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Itchy Toxicodendron Plant Dermatitis: Comparison
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Please note this is a comparison between Version 4 by Vicky Zhou and Version 5 by Vicky Zhou.

Plants such as the Toxicodendron species, consisting of poison ivy, poison oak, and poison sumac, largely contribute to allergic contact dermatitis with itch as a predominate symptom. Many individuals are affected by this skin condition, with approximately 50% to 70% of adults in North America demonstrating a degree of clinical sensitivity to this species of plants. 

  • allergic contact dermatitis
  • itch
  • Toxicodendron species
  • poison ivy
  • poison oak
  • poison sumac

1. Introduction

The most common cause of allergic contact dermatitis in the US is exposure to plants, specifically the Toxicodendron species, which include poison ivy, poison oak, and poison sumac. Contact with this species of plants causes a weeping rash that is largely characterized by significant pruritus. Allergic contact dermatitis is a common skin condition that affects millions of people per year, with anywhere between 10 to 50 million cases yearly, and it is a significant medical condition that occurs frequently [1]. Urushiol is the major allergen that elicits the response in the Toxicodendron species and it is dispersed throughout the plant including the leaves, stems, and roots [2]. The reaction occurs via direct contact with any part of the plant, as well as from indirect exposure to contaminated sources, such as clothing, shoes, and pets.
Pruritus is a significant manifestation of rash; other characteristics include an eruption of delineated erythematous vesicles, papules, and edema. For many years, the treatment of allergic contact dermatitis has not changed but recent understanding of the underlying mechanism of itch can contribute to both the treatment and prevention.

2. Clinical Features

Individuals who are sensitized to poison ivy, poison oak, and poison sumac will develop an acute response in response to re-exposure. Classically, the dermatitis that develops is described as a pruritic eczematous eruption that is often in the form of delineated streaks where contact with the plant brushed the surface of the skin [3]. The sharp demarcated eruptions consist of erythematous papules and vesicles that typically present within 24–48 h following exposure, however this can range from 5 h to 15 days in some individuals [4]. The clinical presentation of linear markings and sharp borders is a key feature that aids in the identification of this plant dermatitis.
Initially, individuals may experience erythema, edema, and an eruption of papules followed by vesicles and bullae. In more mild cases, vesicles and bullae may not occur. Fluid from vesicles and bullae have not been found to contain antigen load and therefore do not contribute to the dissemination of the disease. Variations can occur in an individual due to differing concentrations of antigen and time of exposure. Occupational workers can experience additional sequelae of generalized dermatitis and respiratory tract inflammation due to aerosolization of urushiol in wildfire smoke [5].

