Anaphylactoid reaction, mediators

Type I hypersensitivity reactions (immediate hypersensitivity or anaphylaxis) are immunologic responses to a foreign antigen to which a patient has been previously sensitized. Anaphylactoid reactions are not immunoogically mediated however, symptoms and treatment are similar. 

Most anaphylactoid reactions are due to a direct or chemical release of histamine, and other mediators, from mast cells and basophils. Immune-mediated hypersensitivity reactions have been classified as types I-IV. Type I, involving IgE or IgG antibodies, is the main mechanism involved in most anaphylactic or immediate hypersensitivity reactions to anaesthetic drugs. Type II, also known as antibody-dependent hypersensitivity or cytotoxic reactions are, for example, responsible for ABO-incompatible blood transfusion reactions. Type III, immune complex reactions, include classic serum sickness. Type IV, cellular responses mediated by sensitised lymphocytes, may account for as much as 80% of allergic reactions to local anaesthetic. 

BETA-BLOCKERS X-RAY CONTRAST SOLUTIONS Beta-blockers are associated with T risk of anaphylactoid reactions to iodinated X-ray contrast materials Uncertain, but postulated that beta-receptors have a role in suppressing the release of mediators of anaphylaxis Consider using low-osmolality contrast media and pretreating with antihistamines and corticosteroids. Stopping beta-blockers a few days before the X-ray is associated with a risk of withdrawal t BP and tachycardia a risk-benefit assessment must therefore be made... 

Alfadolone and alfaxolone are two steroid anesthetics that were used in combination. However, the mixture has been withdrawn because of safety considerations regarding the solvent used, polyethoxylated castor oil (Cremophor EL), which can cause non-IgE-mediated anaphylactic (anaphylactoid) reactions (SED-10,189) (1). 

Non-IgE-mediated anaphylactic (anaphylactoid) reactions suspected to be caused by dextran as used in BCG vaccines have been described (SEDA-16, 375). 

Acute allergic reactions were reported in 48 patients, and included anaphylactic or anaphylactoid reactions and angioedema without shock. Two anaphylactic reactions, one fatal, to parenteral diclofenac have been reported (SEDA-18, 104). Hepatorenal damage (SEDA-15, 100), thrombocytopenia, and hemoljdic anemia mediated by an immune mechanism have been reported (SEDA-16,110). 

Skin rashes due to podophyllotoxin derivatives may be hypersensitivity reactions and can be related to the drug itself or more commonly to the vehicles used. Dose-related, non-IgE-mediated hypersensitivity has been reported in 16 children receiving teniposide (118). Other published reports of hypersensitivity or anaphylactoid reactions to teniposide include degranulation of basophils (119,120), and eight anaphylactic reactions in children, all associated with the use of intravenous teniposide 150 mg/ m (121). 

Many compounds, including a large number of therapeutic agents, stimulate the release of histamine from mast cells directly and without prior sensitization. Responses of this sort are most likely to occur following intravenous injections of certain substances. Tubocurarine, succinyl-choline, morphine, some antibiotics, radiocontrast media, and certain carbohydrate plasma expanders may elicit the response. The phenomenon may account for unexpected anaphylactoid reactions. Vancomycin-induced red-man syndrome involving upper body and facial flushing and hypotension may be mediated through histamine release. 

Anaphyla. is is a type I reaction in which the drug ( ) interacts with IgE lixed to mast cells contrast media) can produce an anaphylaxis-like (anaphylactoid) reaction on first exposure. 

Anaphylactoid reactions are also caused by release of active compounds from mast cells but do not involve prior sensitization or mediation through IgE. 

This test was negative in patients who had experienced anaphylactoid reactions to gelatin derivatives, indicating absence of specific cell-mediated hypersensitivity (Ring 1978 a). Further, the T- and B-cell functions were considered normal as measured by stimulation of the lymphocytes with phytohemagglutinin and pokeweed mitogen. 

Autacoids A 25-year-old woman had a non-IgE-mediated anaphylactic (anaphylactoid) reaction with angioedema and pulmonary edema 24 hours after starting to take oral ciprofloxacin 500 mg bd for pyelonephritis [30" ]. Ventilatory support was required for 4 days. A literature review revealed 64 cases of probable ciprofloxacin-related anaphylactoid reactions and detailed information was available in 22 patients, 10 of whom were HIV positive. The mean age was about 35 years and reactions typically developed minutes to hours after first exposure in the HIV-negative patients and from 5 minutes to 5 days of dosing in... 

The prevalence of acute reactions to gadobutrol, a highly concentrated macro-cyclic gadohnium chelate, has been studied using prospective observational surveillance in 14 299 patients [27 ]. There was at least one adverse reaction in 78 patients (0.55%) and 2 (0.01%) were serious. One was a severe non-IgE-mediated anaphylactic (anaphylactoid) reaction and the other presented with itching and swelling of the throat. The most common adverse reaction was nausea, which occurred in 36 patients. 

Moneret-Vautrin (1979, 1983) has suggested that exogenous histamine and histamine releasers may lead to anaphylactoid reactions when there is functional impairment of the mucosa, either in early childhood before maturation of exclusion mechanisms or later due to intrinsic disease of the gut or to the action of pharmaco-active agents. However, the relevant foods (cheese, egg white, shellfish, nuts) are also those to which evidence of IgE-mediated sensitization is found commonly, and as we have seen, absence of demonstrable specific IgE antibody in the serum does not prove the non-allergic nature of the reaction. This remains an area of potentially useful future research. 

Individuals with hereditary angioneurotic oedema lack serum CT-esterase inhibitor, the inhibitor of the activated first component of hemolytic complement. During an acute episode of this disorder circulating CT-esterase, which is a permeability-increasing factor in human skin, is markedly increased [57, 97, 140, 142, 219, 332]. It is unlikely that a similar mechanism is involved in the anaphylactoid reaction in rats as reactivity is not an absolute phenomenon [32-34, 274]. The final inflammatory mediator(s) of the reaction is, therefore, available for release in both reactor and non-reactor rats. This implies that the trigger mechanism or some intermediary step in the reaction is different in the two types of rat. 

The following criteria have been applied when considering the role of a potential mediator in the anaphylactoid reaction ... 

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