Mechanisms Of Contact Urticaria

CUS can be described in two broad categories: nonimmunological contact urticaria (NICU) and immunological contact urticaria (ICU). The former does not require presensitization of the patient's immune system to an allergen, whereas the latter does. There are, however, contact urticaria reactions of unknown mechanism, and these are unclassified.

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Nonimmunological Contact Urticaria s

NICU is the most frequent immediate contact reaction (4) and occurs, without ja prior sensitization, in most exposed individuals. The symptoms may vary according to the site of exposure, the concentration, the vehicle, the mode of exposure, and the substance itself (5). |

The mechanism of NICU is not well understood. It was previously assumed that histamine was released from mast cells in response to exposure to an eliciting substance. However, the H antihistamines—hydroxyzine and terfenadine—do not inhibit NICU to benzoic acid, cinnamic acid, cinnamic aldehyde, or methyl nicotinate in prick tests, but they do inhibit reactions to histamine itself (5,6). Therefore, mechanisms that do not involve histamine may mediate NICU for these substances.

Evidence suggests that prostaglandins may mediate NICU. Oral and topical nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit nonimmunological reactions (7). Lahti et al. (6), used laser Doppler flowmetry to demonstrate a reduction in NICU-induced erythema in subjects pretreated with NSAIDs. This group believed that inhibition of prostaglandin metabolism may explain this effect.

Supporting this, Morrow et al. (8) demonstrated an increase in plasma PGD2 following the topical application of 1% sorbic acid to the human forearm. The time course of PGD2 peaks correlated temporally with the observed intensity of cutaneous vasodilatation. Notably, histamine and PGE2 levels at peak erythema were not significantly higher than pretreatment levels. This suggests that the release of vasodilatory prostaglandins induced by sorbic acid was selective for PGD2, and that histamine is not involved in sorbic acid contact urticarial reactions. The release of PGD2 was a dose-dependent effect, increasing with greater concentrations of sorbic acid, until reaching a plateau between 1 to 3%. Pretreat-ing the subjects with oral aspirin (325 mg b.i.d. for 3 days) attenuated the observed cutaneous vasodilatation and inhibit release of PGD2. In later studies, based on the same model, this group demonstrated similar results with benzoic acid-and nicotinic acid-induced contact urticaria (9,10).

These studies add evidence to the argument that prostaglandin metabolism is significant in the pathophysiology of CUS. Also, they not only suggest that NSAIDs are useful as a treatment but also that experimental subjects should avoid these drugs when participating in a contact urticaria study.

Ultraviolet A and ultraviolet B light also inhibits immediate nonimmuno-logical contact reactions. Notably this effect can last for 2 weeks after irradiation and inhibits skin sites that were not directly irradiated (7). The authors suggest that there may be a systemic effect rather than simply a local one; however, the mechanism by which ultraviolet light inhibits NICU is not known.

Immunological Contact Urticaria s

ICU is less frequent in clinical practice than the NICU form. It is a type 1 hyper- ja sensitivity reaction mediated by IgE antibodies, specific to the eliciting substance (11). Therefore, prior immune (IgE) sensitization is required for this type of con- «

tact urticaria.

This sensitization can be at the cutaneous level, but also via mucous membranes, for example, in the respiratory or gastrointestinal tracts. Notably, ICU reactions may spread beyond the site of contact and progress to generalized urticaria and, in the most severe case, to anaphylactic shock.

People with an atopic background (personal or family background of eczema, hayfever, or asthma) are predisposed toward the immunological form of contact urticaria.

A well-studied example of ICU is allergy to natural rubber latex (NRL), which is found in a wide variety of products, such as balloons, condoms, and, importantly, surgical or protective gloves. ICU to NRL is a major occupational hazard in occupations that utilize such gloves (e.g., the health care profession).

Typically, latex gloves cause a wheal-and-flare reaction at the site of contact. This can affect either the person wearing the gloves or the person being touched by the wearer. In a study of 70 German patients with contact urticaria, 51% suffered rhinitis, 44% conjunctivitis, 31% dyspnea, 24% systemic symptoms, and 6% severe systemic reactions during surgery (12). In addition to direct skin contact, allergy may be caused by airborne NRL (13). Clearly, sensitized, yet undiagnosed, individuals are at risk when contacting ICU allergens.

Cross allergy can also induce ICU reactions: the patient may be sensitized to one protein but reacts to other proteins that contain the same (or similar) aller-genic molecule. In the example of latex allergy, patients may also experience symptoms from banana, chestnut, and avocado (14). This phenomenon places ICU patients at further risk.

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