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Medical condition From Wikipedia, the free encyclopedia
Urushiol-induced contact dermatitis (also called Toxicodendron dermatitis or Rhus dermatitis) is a type of allergic contact dermatitis caused by the oil urushiol found in various plants, most notably sumac family species of the genus Toxicodendron: poison ivy, poison oak, poison sumac, and the Chinese lacquer tree.[1] The name is derived from the Japanese word for the sap of the Chinese lacquer tree, urushi. Other plants in the sumac family (including mango, pistachio, the Burmese lacquer tree, the India marking nut tree, and the cashew) also contain urushiol,[2] as do unrelated plants such as Ginkgo biloba.[3]
| Urushiol-induced contact dermatitis | |
|---|---|
| |
| Specialty | Dermatology  |
| Symptoms | rashes, itching, inflammation, oozing, and, in severe cases, a burning sensation. |
| Causes | urushiol contact |
As is the case with all contact dermatitis, urushiol-induced allergic rashes are a Type IV hypersensitivity reaction, also known as delayed-type hypersensitivity. Symptoms include itching, inflammation, oozing, and, in severe cases, a burning sensation.
The American Academy of Dermatology estimates that there are up to 50 million cases of urushiol-induced dermatitis annually in the United States alone, accounting for 10% of all lost-time injuries in the United States Forest Service. Poison oak is a significant problem in the rural Western and Southern United States, while poison ivy is most rampant in the Eastern United States. Dermatitis from poison sumac is less common.
Urushiol causes an eczematous contact dermatitis characterized by redness, swelling, papules, vesicles, blisters, and streaking.[4][5] People vary greatly in their sensitivity to urushiol. In approximately 15%[6] to 30%[7] of people, urushiol does not trigger an immune system response, while at least 25% of people have a very strong immune response resulting in severe symptoms.[citation needed]
The rash takes one to two weeks to run its course and may cause scars, depending on the severity of the exposure.[4] Severe cases involve small (1–2 mm), clear, fluid-filled blisters on the skin. Pus-filled vesicles containing a whitish fluid may indicate an infection. Most poison ivy rashes, without infections, will resolve within 14 days without treatment. Excessive scratching may result in infection, commonly by staphylococcal and streptococcal species; these may require antibiotics.
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Urushiol-induced contact dermatitis is caused by contact with a plant or any other object containing urushiol oil.[1] The oil adheres to almost anything with which it comes in contact, such as towels, blankets, clothing, and landscaping tools.[4] Clothing or other materials that touch the plant and then, before being washed, touch the skin are common causes of exposure.[4]
For people who have never been exposed or are not yet allergic to urushiol, it may take 10 to 21 days for a reaction to occur the first time. Once allergic to urushiol, however, most people break out 48 to 72 hours after contact with the oil. Typically, individuals have been exposed at least once, if not several times, before they develop a rash.[8] The rash typically persists one to two weeks, but in some cases may last up to five weeks.
Urushiol is primarily found in the spaces between cells beneath the outer skin of the plant, so the effects are less severe if the plant tissue remains undamaged on contact. Once the oil and resin are thoroughly washed from the skin, the rash is not contagious. Urushiol does not always spread once it has bonded with the skin, and cannot be transferred once the urushiol has been washed away.
Although simple skin exposure is most common, ingestion of urushiol can lead to serious, systemic reactions. Burning plant material is commonly said to create urushiol-laden smoke that causes a systemic reaction, as well as a rash in the throat and eyes. Firefighters often get rashes and eye inflammation from smoke-related contact.[9] A high-temperature bonfire may incinerate urushiol before it can cause harm, while a smoldering fire may vaporize the volatile oil and spread it as white smoke. However, some sources dispute the danger of burning urushiol-containing plant material.[10]
Urushiol is fat-soluble, penetrating the stratum corneum of the skin, then binding to Langerhans cells in the epidermis.[1] The affected cells then migrate to lymph nodes, where T cells become activated, then return to the skin where they stimulate an urushiol-activated dermatitis.[1] The toxic effect is indirect, mediated by an induced immune response.[1] The oxidized urushiols act as haptens, chemically reacting with, binding to, and changing the shape of integral membrane proteins on exposed skin cells.[1] Urushiols are oxidized in vivo, generating a quinone form of the molecules.[11]
Affected proteins interfere with immune system ability to recognize these cells as normal parts of the body, causing a T-cell-mediated immune response.[12] This response is directed at the complex of urushiol derivatives (namely, pentadecacatechol) bound in the skin proteins, attacking the cells as if they were foreign bodies.
Treatment consists of two phases: stopping the urushiol contact that is causing the reaction (this must be done within minutes)[13] and, later, reducing the pain and itching.[4]
Primary treatment involves washing exposed skin thoroughly with soap, cool water, and friction as soon as possible after exposure is discovered.[4] Soap or detergent is necessary because urushiol is an oil; friction, with a washcloth or something similar, is necessary because urushiol adheres strongly to the skin.[4]Commercial removal preparations, which are available in areas where poison ivy grows, usually contain surfactants, such as the nonionic detergent Triton X-100, to solubilize urushiol; some products also contain abrasives.
The U.S. Food and Drug Administration recommends applying a wet compress or soaking the affected area in cool water; topical corticosteroids (available over-the-counter) or oral corticosteroids (available by prescription); and topical skin protectants, such as zinc acetate, zinc carbonate, zinc oxide, and calamine. Baking soda or colloidal oatmeal can relieve minor irritation and itching. Aluminium triacetate, sometimes known as Burow's solution, can also ease the rash.[14]
Showers or compresses using hot (but not scalding) water can relieve itching for up to several hours, though this "also taxes the skin's integrity, opening pores and generally making it more vulnerable", and is only useful for secondary treatment (not for cleaning urushiol from the skin, which should be done with cold water).[15] People who have had a prior systemic reaction may be able to prevent subsequent exposure from turning systemic by avoiding heat and excitation of the circulatory system and applying moderate cold to any infected skin with biting pain.
In cases of extreme symptoms, steroids such as prednisone, triamcinolone, or dexamethasone are sometimes administered to attenuate the immune response and prevent long-term skin damage, especially if the eyes are involved. Prednisone is the most commonly prescribed systemic treatment but can cause serious adrenal suppression, so it must be taken carefully and tapered off slowly.[16] If bacterial secondary infection of affected areas occurs, antibiotics may also be necessary.
Scrubbing with plain soap and cold water will remove urushiol from skin if it is done within a few minutes of exposure.[4][13]
A rarely cited double-blind study in 1982 reported that a course of oral urushiol usually hyposensitized subjects, with the principal side effect, pruritus ani, being reported by 85% of the participants who ingested the urushiol.[22]
Research conducted on urushiol by Mahmoud ElSohly led to the development of PDC-APB, a candidate for a vaccine against skin irritation from poison ivy.[23]
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