Urushiol

Ginkgolic acids are urushiol-type alkylphenols and occur in quantity in the seed coat and to a much lesser extent in the leaves.

From: Trease and Evans' Pharmacognosy (Sixteenth Edition), 2009

Chapters and Articles

Contact Hypersensitivity

P.S. Friedmann, in Encyclopedia of Immunology (Second Edition), 1998

Immunobiology

Activation of the immune system via the epicutaneous contact route is dependent upon several factors.

Antigen potency

Some antigens, such as 2,4-dinitrochlorobenzene (DNCB), pentadecylcatechol (urushiol of poison ivy) and diphenylcyclopropenone (diphencyprone) are potent and can sensitize all subjects. Many organic compounds and inorganic salts of metals such as nickel, cobalt and chromium are weak antigens and appear only to sensitize some subjects.

Genetic factors

In experimental animals there are clearly genetic controls of immune reponsiveness. Thus, inbred guinea pigs of strain XIII can be sensitized with mercury but not chromate or beryllium, whereas animals of strain II can be sensitized with chromate and beryllium but not with mercury. Evidence in humans is less clear-cut. With regard to a strong antigen (DNCB), it seems that everyone can become sensitive but there is a normal distribution of the degree of sensitivity. Family studies have indicated that ‘high responder’ characteristics are transmitted to children. Studies of HLA linkage in subjects with the propensity to form numerous allergic sensitivities to environmental substances have not found positive evidence of genetic control.

Intact lymphatic drainage

Guinea pigs cannot be sensitized if antigen is applied to islands of skin lacking lymphatic drainage. This is because the early stages of the induction process involve circulation of antigen-bearing cells via the lymphatics to the draining lymph nodes.

Antigen-presenting cells

The epidermis is populated with Langerhans cells. These are leukocytes whose function is presentation of antigens to the appropriate CD4+ T lymphocytes. They have long dendritic processes ramifying between the epidermal cells, forming a network likely to be encountered by any organism or antigen which penetrates through the stratum corneum barrier. They are characterized by a formalin-resistant membrane ATPase, a specific cytoplasmic organelle, the Birbeck granule, membrane antigens including CD1a (T6), class II major histocompatibility complex (MHC) antigens and costimulatory molecules B7-1 and B7-2. Langerhans cells also express various adhesion molecules including E-cadherin, probably necessary for maintaining position in the epidermis, and ICAM-1 and LFA-1, necessary for their migration to the regional lymph node and interaction with T cells.

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Poisonous Plants

SUSAN C. SMOLINSKE PHARMD, ... DAVID G. SPOERKE MS, RPH, in Haddad and Winchester's Clinical Management of Poisoning and Drug Overdose (Fourth Edition), 2007

ALLERGIC CONTACT DERMATITIS

Allergic contact dermatitis is the result of a type IV hypersensitivity reaction that requires a previous exposure before symptoms develop. The most common substances known to elicit such a reaction are the urushiol oleoresins. Urushiol contains a mixture of catechols (1,2-dihydroxybenzenes) and resorcinols (1,3-dihydroxybenzenes) and is found in Toxicodendron (poison tree) species, including poison ivy (Toxicodendron radicans), poison oak (Eastern, Toxicodendron toxicarium; Western, Toxicodendron diversilobum), and poison sumac (Toxicodendron vernix). It also includes fruit and nut trees such as gingko (G. biloba), cashew (Anacardium occidentale), and mango (Mangifera indica). Cashew nut shell oil contains cardol, a resorcinol with a similar side chain to poison oak and poison ivy allergens. Members of Ginkgoaceae and Proteaceae contain sensitizing resorcinols.158 In severe cases, type I hypersensitivity reactions may develop.

