Allergic Reaction: Is Initial Exposure Necessary for Allergic Reactions?

[Holocene]

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?

 

[Tsu]

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'm not absolutely sure, I don't believe that that is true. It's a possibility - but not a given. In my job as a Cat Scan Tech., we administer a liquid to patients commonly called 'xray dye'. It is clear liquid that contains iodine and about one in 90,000 people (who have never had the injection) can have a severe anaphylactic reaction to it and most of their body systems shut down immediately. Or they can have numerous exams utilizing this liquid and have absolutley no reaction to it, and then, one day - out of the blue - they have a major reaction to it when administered - even though they've had it before with no problems. Allegric reactions are often random occurances.

 

[hypatia]

Tus is right, it can be the first time, or the 100th time.

 

[Moonbear]

Usually, a first exposure doesn't induce a reaction, or it's only a very mild reaction. A full blown allergic reaction requires a previous exposure. In Tsu's example, one cannot rule out the individual ingredients. For example, x-ray dyes contain commonly used preservatives. Someone may have developed a sensitivity due to previous exposure to the preservative, for example in their cosmetics or detergents.

The sensitizing agent may not need to be the exact one that someone reacts to either. For example, if someone is allergic to one antibiotic, it is likely they will be allergic to others in the same class.

 

[hypatia]

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. Anaphylactoid and Anaphylaxis are both treated the same way.
Some drugs and foods ( morphine,shellfish) may cause an anaphylactoid reaction on the first exposure.
I would think for the majority of the population, it is the act of being sensitized a few times before a allergic reaction occurs. But if either signs of anaphylactoid and anaphylaxis become known, seek help at once.

A small study from American Academy of Pediatrics
http://pediatrics.aappublications.org/cgi/content/full/102/1/e6
Initial reactions usually occurred at home (median age, 24 months for PeaNut and 62 months for Tree, nut) and were considered to result from a first exposure in 72% of cases.

 

[Moonbear]

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.

Here's something else that discusses that, and by chance, they even happen to mention radiologic dyes (x-ray dye) as causative of anaphylactoid reactions.

http://www.postgradmed.com/issues/2002/05_02/rusznak.htm

Hmm...this one mentions radiologic contrast dyes too...and some contraindications for their use; Tsu, if you weren't already aware of these, it might be worth looking into further.

http://www.hon.ch/Library/Theme/Allergy/Glossary/anaphylactoid_reaction.html

 

[Tsu]

Thanks MB!

Yes, we are all VERY aware of the contraindications for contrast media injections. 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. We are more concerned now with renal function and other underlying diseases; diabetes, heart problems (on beta-blockers - as the article mentioned), multiple myeloma... We have a HUGE list of things on our questionaires.

 

[Moonbear]

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

How dare they!

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.

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.

 

[hypatia]

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

Where have you found that they ARE immune-mediated?

http://www.anaesthesiajournal.co.uk/article/PIIS147202990700152X/abstract

3}Anaphylactoid reactions occur through a direct nonimmune-mediated release of mediators from mast cells and/or basophils or result from direct complement activation, but they present with clinical symptoms similar to those of anaphylaxis.

 

[Tsu]

How dare they!

I KNOW! Can you believe that?? It just wrecks my whole day!

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.

This may help clear up the differences between "anaphylactoid" and "anaphylatic". The uses of either may have been what caused the confusion in the first place, but I think it addresses the OP question best. It's from the drug company Merck from this page:

http://www.merck.com/mmhe/sec16/ch185/ch185e.html

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.

 

[Moonbear]

Where have you found that they ARE immune-mediated?

Here's one example (well, 2 examples, but same author):

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.

http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

and

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.

http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

There are some articles by other authors that support this too, basically distinguishing anaphylactic from anaphylactoid by the presence or absence of IgE involvement, but I'm not sure what I can quote of them (they have further restrictions than the usual journals in our library subscription).

 

[hypatia]

opps posted in wrong thread!