Allergic reaction question

Is it true that you can only have an allergic reaction to something AFTER the initial exposure?

For example, the very first time you get exposed to something you could be allergic to, it will do nothing?

I myself, was stung by a hornet when I was 8, and went into a anaphylactoid reaction, An anaphylactoid reaction produces a very similar clinical syndrome but is not immune-mediated.

I just HATE it when my patients try to code out on me!!

Actually the crustacean/mussels part is no longer valid. That used to be a red flag when we used the ionic contrasts, but these days it's a moot point.

Oh, and I didn't catch before...hypatia said that anaphylactoid reactions are NOT immune-mediated. They are, but are not allergic reactions

How dare they!

Thanks for the clarification.

Oh, and I didn't catch before...hypatia said that anaphylactoid reactions are NOT immune-mediated. They are, but are not allergic reactions...i.e., they are not IgE mediated...at least that seems to be the distinction from what I've gathered in some quick reading, such as from the links above. I had come across some assorted other case reports where they were calling such reactions anaphylactic reactions upon first exposures to some drugs, but within the description of the follow-up testing, those patients did not have any IgE response (which had me baffled until hypatia mentioned the anaphylactoid reactions and I dug into them), so it seems to be a commonly confused term, even within the literature and among medical practitioners. I guess in a clinical setting, since both respond to the same treatment, the nuances of mechanism aren't important, though to an allergist they might be.

Anaphylactoid reactions resemble anaphylactic reactions. However, anaphylactoid reactions may occur after the first exposure to a substance—for example, after the first injection of certain drugs, such as polymyxin, pentamidineSome Trade Names
NEBUPENT, PENTAM 300, opioids, or the radiopaque dyes sometimes used with x-ray procedures. Anaphylactoid reactions are not allergic reactions because IgE, the class of antibodies involved in allergic reactions, does not cause them. Rather, the reaction is caused by the substance itself. Aspirin (Some Trade Names: ECOTRIN, ASPERGUM)
and other nonsteroidal anti-inflammatory drugs (NSAIDs) can cause anaphylactoid reactions in some people, particularly those with year-round allergic rhinitis and nasal polyps.

If possible, doctors avoid using dyes with x-ray procedures in people who have anaphylactoid reactions to such dyes. However, some disorders cannot be diagnosed without dyes. In such cases, special dyes that reduce the risk of reactions are used. In addition, drugs that block anaphylactoid reactions, such as prednisone (Some Trade Names: DELTASONE, METICORTEN) diphenhydramine (Some Trade Names: BENADRYL, NYTOL, SOMINEX), or ephedrine, are usually given before the dye is injected.

Where have you found that they ARE immune-mediated?

Toxicology. 2005 Dec 15;216(2-3):106-21.
Szebeni J.

A major goal in modern pharmacotechnology is to increase the therapeutic index of drugs by using nanoparticulate vehicle systems in order to ensure slow release or targeted delivery of drugs. With all great benefits, however, these innovative therapies can carry a risk for acute immune toxicity manifested in hypersensitivity reactions (HSRs) that do not involve IgE but arises as a consequence of activation of the complement (C) system. These anaphylactoid reactions can be distinguished within the Type I category of HSRs as "C activation-related pseudoallergy" (CARPA). Drugs and agents causing CARPA include radiocontrast media (RCM), liposomal drugs (Doxil, Ambisome and DaunoXome) and micellar solvents containing amphiphilic lipids (e.g., Cremophor EL, the vehicle of Taxol). These agents activate C through both the classical and the alternative pathways, giving rise to C3a and C5a anaphylatoxins that trigger mast cells and basophils for secretory response that underlies HSRs. Pigs provide a useful model for liposome-induced CARPA as minute amounts of reactogenic lipomes cause C activation with consequent dramatic cardiovascular and laboratory abnormalities that mimic some of the human symptoms. Consistent with the causal role of C activation in liposome-induced HSRs, a recent clinical study demonstrated correlation between the formation of C terminal complex (SC5b-9) in blood and the presence of HSRs in patients treated with liposomal doxorubicin (Doxil). Overall, the CARPA concept may help in the prediction, prevention and treatment of the acute immune toxicity of numerous state-of-the-art drugs.

Curr Drug Deliv. 2005 Oct;2(4):443-9.

Complement activation-related pseudoallergy caused by amphiphilic drug carriers: the role of lipoproteins.

Szebeni J.

Self-assembling amphiphilic lipids or polymers have been successfully used in pharmacotherapy as drug solvents or carriers, improving the bioavailability of water-insoluble drugs. This review focuses on an unusual hypersensitivity reaction (HSR) caused by a micellar (Cremophor EL, CrEL) and a monomeric block copolymer (poloxamer 188) representative of these systems. The HSRs, also referred to as anaphylactoid or pseudoallergic, are thought to arise as a consequence of complement (C) activation in blood. However, considering that C activation involves the deposition of multiple C and other (immune) proteins on the activator surface, the mechanism by which small, 8-25 nm CrEL micelles or individual poloxamer 188 molecules activate C is not straightforward. Observations on enlarged lipoproteins and de novo formation of abnormally large lipoprotein-like structures in plasma exposed to CrEL or poloxamer 188 raise the possibility that lipoprotein transformation might play a crucial role in C activation by these amphiphilic emulsifiers. Lipoproteins, furthermore, can also provide a negative feedback control on C activation, as suggested by the inhibition of poloxamer 188-induced C activation in the presence of excess exogenous lipoproteins, and the attenuation of liposome-induced and C activation-related hypotension in pigs by precoating the vesicles with lipoproteins. Thus, lipoproteins may be essential in the induction, and they may also play a complex modulatory role in C activation-related pseudoallergy caused amphiphilic drug solvents and carriers.