Occupational exposures to plants represent another common source of toxicity. People working in the tulip industry have known for years of the condition termed “tulip fingers.” This painful hyperkeratosis of the fingertips is caused by exposure to the toxin tuliposide A.159 People working with lilies of the Alstroemeria family have developed a similar condition due to the tuliposide found in Alstroemeria. Tuliposide is hydrolyzed to a butyrolactone, which probably acts as the true allergen in these cases. Cross-reactivity may occur among workers already sensitized to tulips or Alstroemeria species. Occupational exposure to primroses is another cause of allergic dermatitis due to the toxin primin (2-methoxy-6-pentyl-1,4-benzoquinone).160

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Polyphenols in Chronic Diseases and their Mechanisms of Action

Lars Porskjær Christensen, in Polyphenols in Human Health and Disease, 2014

2.1.1 Alk(en)yl Catechols and Alk(en)yl Resorcinols

A common cause of allergic contact dermatitis in central and northern America is exposure to members of the Anarcadiaceae family also known as the “cashew family” or the “sumac family”, affecting 10–50 million Americans per year.92 Members of the Anarcardiaceae plant family that are important in dermatology include Toxicodendron spp. such as poison ivy T. rydbergii (Rydberg’s poison ivy), western poison oak, T. toxicarium (eastern poison oak), poison sumac, T. striatum (Manzanillo) and T. vernicifluum (lacquer tree). Also, mango and Anacardium occidentale (cashew nut) are common causes for allergic contact dermatitis.5,16,18,23,25,26,92,93

The allergenic compounds of the Anacardiaceae family are a mixture of 3-alkyl and 3-alkenyl catechols, sometimes referred to as urushiols, with side chain lengths usually of 15 and/or 17 carbon atoms (116, Figure 62.2).1,5–7,16,17,23–29,94,95 The number of double bonds in 3-alkenyl catechols varies between one and three. The positions of the double bonds of the C15- and C17-carbon side chain can vary, but are usually at positions 8, 11, and 13 for C15-alkenyl catechols and at positions 8, 11, and 14 for C17-alkenyl catechols (Table 62.1, Figure 62.2). Furthermore, the 3-alk(en)yl catechols from different species of the Anacardiaceae differ in the relative proportions of the individual components. For example, in poison ivy, poison sumac and lacquer tree the alk(en)yl groups are predominantly of C15 chain length, whereas in poison oak, Toxicodendron succedaneum (wax tree) the chain length is predominantly C17.17,23,25 Allergenic urushiols have also been found in Ginkgo biloba (Ginkgoaceae) (Table 62.1).58

Allergenic resorcinol derivatives (1725, Figure 62.3) that are closely related to the urushiols have been isolated from species of the Araceae, Anacardiaceae, and Proteaceae families (Table 62.1) and seem to play a significant role in relation to allergenic contact dermatitis caused by plants of these families.7,18–21,30–33,83–86,96–98 In addition, different types of bisalkylresorcinols (e.g., 26 and 27, Figure 62.3) have been isolated from Grevillea spp. (Protaceae) whose allergenicity still needs to be explored,84,98 and Melanorrhoea usitata (Burmese lacquer, Anacardiaceae) contains besides allergenic resorcinol derivatives also a mixture of 3-phenylalkyl catechols and 4-alk(en)yl and 4-phenylalkyl catechols (2833, Figure 62.4) also sometimes referred to as thitsiols, which also may cause allergic contact dermatitis.17,22,23 Moreover, allergenic resorcinol derivatives have been found in plant species of many other families including Asteraceae, Fabaceae, Ginkgoaceae, Gramineae, Iridaceae, Myristicaceae, Myrsinaceae and Primulaceae.19,72,97

Figure 62.3. Chemical structures of some examples of allergenic 5-alk(en)yl resorcinols (17–25) occurring in species of, for example, the plant families Anacardiaceae, Araceae, and Protaceae and examples of bisresorcinols (26, 27), which are characteristic for Grevillea spp. (Protaceae) whose allergenic potential is yet not known.

Figure 62.4. Chemical structures of some 3-phenylalkyl catechols (28, 29) and 4-alk(en)yl and 4-phenylalkyl catechols (30–33) occurring in Melanorrhoea usitata (Burmese lacquer) lacquer sap that may cause allergic contact dermatitis.

