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The Pathophysiology of Latex Allergy
- all the Immunology you need to know
- An allergic reaction is one mediated by immunologic
mechanisms i.e. the interaction of a foreign molecule, or antigen,
with host antibodies and/or effector cells.
- A life-threatening allergic reaction mediated by
antibodies is known as anaphylactic. When antibodies
are not responsible for the reaction, it is termed
anaphylactoid and may involve complement activation or
non-immunologic release of histamine.
- Anaphylactic and anaphylactoid reactions cannot be
distinguished by clinical observation.
- Antigen binding to IgE antibodies initiates
anaphylaxis. Prior exposure to the antigen, or a substance
of a similar structure is required to produce sensitisation. On
re-exposure, binding of the antigen bridges to immunospecific IgE
antibodies located on the surfaces of mast cells and basophils,
liberating histamine and other inflammatory mediators, such
as leukotrienes, prostaglandins and kinins.
The liberated mediators produce a respiratory, cardiovascular and
cutaneous symptom complex. See Diagnosis of
Anaphylaxis.
- Intra-operative latex anaphylaxis is immunologic and mediated
by IgE
- Latex can also result in reactions that are limited to the
skin. This type of allergy is not IgE-related and is classified
immunologically as a Type IV reaction (anaphylaxis is Type
I). Clinically this is seen as rubber glove eczema in health care
workers, contact stomatitis in those using rubber orthodontic
appliances, and condom dermatitis. These reactions are not
life-threatening, are unrelated to the proteins that incite Type I
reactions and are probably due to chemicals
(mercaptothiobenzothiazole, tetramethyliuram) added to rubber
during processing.
- Type IV reactions (contact dermatitis) occur mostly in
patients with occupational exposure to latex. But note that
contact dermatits, especially in atopic individuals, may portend
future systemic (Type I - anaphylactic) sensitivity.
