Botanical Briefs: Contact Dermatitis Induced by Western Poison Ivy (Toxicodendron rydbergii).

"Leaves of three, leave it be" serves as an apt caution for avoiding poison ivy (Toxicodendron species) and its dermatitis-inducing sap. Toxicodendron contact dermatitis (TCD) poses a notable burden to the American health care system by accounting for half a million reported cases of allergic contact dermatitis (ACD) annually. Identifying and avoiding physical contact with the western poison ivy (Toxicodendron rydbergii) plant prevails as the chief method of preventing TCD. This article discusses common features of T rydbergii as well as clinical manifestations and treatment options following exposure to this allergenic plant.

Evaluation and Management of Toxicodendron Dermatitis in the Emergency Department: A Review of Current Practices.

Toxicodendron dermatitis is an underappreciated disease seen in the emergency department. Although self-limiting, symptoms can be distressing and can last for weeks if untreated, particularly with re-exposure. Continuing research has improved our understanding of specific inflammatory markers that are associated with exposure to urushiol-the compound responsible for Toxicodendron dermatitis-although consensus for treatment remains varied and poorly supported. Owing to the lack of recent primary literature on the topic, many providers rely on historical precedent, expert opinion, and personal experience when treating this disease. This article provides a narrative review of the literature currently available on the effects of urushiol on key molecular and cellular functions and the prevention and treatment of Toxicodendron dermatitis.

Poison Ivy Dermatitis Treatment Patterns and Utilization: A Retrospective Claims-based Analysis.

INTRODUCTION: Poison ivy (toxicodendron) dermatitis (TD) resulting from contact with poison ivy, oak, or sumac is a common form of allergic contact dermatitis that impacts millions of people in the United State every year and results in an estimated 43,000 emergency department (ED) visits annually. Our objective in this study was to evaluate whether healthcare utilization outcomes are impacted by prescription practices of systemic corticosteroids. METHODS: We used a health claims database from 2017-2018 of those treated for TD. Descriptive statistics and logistics regression models were used to characterize trends. RESULTS: We included in this analysis 115,885 claims from 108,111 unique individuals (93.29%) with 7,774 (6.71%) return claims within 28 days. Of the return claims, 470 (6.05%) were to the ED. Emergency clinicians offered no oral corticosteroid prescription 5.27% (n = 3,194) of the time; 3276 (86.26%) prescriptions were for a duration of 1-13 days, 410 (10.80%) were for 14-20 days, and 112 (2.95%) were for >21 days. Further, we found that shorter duration oral corticosteroids (odds ratio [OR] 1.30; 95% confidence interval 1.17-1.44; P <0.001) and initial treatment for TD at the ED compared to primary care clinicians (OR 0.87 [0.80, 0.96]; P <0.001) and other non-dermatologists (OR 0.89 [0.80, 0.98]; P = 0.01) places patients at an increased risk for return visits with healthcare clinicians when controlling for drug group, duration of treatment, and initial treatment location. CONCLUSION: Despite recommendations to treat TD with oral steroids for at least 14 days, most emergency clinicians offered this treatment for shorter durations and was associated with return visits. Emergency clinicians should consider treatment of two to three weeks when providing systemic steroid coverage when there are no limiting contraindications, especially as patients who present to the ED may do so with more severe disease. Additional education may be needed on appropriate treatment pathways for TD to reduce healthcare utilization associated with undertreatment.

Black-Spot Toxicodendron Dermatitis With Varied Presentation.