The alk(en)yl catechols are readily oxidized to the corresponding ortho-quinones, which are highly reactive towards nucleophilic sites in proteins. Thus the quinones are the actual haptens reacting with skin proteins to form antigens, and thus the urushiols are regarded as prohaptens as they need to be oxidized to their more reactive analogs to become allergenic (Figure 62.1). Moreover, it has been shown that olefinic C15 and C17 urushiols are the most allergenic.15,99–101 Thus the lack of saturation but also the length of the aliphatic chain is important for the allergenicity of urushiols. It has been shown that shortening of the aliphatic chain by β-oxidation plays an important role in processing and activation of urushiols in vivo in order to become allergenic.15 Hence it appears that the allergenicity of urushiols depends on both their reactivity towards proteins and bulkiness of the aliphatic chain. The latter could indicate that the reactivity of the urushiols to some extent results from van der Waals forces. Aliphatic catechols have been demonstrated to possess greater allergenicity than the corresponding resorcinols. The reason for the allergenicity of aliphatic resorcinols is not known, but in considering possible mechanisms of alkylresorcinol-induced sensitivity, it should be noted that because both hydroxyl groups and the chain are in a meta-position, they do not directly form ortho-quinones. However, during the oxidation of the dihydroxybenzene nucleus a 1,2,4-trihydroxyalkylbenzene can be formed.97 Further oxidation of this molecule may result in the formation of an ortho-quinonic form, active for allergy induction. Therefore, the sensitizing activity of the alk(en)yl resorcinols appears to be, in fact, attributed to the products of their oxidation.97

Contact dermatitis due to alk(en)yl catechols and resorcinols primarily results from the direct contact with the oleoresin of the bruised or injured plants. Therefore, the best method for preventing allergic contact dermatitis caused by these allergens is to avoid contact with plants and/or plant products containing the allergens.5,16,17,25 However, this can be difficult as some plant species are used for manufacturing foods; such as mango and cashew nut and others that are used by the lacquerware industry. Lacquer tree, Burmese lacquer and wax tree produce a milky juice or sap, utilized in the manufacture of a durable lacquer used to varnish on furniture, floors, tea pots, canes, ornaments etc. Lacquer allergy is thus a serious occupational skin disease in East Asia, as direct contact with lacquer sap is inevitable for lacquerware workers.5,17

Contact dermatitis caused by plant species of the Anacardiaceae family usually appears within 2–4 days; however, it may appear as late as 2 weeks after contact with the allergens. Contact dermatitis caused by Toxicodendron spp. is characterized by intense pruritus and an erythematous reaction followed by the appearance of multiple papules and vesiculo-bullous lesions in a linear distribution on the legs and arms. The face, neck, and genitalia are also commonly affected and usually show intense edema. The dermatitis has a self-limiting course, normally lasting between 1–2 weeks.1,5,16,25,102,103

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Toxicodendron (Rhus) Allergic Contact Dermatitis

Philip Buttaravoli MD, FACEP, in Minor Emergencies (Second Edition), 2007

What Not To Do:

Do not have the patient use heavy-duty skin cleansers, alcohol, or other strong solvents to remove any remaining antigen. This would be ineffective and may do harm. Strong soap and scrubbing merely irritate the skin and are not more effective than mild soap and gentle washing.

Do not try to substitute prepackaged steroid regimens (Medrol Dosepak, Aristopak). The course is not long enough and may lead to a flare-up.

Do not allow patients to apply fluorinated corticosteroids such as Lidex or Valisone for more than 3 weeks to the face or intertriginous areas, where they can produce thinning of skin and telangiectasias. A 10- to 14-day course should not be a problem. Any significant involvement of the face should be treated with systemic corticosteroids.

Do not institute systemic steroids in the presence of severe secondary infections such as cellulitis or erysipelas. Also, do not start steroids if there is a history of tuberculosis, peptic ulcer, diabetes, herpes, or severe hypertension without careful monitoring and/or specialty consultation.

Do not recommend OTC topical steroid preparations. They are not potent enough to be effective.

Do not prescribe topical steroids if systemic steroids are being given. They should no longer be necessary.

Do not recommend the use of topical antihistamines (which do not reduce itching) or topical benzocaine because of the added risk for the development of a second allergic contact dermatitis. Topical antibiotics with neomycin should be avoided for the same reason.

Discussion

Poison ivy is the most ubiquitous of the four species of the Toxicodendron genus of the Anacardiaceae plant family, which also includes poison sumac and two species of poison oak. In the United States, these four species of plants are responsible for more cases of allergic contact dermatitis than all other contact allergens combined. The strongly sensitizing allergen of Toxicodendron plants is urushiol, a catechol derivative found in the plants' sap. It is also found in the Japanese lacquer tree, mango rinds, cashew shell oil, and the seed coat of the ginkgo tree. When exposed to oxygen, urushiol easily oxidizes and, after polymerizing, becomes a shiny black lacquer. Urushiol is found not only in the leaves but also in vines (aerial roots), stems, and root systems.

