CONTACT
URTICARIACONTACT
URTICARIA'Urticaria' is derived from the Latin term urtica, meaning nettle, a plant with toothed leaves covered with hairs that contain a stinging fluid. Urtica is further derived from the Latin uro meaning ‘to burn’ or ‘burn up’ in the sense of ‘to irritate, chafe, or rub sore’. Not surprisingly, the plant family Urticaceae is the most notorious family for causing urticaria.
TOXIN-MEDIATED
URTICARIA ( TMU )
Toxin-mediated (non-immunologic) contact urticaria occurs without prior sensitization in most individuals who contact plants such as nettles. Most cases of contact urticaria due to plants are toxin-mediated and do not involve a Type I hypersensitivity reaction. Such plant species possess sharp hairs known as trichomes on the surfaces of leaves and stems. The proximal silicaceous hair attaches to a distal calcified portion with a terminal bulb. When rubbed against, the bulb is dislodged at a predetermined line from the end of the hair revealing a beveled, hypodermic needle-like, silicaceous hollow. These release irritant chemical cocktails (containing histamine, acetylcholine, and 5-hydroxytryptamine) that supposedly act as a defense mechanism against plant-eaters.13-15 These plants have been used since antiquity as counterirritants in folk medicine.16
Table
2. The most common plants causing toxin-mediated
urticaria15,17
|
|
|
|
|
|
Urticaceae (Nettle family; 550 spp. worldwide) |
Urtica |
dioica, urens, pilulifera |
'stinging nettles', world-wide |
|
|
Laportea |
canadensis |
NE USA 5-foot tall perennial herb, wood nettle |
|
|
Dendrocnide |
gigas, moroides, photinophylla |
Australian stinging tree-shrubs |
|
Euphorbiaceae (Spurge family) |
Acidoton |
urens |
tropical America |
|
|
Cnidosculus |
stimulosus |
SE USA; 'tread-softly', 'spurge nettle', 'bull nettle' |
|
|
Cnidosculus |
spp. |
'spurge nettles' of tropical Americas |
|
Loasaceae (Loasa family) |
Blumenbachia, Caiophora, Cevallia, Eucnide, Fuertesia, Gronovia, Loasa, Mentzelia |
spp |
cultivated as ornamentals; SW USA, Mexico, S. America |
|
Hydrophyllaceae (Water-leaf family) |
Wigandia |
caracasana |
N. America herbs and sub-shrubs |
Members of the family Urticaceae account for the majority of contact urticaria throughout the world.19 The most common culprit in the United States is the stinging nettle (Urtica dioica). Stinging nettle grows throughout the world, except in the lowland trpoics. It is well-entrenched in American soil, especially in moist woods, road sides, and waste places (Figure 1).17,19,20 The spurge nettle, bull nettle, or 'tread-softly' (Cnidosculus stimulosus) is also a common cause of contact urticaria.17,20 Urtica urens has also been reported to cause allergic contact dermatitis.21 Reactions to these, plants, however, pale in comparison to those elicited by members of the Dendrocnide genus of the Urticaceae family. Mostly found in Eastern Australia rain forests, these trees grow up to 40 meters in height. Young shoots are covered with stiff stinging hairs. Urticaria from these may be severe and last for weeks, and contact with water or cold objects reactivates the urticaria.16 Severe, intermittent, stabbing pains may follow the course of lymphatics. Many equine deaths and one human death due to Dendrocnide members have been documented. 15
Clinical Symptoms
Patients experience short-lived burning and itching with wheals. In a controlled trial, wheals achieved maximal size between 3 and 5 minutes after contact. Erythema faded in 1-2 hours, but a persistent tingling sensation lasted 12 hours or more.18 At 5 minutes, dermal edema and telangiectasia with or without mild spongiosis were seen. At 12 hours, edema had resolved but vasodilation persisted. Some patients had neutrophilic and lymphocytic spongiosis. Mast cell numbers were increased in the papillary dermis at 12 hours but not at 5 minutes. While histamine, acetylcholine, and 5-hydroxytryptamine explain the early reaction (Triple response of Lewis), they do not account for the persistent paresthesias.13 This indicates that other mediators may cause secondary release of neurotoxic inflammatory mediators. Most stings are benign, self-limited, and require no treatment.19
IMMUNOLOGIC CONTACT URTICARIA ( ICU )
Type I hypersensitivity reactions require that individuals have been previously sensitized to an allergen in the plant. The allergen must contact IgE on mast cells and cause symptoms within one to two hours to be considered a true 'contact urticaria'.22 The release of vasoactive mediators leads to local urticaria and rarely may cause a 'contact urticaria syndrome' that includes local wheals with systemic symptoms in the nose, throat, lungs, gastrointestinal tract, or cardiovascular system. The main factor seems to be histamine since simultaneous preinjection with compound 48:80 (a mast cell degranulator) and an antihistamine reduces or blocks the clinical response. Prostaglandins, kinins, and leukotrienes probably augment the inflammatory response.14