This article describes the clinical presentation, differential diagnosis, and treatment of 2 unrelated cases with different presentations of black-spot Toxicodendron dermatitis. In the first case, a healthy 7-y-old male presented with a rash consisting of black dots with localized surrounding erythema on the left arm. The rash then progressed to a vesicular, pinpoint, raised rash spreading to the face, arms, and neck. In the second case, a 4-y-old male presented with non-pruritic, black, flat, non-erythematous lesions that did not progress. This patient's older sibling had been diagnosed with poison ivy 1 wk prior, and they attended the same child care where the poison ivy was thought to be acquired. In both cases, diagnosis of black-spot Toxicodendron dermatitis was made. The black spot of Toxicodendron dermatitis is caused by urushiol oxidation on exposure to air. The subject may or may not go on to develop allergic contact dermatitis after the exposure. Diagnosis of this dermatitis is made on clinical presentation, with careful consideration of history, distribution, and lesion morphology. When allergic dermatitis does develop as in the first case, systemic treatment with oral steroids is recommended. In both of these cases the black dots completely resolved in 2 to 3 wk. Dermatologic referral for dermoscopy and biopsy may be necessary if the dermatosis does not resolve as anticipated.

Establishing Consensus on the Treatment of Toxicodendron Dermatitis.

BACKGROUND: Toxicodendron dermatitis (TD) is a common form of allergic contact dermatitis that affects millions of Americans every year. Studies have shown that although there are general recommendations for the treatment of TD, there are no treatment algorithms for clinicians to follow when patients present with TD. OBJECTIVE: The objective of this study was to achieve consensus on the treatment of TD to create practical guidelines for physicians who treat TD. METHODS: Data were collected from March 2020 to April 2021. This study included semistructured focus groups and a Delphi Study with dermatologists to achieve consensus. RESULTS: A total of 51 dermatologists were included in the Delphi. Final agreement with proposed severity criteria ranged from 90.9% to 100.0%. Primary indicators of disease severity were body surface area, presence and severity of pruritus, and anatomic locations of eruptions with 77.4% agreement. Final agreement for the treatment algorithm was over the threshold majority agreement at 67.6%. CONCLUSIONS: Literature guiding the treatment of TD is scarce. The use of the Delphi method and focus groups can help expand dermatological resources both within dermatology and to other specialties that may need to treat skin conditions.

Botanical Briefs: Toxicodendron Dermatitis.

Toxicodendron dermatitis is a type IV hypersensitivity reaction resulting from exposure to urushiol found in poison ivy, poison oak, and poison sumac. The dermatitis presents as a pruritic erythematous rash with vesicles and bullae in areas that were in contact with the plant. Symptoms present after 24 to 48 hours and can be managed with a variety of treatments, depending on severity. Avoidance is the principal way to prevent Toxicodendron dermatitis, highlighting the importance of educating patients on identification of plants.

Plant Dermatitis: More Than Just Poison Ivy.

Plants can cause allergic contact dermatitis (ACD), mechanical irritant contact dermatitis, chemical irritant contact dermatitis, light-mediated dermatitis, and pseudophytodermatitis. Allergic contact dermatitis to chemicals in the Toxicodendron genus, which includes poison ivy, poison oak, and poison sumac, is the most common cause of plant ACD; however, many other plants, such as Compositae, Alstroemeriaceae, and Rutaceae plants also are important causes of dermatitis. In individuals with recurrent ACD from plants other than Toxicodendron, patch testing can be used to identify the source of allergic reactions to plant species. This article provides an overview of the various plant dermatoses, common culprits of plant dermatitis, and diagnostic and therapeutic options for plant dermatoses.

Systemic contact dermatitis induced by Rhus allergens in Korea: exercising caution in the consumption of this nutritious food.

Systemic contact dermatitis (SCD) develops when a person who was previously sensitized to an allergen is exposed to the same allergen via the systemic route. In East Asia, the use of lacquer for polishing furniture is common and a part of the traditional culture. Contact exposure to tableware polished with Rhus lacquer may lead to sensitization. In Korea, SCD is commonly observed after systemic exposure to Rhus, a nutritious food item consumed because of the common belief of it improving the immune system. In this study, we reviewed the medical records of 21 Korean patients with SCD caused by Rhus ingestion. We found that the most significant epidemiological factor for SCD was the season of the year. Furthermore, 66.67% of the patients presented with leucocytosis and 23.81% showed increased liver enzyme levels. It is important to educate people on the risks associated with the systemic ingestion of Rhus.