In an area where Toxicodendrons grow, Toxicodendron dermatitis should be suspected in anyone with severe acute allergic contact dermatitis. In the summer, any contact dermatitis of unknown cause should be considered Toxicodendron dermatitis until proven otherwise.

This is an allergic contact dermatitis that is T cell–mediated and develops in genetically susceptible individuals following skin contact with urushiol. This allergen induces sensitization in more than 70% of the population, may be carried by pets, and is frequently transferred from hands to other areas of the body that may unfortunately include the genital area. Broad areas of redness and dermatitis are generally due to rubbing. There is always pruritus, which most often is intense. If there is no itching, it is almost certainly not Toxicodendron dermatitis.

The gradual appearance of the eruption over a period of several days is a reflection of the amount of antigen deposited on the skin and the reactivity of the site, not an indication of any further spread of the allergen. The vesicle fluid is a transudate, does not contain antigen, and will not spread the eruption to elsewhere on the body or to other people. The rash only seems to spread because different areas of the body have different thicknesses of stratum corneum leading to different rates of absorption of antigen and, therefore, different rates of eruption. The allergic skin reaction usually runs a course of about 2 weeks, sometimes longer, and is not shortened by any of the previously mentioned treatments (except possibly in the case of Zanfel). The aim of therapy is to reduce the severity of symptoms. It is not currently clear whether we are able to shorten the course of this reaction. Those skin areas with the greatest degree of initial reaction tend to be affected the longest. In a dry environment, the allergen can remain under fingernails for several days and on clothes for longer than 1 week.

Urushiol is degraded by soap and water. Once urushiol touches the skin, however, it begins to penetrate in minutes. It is completely bound to the skin within 8 hours and is probably no longer affected by normal soap and water after 1 to 6 hours. Zanfel Poison Ivy Wash is an OTC soap mixture of ethoxylate and sodium lauryl sarcosinate surfactants that is claimed, by its manufacturer, to render urushiol totally inactive by complementing the polarity of the urushiol to form a micelle. This is said to allow the urushiol to be rinsed away with water at any point during the dermatitis cycle. During the first 3 days, multiple washings may be necessary. Clinical trials to support the manufacturer's claims are in progress. A 1-ounce tube costs approximately $40.00 and is supposed to be enough for 15 applications to an area the size of an adult forearm. The manufacturer also claims that often Zanfel will eliminate the itching of Toxicodendron dermatitis with no further treatment. Zanfel is specific for urushiol; it does not work on other causes of allergic contact dermatitis.

Washing skin immediately after exposure can abort the rash. Washing clothes in a standard washing machine will inactivate the antigen remaining on the patient's clothing as long as they have no black lacquer deposits causing visible staining. Shoes, tools, and sports equipment may require separate cleansing and can be the source of late spread. They should at least be rinsed with copious amounts of water. Pets suspected of harboring urushiol should be bathed.

Poison ivy dermatitis can sometimes be confused with phytophotodermatitis, which is a nonallergic skin reaction to psoralens, which react with ultraviolet light to cause blister formation and burning pain in the skin rather than pruritus. The most common causes are lime juice, weeds, or plants of the Apiaceae family (parsley, celery, parsnip) and other members of the Rutaceae family (includes citrus fruits). Redness, swelling, blisters, and bizarre configurations appear 24 hours after contact with the psoralens and ultraviolet light from the sun or a tanning booth. Within 1 to 2 weeks, patients will develop dark streaks wherever the initial rash occurred. This color will last for months to years, and the involved skin will often remain very sensitive to UV light.

