CD1a on Langerhans cells controls inflammatory skin disease.

CD1a is a lipid-presenting molecule that is abundantly expressed on Langerhans cells. However, the in vivo role of CD1a has remained unclear, principally because CD1a is lacking in mice. Through the use of mice with transgenic expression of CD1a, we found that the plant-derived lipid urushiol triggered CD1a-dependent skin inflammation driven by CD4(+) helper T cells that produced the cytokines IL-17 and IL-22 (TH17 cells). Human subjects with poison-ivy dermatitis had a similar cytokine signature following CD1a-mediated recognition of urushiol. Among various urushiol congeners, we identified diunsaturated pentadecylcatechol (C15:2) as the dominant antigen for CD1a-restricted T cells. We determined the crystal structure of the CD1a-urushiol (C15:2) complex, demonstrating the molecular basis of urushiol interaction with the antigen-binding cleft of CD1a. In a mouse model and in patients with psoriasis, CD1a amplified inflammatory responses that were mediated by TH17 cells that reacted to self lipid antigens. Treatment with blocking antibodies to CD1a alleviated skin inflammation. Thus, we propose CD1a as a potential therapeutic target in inflammatory skin diseases.

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.

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.

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.

IL-33/ST2 signaling excites sensory neurons and mediates itch response in a mouse model of poison ivy contact allergy.

Poison ivy-induced allergic contact dermatitis (ACD) is the most common environmental allergic condition in the United States. Case numbers of poison ivy ACD are increasing due to growing biomass and geographical expansion of poison ivy and increasing content of the allergen, urushiol, likely attributable to rising atmospheric CO2 Severe and treatment-resistant itch is the major complaint of affected patients. However, because of limited clinical data and poorly characterized models, the pruritic mechanisms in poison ivy ACD remain unknown. Here, we aim to identify the mechanisms of itch in a mouse model of poison ivy ACD by transcriptomics, neuronal imaging, and behavioral analysis. Using transcriptome microarray analysis, we identified IL-33 as a key cytokine up-regulated in the inflamed skin of urushiol-challenged mice. We further found that the IL-33 receptor, ST2, is expressed in small to medium-sized dorsal root ganglion (DRG) neurons, including neurons that innervate the skin. IL-33 induces Ca2+ influx into a subset of DRG neurons through neuronal ST2. Neutralizing antibodies against IL-33 or ST2 reduced scratching behavior and skin inflammation in urushiol-challenged mice. Injection of IL-33 into urushiol-challenged skin rapidly exacerbated itch-related scratching via ST2, in a histamine-independent manner. Targeted silencing of neuronal ST2 expression by intrathecal ST2 siRNA delivery significantly attenuated pruritic responses caused by urushiol-induced ACD. These results indicate that IL-33/ST2 signaling is functionally present in primary sensory neurons and contributes to pruritus in poison ivy ACD. Blocking IL-33/ST2 signaling may represent a therapeutic approach to ameliorate itch and skin inflammation related to poison ivy ACD.

Poison Ivy, Poison Oak, and Poison Sumac.

This JAMA Patient Page describes allergic skin reactions from contact with poison ivy, poison oak, and poison sumac plants, and how to treat rashes caused by these plants.

Prevention of poison ivy dermatitis with oral homeopathic Rhus toxicodendron.

Acute allergic contact dermatitis to poison ivy is acommon and miserable dermatosis which affectsmillions of Americans each year. Preventativemeasures, such as avoidance, protective clothing,barrier creams, soaps, and solvents often fail despiteour patients' best attempts. Severe allergic reactionsto poison ivy are a significant source of decreasedemployee productivity owing to inability to work anda major health care expenditure. Patients may haveto leave their jobs and discontinue favorite outdoorrecreational activities as a result of severe urushiolsensitivity. Thus, a simple and effective method ofpreventing poison ivy dermatitis would be of greatbenefit to clinical dermatologists and their patients.Complementary and alternative medical practitionerscommonly prescribe homeopathic poison ivyproducts by mouth for the prevention of poisonivy dermatitis. Yet, conventional dermatologists aremostly unaware of this little known clinical pearl. Theauthor discusses two open studies and anecdotalexperience with administration of homeopathicpoison ivy in the prevention of acute allergic contactdermatitis related to poison ivy exposure. Potentialadvantages could include patient acceptability,ease of administration, affordability, and availability.Randomized clinical trials are needed to furtherevaluate the safety and efficacy of this interesting andpromising clinical tip.