Urushiol Compounds Detected in Toxicodendron-Labeled Consumer Products Using Mass Spectrometry.

BACKGROUND: Urushiol, the culprit allergen in Toxicodendron plants such as poison ivy, is an oily mixture of 15 and 17 carbon side chain alk-(en)-yl catechols. Recently, consumer products have been identified that contain Toxicodendron as an ingredient on their label; however, no studies have assessed whether urushiol is indeed present within these products. OBJECTIVE: The aim of the study was to determine whether urushiol compounds are present in consumer products labeled as containing Toxicodendron species. METHODS: Gas chromatography-mass spectrometry and liquid chromatography-tandem mass spectrometry were performed on 9 consumer products labeled as containing Toxicodendron species, including topical homeopathic remedies. Single ion monitoring gas chromatography-mass spectrometry was programmed in selective ion mode to detect 3-methylcatechol characteristic fragment ions of alk-(en)-yl catechols after silanization. Similarly, single ion monitoring liquid chromatography-tandem mass spectrometry was programmed to detect 4 urushiol pentadecylcatechols and 5 urushiol heptadecylcatechols using previously reported mass-to-charge ratios. RESULTS: Gas chromatography-mass spectrometry detected alk-(en)-yl catechols in 67% (6/9) of the products tested. Liquid chromatography-tandem mass spectrometry detected multiple urushiol pentadecylcatechols and heptadecylcatechols in 44% (4/9) of the products tested. CONCLUSIONS: Alk-(en)-yl catechols and multiple urushiols were detected in consumer products listing Toxicodendron species as an ingredient. Clinicians should be aware of these known allergenic ingredients in consumer products.

Transcriptome profiling reveals Th2 bias and identifies endogenous itch mediators in poison ivy contact dermatitis.

In the United States, poison ivy exposure is the most common naturally occurring allergen to cause allergic contact dermatitis (ACD). The immune and pruritic mechanisms associated with poison ivy ACD remain largely unexplored. Here, we compared skin whole transcriptomes and itch mediator levels in mouse ACD models induced by the poison ivy allergen, urushiol, and the synthetic allergen, oxazolone. The urushiol model produced a Th2-biased immune response and scratching behavior, resembling findings in poison ivy patients. Urushiol-challenged skin contained elevated levels of the cytokine thymic stromal lymphopoietin (TSLP), a T-cell regulator and itch mediator, and pruritogenic serotonin (5-HT) and endothelin (ET-1), but not substance P (SP) or histamine. The oxazolone model generated a mixed Th1/Th2 response associated with increased levels of substance P, 5-HT, ET-1, but not TSLP or histamine. Injections of a TSLP monoclonal neutralizing antibody, serotonergic or endothelin inhibitors, but not SP inhibitors or antihistamines, reduced scratching behaviors in urushiol-challenged mice. Our findings suggest that the mouse urushiol model may serve as a translational model of human poison ivy ACD study. Inhibiting signaling by TSLP and other cytokines may represent alternatives to the standard steroid/antihistamine regimen for steroid-resistant or -intolerant patients and in exaggerated systemic responses to poison ivy.

Poison Ivy, Oak, and Sumac Dermatitis: What Is Known and What Is New?

Poison ivy, poison oak, and poison sumac are the most common causes of clinically diagnosed allergic contact dermatitis in North America. Approximately 50% to 75% of the US adult population is clinically sensitive to poison ivy, oak, and sumac. We reviewed the botany and history of these plants; urushiol chemistry and pathophysiology, clinical features, and the prevalence of allergic contact dermatitis caused by these plants; and current postexposure treatment and preventive methods, including ongoing investigations in the development of a vaccine (immunotherapy). Although extensive efforts have been made to develop therapies that prevent and treat contact dermatitis to these plants, there lacks an entirely effective method, besides complete avoidance. There is a need for a better therapy to definitively prevent allergic contact dermatitis to these plants.

You're the Flight Surgeon.

Solana NM. You're the flight surgeon: black spot poison ivy. Aerosp Med Hum Perform. 2017; 88(7):700-702.