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Hallucinogenic, allergenic, teratogenic and other toxic plants

William Charles Evans BPharm BSc PhD DSc FIBiol FLS FRPharmS, ... Daphne Evans BA MA, in Trease and Evans' Pharmacognosy (Sixteenth Edition), 2009

Rhus (Toxicodendron) spp

Rhus radicans (poison ivy), R. toxicodendron (poison oak), R. diversiloba (Pacific poison oak) and R. vernix (poison sumach, poison elder) (Anacardiaceae) contain contactant allergens which produce severe dermatitis associated with watery blisters which burst and quickly spread across the skin. The allergens are contained in the plant sap and are easily transmitted (on clothing, hands, animal fur and even as the result of bush fires). These compounds are known as urushiols and belong to a class of alkenyl polyphenols found in the Anacardiaceae. They constitute an interesting chemotaxonomic group and are an example of the use of a starter other than acetyl-CoA in fatty-acid synthesis by which C2 units derived from malonate are added to an unsaturated fatty acid; subsequent cyclization forms, as one example, the urushiols. With the exception of the cultivated sumach, which does not appear to be troublesome, these plants are not found in Britain, but they constitute a considerable hazard in the USA, where poison ivy, in particular, is particularly widespread as a woody vine. Lacquer, used in the sixteenth and seventeenth centuries for producing an oriental-type finish on furniture, was derived from R. vernicifera, and its use constituted an industrial hazard for the craftsmen. Similar compounds to the above have been isolated from the fruit pulp of Ginkgo biloba and from the glandular trichomes of annual Phacelia spp. (Hydrophyllaceae) of the Californian Mojave desert. The dermatitic action of these compounds is consistent with oxidation of the allergen to a quinone which then binds covalently to a protein nucleophile giving an antigenic complex.

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Contact Dermatitis

In Diagnostic Pathology: Nonneoplastic Dermatopathology (Second Edition), 2017

Environmental Exposure

ACD

Depends on sensitization, usually requires at least 2 exposures to exogenous antigen, and occurs only in sensitized individuals

Depending on degree of sensitization, even small amounts of antigen can elicit a reaction and sensitization may occur after only 2 exposures

Common allergens include nickel, fragrances, cosmetics, urushiol found in Rhus and Toxicodendron spp. (poison ivy/oak/sumac), formaldehyde, topical antibiotics, latex, rubber, balsam of Peru

ICD

Acute form can occur upon even single exposure to toxic agent with severe cases resulting in necrosis

Effects depend on concentration of toxic agent with strong chemicals causing immediate reactions

Commonly due to repeated or continuous exposures to alkaline soaps/detergents, organic solvents, and excess moisture (hand, diaper area, colostomy site)

Common irritants include acids, alkalis, cement, metal salts, phenols, kerosene, ethylene glycol, lime acids, plants, alcohol solvents, acetone, fiberglass

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Plants, Poisonous (Humans)

M. Banasik, T. Stedeford, in Encyclopedia of Toxicology (Third Edition), 2014

Introduction

Plant toxins have a long and colorful history. The toxins present in some types of plants have historically been used as tools for assassins (e.g., poison hemlock), treatments for various diseases (e.g., autumn crocus), pesticides (e.g., strychnine), and food flavoring (e.g., habañero). Unintentional exposures are commonplace, and most individuals have at one time or another been exposed to plants, which cause some degree of discomfort. For example, dermal exposures to poison ivy (Toxicodendron radicans) may result in various degrees of itching and rash from the urushiol compounds in the plant's sap. These effects are most often of limited consequence. However, in the United States alone, there are over 100’000 reported plant exposures to poison control centers per year. These exposures are typically of minimal toxicity, especially when the exposures occur in children. For example, between 1983 and 2009, 45 fatalities have been recorded with children less than five years of age. Fatalities are, however, not uncommon when exposures occur from intentional ingestion to inflict harm or for substance abuse reasons.

Oral, dermal, and inhalation exposures are all possible, although the toxicity by these routes may vary considerably. Further, even when exposures occur, the potential for adverse effects may be low depending on the form in which the toxin is presented. For example, apple seeds contain amygdalin, a cyanide-containing compound. Despite the known toxicity of cyanide (see Cyanide), the seeds must be chewed or pulverized to release the amygdalin. Once this occurs, amygdalin may be hydrolyzed in the gastrointestinal tract to release cyanide.

