten-specific IgE antibodies. Since many patients experience igE-mediated anaphylactic reactions upon first contact with a myorelaxant, a previous latent sensitivity to some cross-reactive epitope (e.g. quaternary ammonium group) must be postulated. In sensitized individuals possessing drug-specific IgE antibodies, the elicitation of anaphylactic reactions classically requires bridging on the surface of IgE loaded mast cells/basophils by allergens which are functionally at least bivalent (two or more reactive epitopes by allergen molecule). In some cases, myorelaxant molecules, chemically appearing as mirror molecules may be functionally bivalent and elicit anaphylactic reactions apparently directly. In most instances, however, when the responsible drug only contains one reactive epitope per molecule, alternative mechanisms and rapid formation of functionally polyvalent drug allergens in tissue have to be postulated in order to explain the rapid elicitation of anaphylactic reactions by molecules which appear to be immunologically monovalent in vitro. Indeed, in most instances, monovalent haptens and drugs appear to be inhibitors rather than elicitors of IgE-mediated reactions.

Allergy to latex surgical gloves: An unfamiliar cause of intraoperative anaphylaxis

Natural rubber products, including surgical gloves, are known to be associated with contact dermatitis in allergic individuals. These cell-mediated immune reactions are usually not serious. However, an increasing number of reports have appeared recently in the medical literature concerning the association of latex with type I IgE-mediated anaphylactic reactions. We report on a patient with a history of cutaneous sensitivity to latex who experienced an intraoperative anaphylactic reaction felt to be secondary to latex surgical gloves. This report is intended to familiarize clinicians with this unexpected cause of intraoperative anaphylaxis.

Mechanism of antianaphylactic action of beta-agonists in allergic inflammation of air pouch type in rats.

Using an experimental model of allergic inflammation of air pouch type in rats, the mechanism of antiallergic action of beta-agonists was examined. In this model an immediate increase in vascular permeability and histamine level in the pouch fluid was observed after injecting the antigen (azobenzene arsonate-conjugated acetyl bovine serum albumin) solution into the preformed air pouch on the back of the sensitized rats. The same type of reaction was inducible by injecting anti-rat IgE into the preformed air pouch, but not IgG2a. This fact indicates that the immediate increase in vascular permeability and histamine level is an IgE-mediated anaphylactic reaction. When beta-agonists such as isoproterenol, procaterol and salbutamol were injected into the air pouch together with the antigen, the anaphylactic increase in vascular permeability was suppressed dose-dependently without concomitant decrease in histamine level in the pouch fluid. In contrast, disodium cromoglycate, an inhibitor of degranulation of mast cells, the anaphylactic vascular permeability increase was suppressed in parallel with a decrease of the histamine level. Propranolol, a beta-antagonist, counteracted the effect of beta-agonists. Serotonin-induced vascular permeability was also suppressed dose-dependently by treatment with beta-agonists. Furthermore, vascular permeability in the postanaphylactic phase of the present experimental model was also suppressed by isoproterenol. These results indicate that beta-agonists exert their antiallergic effect by inhibiting the reactivity of local vasculature to chemical mediators released from mast cells.

The Restaurant Syndromes

Anaphylactic or anaphylacticlike (anaphylactoid) reactions while dining occur with a disturbing frequency. These cases present as medical emergencies. The onset of symptoms may occur from minutes to two hours after ingestion. Some of the monosodium glutamate reactions (bronchospasm) may occur up to 14 hours later. Causative factors usually consist of food allergens (eg, peanuts), preservatives (metabisulfites), color additives (tartrazine), flavor enhancers (monosodium glutamate [MSG]), and food toxins (eg, scombroidosis). Understanding and diagnosing the cause of these reactions is extremely important to prevent recurrence and possibly fatal reactions. In addition, some of these color additives and preservatives are found in certain drugs and can cause similar adverse reactions. Allergy to food antigens are IgE-mediated anaphylactic reactions, usually occurring within 30 minutes and up to two hours after ingestion. They are associated with a history of atopy and ingestion of known food allergens such as peanuts, egg, fish, and walnuts, together with

Identification and partial purification of species-specific allergens from Triatoma protracta (Heteroptera:Reduviidae)

This article describes the immunochemical characterization of allergens from Triatoma protracta, a hematophagous insect that causes IgE-mediated anaphylactic reactions when it bites sensitized allergic persons. Comparison of the allergenic potency of T. protracta salivary gland extract, thoracic and abdominal hemolymph, and a whole body extract by RAST inhibition demonstrated that salivary glands were the main source of T. protracta allergens. Concentrated salivary gland extracts were purified by gel filtration and isoelectric focusing. Fractions were tested for allergenic activity by RAST inhibition and for protein purity by polyacrylamide gel electrophoresis and immunoelectrophoresis. Two protein peaks were obtained on gel filtration. The high-molecular-weight peak contained a 70,000 MW protein/glycoprotein that had little allergenic activity. The low-molecular-weight peak comprised six proteins, molecular weight 17,000 to 25,000, and T. protracta allergen(s) eluted in parallel with this peak. These proteins were resolved by isoelectric focusing, and two fractions, pI 6.7 to 7.3 and pI 8.2, contained most of the allergenic activity. By RAST, 25 28 sera from T. protracta-allergic patients contained IgE antibody to these fractions, suggesting that they were major allergens. Each fraction demonstrated a single precipitin arc on immunoelectrophoresis and two bands, molecular weight 18,000 to 20,000, on gel electrophoresis. Cross-inhibition radioimmunoassays demonstrated that each fraction completely inhibited binding of the other fraction to IgE antibody, suggesting that they contained different isoelectric forms of the same allergen.

Effects of antihistamines and indomethacin on hyperosmolar-induced vasodilation.

The circulatory effects of iv injections of hyperosmolar solutions were studied both in intact dogs with aortic flow probes and in dogs using a standard right heart-bypass preparation. Serial iv injections of 20 ml of 10% NaCl or 50 ml of 25% mannitol produced reproducible episodic vasodilation characterized by falls in mean aortic pressure from 99 +/- 10 (SE) to 61 +/- 6 Torr and increases in aortic flow from 2.20 +/- 0.06 1/min to 3.12 +/- 0.28 (P less than 0.01). Systemic vascular resistance decreased (P less than 0.01) with each injection and serum osmolarity increased (P less than 0.01); however, there was a poor correlation between these two variables (r = -0.24). Because the mechanism of these physiological changes is unclear, the following experiments were performed to determine whether they were due to the release of vasoactive chemical mediators. We measured arterial and venous plasma histamine, a mediator released systemically in IgE-mediated anaphylactic reactions, but found no changes in histamine levels. Furthermore, pretreatment with both H1 and H2 blockers (diphenhydramine and cimetidine), agents that blocked histamine-induced hypotension, did not prevent hyperosmolar vasodilation. Also, indomethacin (a cyclooxygenase pathway inhibitor of prostaglandin synthesis) did not affect hyperosmolar vasodilation or the fall in systemic vascular resistance. Therefore, hyperosmolar vasodilation is not caused by the systemic release of histamine or by the effects of prostaglandins. The mechanism of these reactions is unknown, but it may be due to direct local effects of hyperosmolar solutions on vascular smooth muscle, perhaps mediated by local fluid and electrolyte shifts.