Vesicular erythema migrans: an atypical and easily misdiagnosed form of Lyme disease.

Erythema migrans is the initial sign in the majority of patients infected with Borrelia, the genus of spirochetes that causes Lyme disease. Early identification and treatment decrease the risk of progression to later stages of disease. Although a "bull's eye" appearance owing to lesional clearing is considered classic for erythema migrans, this feature is surprisingly often lacking among patients in the United States. Furthermore, cutaneous Lyme disease can exhibit a wide range of morphologic variability in a minority of patients. Herein, we describe the case of a patient with Lyme disease in which the presence of atypical vesicular features, in conjunction with the initial absence of clearing, resulted in multiple misdiagnoses and delayed treatment. We also review the literature on the epidemiology and management of erythema migrans for cases in which the diagnosis may pose a challenge.

Plant Dermatitis.

Plant dermatitis is a common pathology that plagues those who work and recreate in the North American outdoors. The most common plant family to cause dermatitis is the Toxicodendron genus, which includes the plants known by the common names of poison ivy, poison oak, and poison sumac. While mortality is usually quite low for this pathology, the incidence and prevalence of the disease leads to substantial healthcare burden and financial implications across the population. The mainstays of treatment have focused on prevention, corticosteroids, and antihistamines.

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.

Innovation in prevention of poison oak contact dermatitis.

Poison oak-induced contact dermatitis poses a significant challenge due to its urushiol oil-induced allergic reactions. Conventional preventive measures like avoidance and post-exposure cleansing are often impractical, necessitating innovative strategies. This comprehensive review explores emerging technologies and formulations for preventing poison oak dermatitis. Literature search via PubMed and Covidence identified 13 relevant studies, with six discussing preventive measures. Barrier methods, including occlusive creams and protective clothing, showed promise in reducing dermatitis risk. Immunotherapy, although investigated, requires further development. Complete avoidance, while effective, is often impractical. The complexity of poison oak management underscores the need for ongoing research to develop more effective preventive measures. This review highlights the current landscape, identifies gaps in knowledge, and emphasizes the importance of continued research for improved prevention and management of poison oak-induced dermatitis.

Urushiol detection using a profluorescent nitroxide.

A method to visually detect minute amounts of urushiol, the toxic catechol from poison oak, poison ivy, and poison sumac, has been developed utilizing the reaction of a profluorescent nitroxide with the B-n-butylcatecholboronate ester formed in situ from urushiol and B-n-butylboronic acid. The resulting N-alkoxyamine is strongly fluorescent upon illumination with a fluorescent lamp, allowing the location of the toxic urushiol contamination to be visualized. This methodology constitutes the groundwork for the future development of a spray to detect urushiol to avoid contact dermatitis, as well as to detect catecholamines for biomedical applications.

Dermoscopy of black-spot poison ivy.

Black-spot poison ivy is an uncommon presentation of poison ivy (Toxicodendron) allergic contact dermatitis. A 78-year-old sought evaluation of a black spot present on her right hand amid pruritic vesicles. The presentation of a black spot on the skin in a clinical context suggesting poison ivy is indicative of black-spot poison ivy. Dermoscopy revealed a jagged, centrally homogeneous, dark brown lesion with a red rim. A skin sample was obtained and compared against a poison ivy standard using ultra-fast liquid chromatography-tandem mass spectrometry (UFLC-MS/MS). This finding confirmed the presence of multiple urushiol congeners in the skin sample. Black-spot poison ivy may be added to the list of diagnoses that show a specific dermoscopic pattern.

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.

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.

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.