A detailed discussion of the environmental fate and behavior, toxicokinetics, and all possible toxic effects of each agent (including genotoxicity, carcinogenicity, effects on immune and reproductive systems, and potential for harming developing organisms) in cases of overexposure is beyond the scope of this broad overview. Other sources, including some other entries in this encyclopedia, should be consulted if readers have more specific concerns about an individual toxin or class discussed here. For example, some basic summary information on clinical management of plant poisonings can be found in the first Further Reading recommendation listed, and local poison centers are also often good resources in cases of suspected poisonings. Instead, the discussion of toxicities focuses here on mechanisms of action and the most important acute and chronic effects recognized to date from human exposures. These plants may also cause toxicity in other species (see Plants, Poisonous (Animals)). Finally, it should be noted that the ‘dose makes the poison’ and that ingestion of small quantities of the plants discussed herein may not necessarily result in the effects identified. Rather, these effects represent a spectrum of potential adverse health outcomes that may occur depending on the quantity of the plant consumed. Consider, for example, the case mentioned about amygdalin in apple seeds. Each seed normally contains only a small amount of amygdalin. Therefore, the dose of cyanide a person could be exposed to after occasional inadvertent consumption of an apple seed or two should not be considered a serious health risk. The nutritional benefits of consuming apples are considerably greater than the risk of cyanide poisoning as long as one avoids eating too many apple seeds. This is certainly not the case with all of the plant toxins discussed herein. Some are so potent that very small quantities can pose very significant health risks.

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Eczematous Eruptions in Childhood

Amy S. Paller MD, Anthony J. Mancini MD, in Hurwitz Clinical Pediatric Dermatology (Fifth Edition), 2016

Poison Ivy (Rhus) Dermatitis

In the United States, poison ivy, poison oak, and poison sumac produce more cases of ACD than all other contactants combined.327 The plants causing poison ivy dermatitis are included under the botanical term Rhus and are Toxicodendron species. Poison ivy and poison oak are the principal causes of Rhus dermatitis in the United States. Regardless of the specific Rhus plant, the clinical appearance of the dermatitis may be identical. The Rhus group belongs to the family of plants known as Anacardiaceae, and cross reactions may occur. These include furniture lacquer derived from the Japanese lacquer tree, oil from the shell of the cashew or Brazil nut, the fruit pulp of the gingko tree, and the marking nut tree of India, from which a black “ink” used to mark wearing apparel is produced. The ACD to this ink is termed dhobi itch. The rind of the mango also cross reacts, and the possibility of contact dermatitis to Rhus should be considered in children with perioral dermatitis after eating mango or on the hands of mango pickers328 (Fig. 3-55).

The poison ivy plant (Fig. 3-56) characteristically shows three leaflets notched at the edge. It grows luxuriantly as a tall shrub or woody rope-like vine in vacant lots, among grasses, and on trees or fences throughout all sections of the United States except the extreme southwest. Poison sumac grows as a shrub or tree, never as a vine. It has 7 to 13 leaflets (arranged in pairs along a central stem), with a single leaflet at the end, is relatively uncommon, grows less abundantly, and is found only in woody or swampy areas primarily east of the Mississippi River. Poison oak, conversely, grows as an upright shrub, is most prominent on the West Coast, and is not a problem in the eastern United States. Although Rhus dermatitis is more common in the summer, the eruption may occur at any time of year by direct contact with the sensitizing allergen from the leaves, roots, or twigs of the plants.

The eruption produced by poison ivy and related plants is a delayed contact hypersensitivity reaction to an oleoresin (urushiol) of which the active sensitizing ingredient is a pentadecylcatechol. It is characterized by itching, redness, papules, vesicles, and bullae (Fig. 3-57). Although often irregular and spotty, a linear distribution is highly characteristic because of scratching and transfer of the urushiol oleoresin (Koebner phenomenon). When contact is indirect, such as from a pet that has the oleoresin on its fur, the dermatitis is often diffuse, thus making the diagnosis more difficult unless the true nature of exposure is suspected. In the fall, when brush and leaves are burned, it must be remembered that the sensitizing oil may be vaporized and transmitted by smoke to exposed cutaneous surfaces, often presenting as a diffuse facial dermatitis with periorbital swelling (Fig. 3-58).

Rhus dermatitis usually first appears in susceptible, sensitized individuals within 1 to 3 days after contact with the sensitizing oleoresin; in highly sensitive individuals it may occur within 8 hours of exposure. Such temporal differences are probably the result of the degree of exposure, individual susceptibility, and variation in cutaneous reactivity of different body regions.