Most affected individuals have been long-time food-handlers, atopic patients, or both, with the contact urticaria exacerbating existing atopic dermatitis (known as 'protein contact dermatitis').23 Although contact urticaria is more common among atopic patients, reactions to poison ivy are less common.14 Within 30 minutes of contacting certain foods, affected individuals experience pruritus, erythema, urticarial swelling, and even dyshidrotic-like vesicles. Sometimes, individuals experience only symptoms of pruritus and burning.14, 22 While the inciting agent may cause urticaria at higher doses, this subjective phenomenon experienced at lower doses has no name.14 Theoretically, any plant could cause contact urticaria, but continued exposure on the wet, macerated skin of food handlers has caused certain foodstuffs (eg. potatoes) to be the most notorious offenders. 15 Even in those without atopic dermatitis, repeated urticarial reactions can cause eczematous eruptions. Cooking, processing, deep-freezing, or crushing fruits and vegetables generally reduce their allergenicity.14
Examples of reported urticants include some common vegetables, fruits, herbs, nuts, shrubs, algae, lichens, trees, and grasses. In one review, potatoes were the most frequent culprits.14 Celery (Apium graveolens) is the most likely plant to cause a generalized urticarial or anaphylactoid reaction. 15 Individuals with Type I reactions to rubber products (proteins derived from the latex of the rubber tree Hevea brasiliensis) may also cross-react with apples and bananas.23
Testing for contact urticaria6, 8
At least seven different tests, all using suspected plant materials, have been recommended for diagnosing plant contact urticaria. The test of choice for TMU is the 'open application test' and for ICU is the 'scratch chamber test'. Serologic tests such as the radioallergosorbent test (RAST) provide less information than prick or scratch-chamber tests. While the work-up of such patients is difficult, office testing of suspected allergens may assume one of the seven methods presented below:
1) Use test14, 23 - The patient handles the plant or plant product as when the original eruption was elicited.
2) Rub test (open patch test)14 - The suspected urticant is rubbed on normal or diseased skin of the forearm or back. The site is observed for one hour. Erythema and edema constitutes a positive reaction that is more easily recognized on normal skin.
3) Skin application food test (closed patch test)14, 23 - The potential allergen is applied to the skin and occluded by a Finn test chamber plaster (Scanpor, Epitest Ltd, Helsinki, Finland). The patch is examined at 10, 20, 30, and 60 minutes for erythema and edema.
4) Prick testing14,15,23 - Prick testing is more sensitive than the skin application food test, but it is potentially the most hazardous method. Place a small piece of plant material on the forearm. Make superficial pricks through the plant material with a blood lancet or hypodermic needle. Care must be taken not to induce bleeding. After observing for an immediate reaction, the site should be covered for 15-20 minutes.
5) Scratch test14,15 - The scratch and prick tests are more sensitive than the contact tests because urticarial allergens are often high molecular weight proteins that poorly penetrate intact skin. In this test, a 5-mm long scratch is made on the back or forearm. Test material is applied for 10-15 minutes and read every 15 minutes for an hour.
6) Scratch chamber technique14,15,23 - This is performed the same as the scratch test, except that the scratch site and test material are occluded with a Finn test chamber for 15 minutes. Readings should be done at removal (15 minutes) and every 15 minutes for one hour. This is the most sensitive available test. After reading, the chamber can be replaced for 48 hours to test for delayed hypersensitivity testing.
7) Open Application Test14 - The method of choice for diagnosing toxin-mediated urticaria requires that 0.1 ml of the suspected urticant be spread on a 3 x 3 cm area of skin. Dilution series are often used. The sites are observed every 10-15 minutes for an hour. Maximal erythema and edema typically occur 30 to 40 minutes after application. Test sites should be examined at 24 hours for irritant reactions.
N.B.: For the above tests, various references recommended final readings at 15 to 60 minutes. To avoid the risk of missing a later reaction, I have recommended reading test sites out to 60 minutes.
For unusual plant products, 10-20 controls (such as clinic staff) should be tested so that toxin-mediated urticaria and irritant dermatitis can be excluded as causes. Serologic tests such as the radioallergosorbent (RAST) test usually do not convey as much information as prick or scratch-chamber tests. 15
Treatment of contact urticaria
Prevention is the preferred form of treatment, but oral antihistamines are sometimes helpful. Of course, parenteral epinephrine is required for anaphylactic reactions.
|
Advance to the next section:  |
|
|