3. Treatment and Prevention

The treatment and prevention of Toxicodendron dermatitis has not changed for many years [6]. The main goal of treatment is therapeutic relief aimed at alleviating many of the symptoms that individuals experience, predominately pruritus. Baths with baking soda and colloidal oatmeal and the use of cold compresses can help improve the itch. Additionally, over the counter topical treatment includes the use of cooling agents, such as calamine lotion, which aids in relieving dryness and reducing itch with menthol and phenol [7][8].
The mainstay of treatment has been corticosteroids. Specifically, high potency topical steroid clobetasol has been found to be most effective during the early reaction [6]. Alternatives to higher potency steroids are mid-potency topical steroids, such as triamcinolone and betamethasone, which may be a better alternative due to lower cost [6]. In children, the use of low potency topical corticosteroids such as hydrocortisone can be used to prevent side effects such as atrophy of the skin [9]. Systemic corticosteroids may be used in severe and widespread cases. Cases that can benefit from the use of systemic steroids include individuals with greater than 20% body surface area affected, extensive vesicles, bullae, blistering, and itch, as well as involvement of sensitive areas such as the face or genitals [10]. Oral prednisone can be initiated at 1 mg/kg/day with a maximum dose of 60 mg/day for severe cases and should be continued for 2–3 weeks with tapering [11]. Alternatively, the use of intramuscular injection of triamcinolone for 3 weeks has been found to be therapeutic in severe cases and demonstrated increased compliance. One consideration when using triamcinolone intramuscular injections is the risk of rebound if the course of treatment is not sufficient [12]. Furthermore, the rebound dermatitis appears to be more steroid-resistant, so management of systemic steroid treatment must be closely followed [13]. The use of long-term systemic corticosteroids is limited by side effects such as risk of infection, hyperglycemia, and hypertension amongst other systemic effects [6].
The use of antihistamines has limited efficacy, considering the histamine-independent cascade that underlies the mechanism of itch [14][15]. While the effect is limited, antihistamines are still considered one of the treatments for allergic contact dermatitis from the Toxicodendron species. Therefore, the newer studies on the IL-33/ST2 signaling cascade and thymic stromal lymphopoeitin (TSLP) show that it can be useful in treating the underlying mechanism of itch in unresponsive patients undergoing treatment with steroids and antihistamines or when contraindications are present.
Use of topical immunomodulators that reduce itch, such as tacrolimus and pimecrolimus, was reported in a few case reports [6]. Tacrolimus and pimecrolimus are calcineurin inhibitors that diminish the immunological cascade by decreasing cytokine production as well as the activation of T cells and Langerhans cells in the dermal skin [16][17]. One study analyzed the use of topical tacrolimus ointment 0.1% in patients with orbital allergic contact dermatitis and found a significant improvement in symptoms and a positive trend in reduction of itch [18]. A randomized controlled trial compared the efficacy of tacrolimus ointment 0.1% to vehicle ointment and found it superior at minimizing dermatitis and that it significantly reduced pruritus [19].
ThWe authors have also used a compounded Topical JAK/STAT inhibitor that reduced poison ivy itch. JAK/STAT pathway inhibition can decrease many cytokines that are involved in inflammatory processes [20]. As an emerging treatment, JAK/STAT inhibitors have been approved for use in rheumatoid and psoriatic arthritis, and are undergoing investigation for treatment of atopic dermatitis, dermatomyositis, and numerous other skin conditions. The use of topical JAK/STAT inhibitors requires further evaluation; however, there is evidence that shows promising efficacy in reducing itch in the treatment of allergic contact dermatitis.
Prevention can be achieved by various modalities, such as limiting exposure to Toxicodendron species, washing of affected areas, pretreatment with topical barriers, and desensitization [6]. Upon exposure, washing the affected areas immediately can breakdown the oily sap containing urushiol and prevent a reaction [6]. Significant water flushing can effectively remove urushiol from the skin; flushing within 10 min can remove 50%, flushing within 15 min can remove 25%, and flushing within 30 min can remove 10% of urushiol substance [5]. Following 30 min, breakdown of urushiol and penetration of skin is likely to occur. Additionally, there is some evidence that suggests the use of chemicals that inactivate urushiol and soap as effective methods to remove urushiol from the skin [6]. The chemical inactivator Tecnu, the oil remover Goop, Dial Ultra dishwashing soap, and Zanfel soap have all been found to significantly remove urushiol from the skin [21][22]. Additionally, pretreatment with topical barriers such as quarternium-18 bentonite, linoleic acid, Hollister Moisture Barrier, and Hydropel have also demonstrated efficacy at preventing or limiting the extent of reaction to urushiol [23][24][25]. One longstanding practice implemented by Native Americans is desensitization to urushiol by ingesting poison ivy leaves; however, this mechanism is controversial [26]. Previous findings have shown that ingestion or parenteral intake of urushiol demonstrates hypo-sensitization rather than desensitization. However, further studies did not find hypo-sensitization to be statistically significant in human models [27][28]. Moreover, there have been reports of increased pruritus and urticaria with ingestion or injection of urushiol [5].
In addition to these treatments, there are currently clinical trials investigating the use of a vaccine injection to prevent poison ivy, oak, and sumac-derived contact dermatitis [6]. The name of the immunomodulating injection is 3-pentadecyl-1,2-phenylene bis (4-(4-aminophenyl)butanoate) (PDC–APB). A recent animal study, published in 2018, revealed that administration of intramuscular injection PDC–APB resulted in a very mild or nonexistent skin reaction following urushiol exposure in the experimental animal group when compared with the control animal group [29]. Currently, there is a phase I trial for the use of PDC–APB that will explore the efficacy and safety of its use against urushiol [30].
Overall, the landscape of treatment for allergic contact dermatitis from poison ivy, poison oak, and poison sumac is directed at eliminated or diminishing itch and has not substantially changed over the last few years. However, developments in understanding the primary mechanisms of itch can impact upcoming treatment mechanisms and decrease pruritus in affected individuals.

4. Conclusions

Toxicodendron dermatitis is one of the most common causes of allergic contact dermatitis and affects millions of individuals in the US yearly. Exposure to poison ivy, poison oak, and poison sumac in sensitized individuals evokes a weeping erythematous eruption of papules and vesicles that are highly pruritic. Many of the treatments for allergic contact dermatitis target the symptom of itch. There have been advancements in understanding the pathophysiology of itch in allergic contact dermatitis from urushiol that highlight the IL-33/ST2 pathway and cytokine TSLP. While management of urushiol-mediated allergic contact dermatitis has been unchanged, the effective targeting of underlying itch mechanisms can provide innovative treatments.

References

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