About 70% of the population of the United States would acquire Rhus dermatitis if exposed to the plants or the sensitizing oleoresin contained in its leaves, stems, and roots. The result is an acute eczematous eruption that, barring complications or reexposure to the offending allergen, persists for 1 to 3 weeks. Since the undiluted sap from plants of the Toxicodendron species turns black when exposed to dry surfaces and skin, dramatic black lacquer- or enamel-like deposits on the skin (“black spot poison ivy”) and clothing of individuals exposed to poison ivy or other urushiol-containing plants may rarely be seen.329,330 These spots typically cannot be removed with soap and water and may precede the development of typical dermatitis.

The best prophylaxis, as with any type of ACD, is complete avoidance of the offending allergen. Patients should be instructed in how to recognize and avoid members of the poison Rhus group. When poison ivy is present in the garden or in children's play areas, chemical destruction or physical removal is indicated. Heavy-duty vinyl gloves should be used if the plants are uprooted, because the urushiol is soluble in rubber and can penetrate latex gloves.331 No topical measure is totally effective in the prevention of poison ivy dermatitis, but certain commercially available barrier preparations with quaternium-18 bentonite (organoclay) have been shown to diminish reactivity significantly (IvyBlock, StokoGard, Hollister Moisture Barrier, Hydropel).332 Desensitization to the oleoresin of poison ivy by systemic administration of Rhus antigen is unreliable and should be reserved only for extremely sensitive individuals who cannot avoid repeated exposure to the antigen. Systemic reactions are not uncommon with the use of hyposensitization procedures.

In an effort to minimize the degree of dermatitis, individuals with known exposure should wash thoroughly with soap and water as rapidly as possible so that removal of the oil is accomplished, preferably within 5 to 10 minutes of exposure. If the oleoresin is not carefully removed shortly after exposure, the allergen may be transmitted by the fingers to other parts of the body (particularly the face, forearms, or male genitalia) (Fig. 3-59). However, the fluid content of vesicles and bullae is not contagious and does not produce new lesions. Thus unless the sensitizing antigen is still on the skin, the disorder is neither able to be spread on an individual nor contagious from one person to another.

Complete change of clothing is advisable, and whenever possible, contaminated shoes and clothing should be washed with soap and water or cold water mixed with alcohol to remove the urushiol. Harsh soaps and vigorous scrubbing offer no advantage over simple soaking and cool water. Thorough washing may not prevent a severe dermatitis in highly sensitive persons. It may, however, reduce the reaction and prevent spread of the oleoresin. When early washing is not feasible, it is worthwhile to wash at the first opportunity in an effort to remove any oleoresin remaining on the skin or clothing and thus prevent its transfer to other parts of the body.

In the management of mild Rhus dermatitis, treatment with an antipruritic “shake” lotion such as calamine lotion is helpful. Topical preparations containing potential sensitizers such as diphenhydramine or benzocaine should be avoided. As in other acute eczematous eruptions, cool compresses with plain tap water or Burow solution are soothing, help remove crusts, and relieve pruritus. Administration of potent topical corticosteroids and systemic use of antihistamines and antipruritic agents are helpful. Because the acutely involved areas tend to be vesicular and weeping, creams and lotion forms of topical steroids are more commonly used than occlusive ointments.

In severe, more generalized cases of Rhus dermatitis, short-term systemic corticosteroid treatment may be indicated. Systemic corticosteroid therapy may be initiated with dosages of 1 mg/kg per day of prednisone or its equivalent. Steroids should be tapered gradually over 2 to 3 weeks. Premature termination of systemic corticosteroids may result in a rapid rebound, with return of the dermatitis to its original intensity.

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Diaper Area Eruptions

Alfons Krol, Bernice Krafchik, in Neonatal Dermatology (Second Edition), 2008

Allergic Contact Dermatitis

Allergic contact dermatitis (ACD) may occur in the diaper region after exposure to fragrances, dyes, other components of the diaper itself, or to products applied by the parents to diapered skin.38 Weston39 has shown that ACD may account for up to 20% of all cases of childhood dermatitis, refuting the notion that ACD is rare in children. Sensitization may begin as early as 6 months of age.40 Allergens that infants and children have become sensitized to include urushiol (poison ivy), nickel (in metal snaps on clothing), thimerosol, neomycin, chromates, Balsam of Peru, and formaldehyde and related preservatives.41

A specific form of ACD on the outer buttocks and hips was determined by patch testing to be due to rubber components in the elastic bands of the diapers. The authors termed this entity ‘Lucky Luke Dermatitis’ after the cartoon character who carries his gun holster in the same area42 (Fig. 16-10). Recently Alberta et al.43 reported several infants with ACD caused by the various blue, pink, and green dyes used in diapers. Changing to dye-free diapers quickly alleviated the rash. ACD may be present in the same areas of the diaper as IDD, but the morphology of the lesions is different in ACD, beginning with erythema and small vesicles and leading to an eczematous eruption with red papules or vesicles overlying areas of edema.38 Treatment with a medium-strength topical steroid provides rapid relief of symptoms, but removing the offending allergen is key to preventing recurrences.

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Immunology of the Skin

Hui Xu, ... Craig A. Elmets, in Clinical Immunology (Sixth Edition), 2023

Environmental Challenges and the Skin-Associated Lymphoid Tissue

Chemicals

Environmental chemicals that are able to breach the cutaneous physical barrier are often identified by the host, correctly or incorrectly, as unwelcoming molecules that should be neutralized or eliminated by the immune system. When this occurs to a seemingly innocuous molecule, it causes allergic contact dermatitis. Examples include urushiol, the active moiety in poison ivy, oak, and sumac, and nickel sulfate, responsible for the dermatitis caused by nickel-containing jewelry. Once beyond the stratum corneum, these chemicals bind to epidermal proteins, generating “modified self” proteins as immunogenic complete antigens. Animal models of allergic contact dermatitis have been studied extensively to understand the mechanism of action of T-cell-mediated adaptive immune responses in the skin.

Solar Ultraviolet Radiation

Sunlight is the major environmental agent to which skin is exposed. Injudicious exposure to UV spectrum can lead to sunburn, skin aging, skin cancers, and photosensitivity diseases, many of which have an immunological pathogenesis. Although much of the investigation into the immunological effects of UVR was conducted in animal models, many of the observations have been corroborated in humans.

In mice, as in humans, chronic exposure to UVR results in the development of highly antigenic skin tumors, capable of stimulating a vigorous antitumor response in untreated mice. Despite their antigenic nature, these tumors grow progressively in their original host. This apparent paradox was resolved in studies showing that, in addition to producing mutant neoplastic cells, UVR also impairs cell-mediated immune surveillance, which, under normal circumstances, eliminates mutant cells before they develop into clinically apparent tumors. Thus, mutant cells progress to become tumors only in an environment of immune suppression. For example, organ transplant recipients who are treated with immunosuppressive medications have a greatly increased risk of developing aggressive skin cancers.30

UVR mediates its effects on the immune system by perturbing the function of skin APCs. UV-irradiated APCs are poor stimulators of Th1 cells but are able to activate Tregs, which promote antigen-specific immunological tolerance. Enhanced production of the suppressive cytokines IL-10 and TGF-β, as well as by a reduction in the Th1 activation cytokine IL-12 also play a role. It may seem surprising that an environmental carcinogen, such as UVR, suppresses immunological function in skin. One proposed hypothesis is that altered epithelial proteins are constantly generated by UVR exposure, necessitating chronic induction of immune tolerance to UVR-damaged proteins to preserve the integrity of the skin barrier.

The immunosuppressive effect of UVR has been exploited for therapeutic purposes. UVR phototherapy is used to suppress pathological immune responses in such inflammatory skin diseases as psoriasis and atopic dermatitis.30

On the Horizon

Development of small-molecule inhibitors of JAK/STAT signaling that can be given orally or topically for the treatment of psoriasis.

Elucidation of the mechanisms underlying comorbidities, such as metabolic syndrome and major adverse cardiovascular events in patients with psoriasis.

Development of new cytokine inhibitors to treat a spectrum of skin diseases (such as IL-17 and IL-23 inhibitors for the management of hidradenitis suppurativa).

Targeting of dendritic cell subsets (DCs) in order to optimize vaccination.

Use of cytokines or cytokine inhibitors to manipulate cutaneous immune responses in immunologically mediated skin diseases (such as vitiligo, alopecia areata, cutaneous lupus erythematosus, and dermatomyositis).

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URL: https://www.sciencedirect.com/science/article/pii/B978070208165100023X