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Contact dermatitis (CD) is a common inflammatory skin disease caused by exposure to contact allergens and irritants. It is also the most common reason of occupational dermatitis and contributes greatly to hand dermatitis and facial dermatitis. Besides the two major forms of contact dermatitis: allergic contact dermatitis and irritant contact dermatitis, other subtypes of CD have been recognized including immediate skin reactions, photoinduced contact dermatitis, systemic contact dermatitis, and non-eczematous contact dermatitis. CD is a great imitator which can mimic many kinds of skin diseases, such as atopic dermatitis, lichen planus, and angioedema. For the diagnosis of CD, a complete medical history, including occupational history, is very important. It can give a clue of CD and provide a list of suspected substances. Besides the well-known diagnostic test, patch testing, there are many other diagnostic tests can be used to help diagnosis of CD and identify the causative allergens, including photopatch test, skin tests for detecting of immediate contact reactions, serum allergen-specific IgE test, and qualitative and quantitative testing of allergen in the suspected materials patients exposed to and challenge test. Before the treatment, the suspected irritants or allergens should be avoided completely. This includes both the removal of the patient from the environment that contains those substances and the promotion of the metabolism and expulsion of the allergens that have been absorbed by the body. In addition, it is also important to restore the skin barrier and reduce skin inflammation through multiple treatments, such as emollients, topical corticosteroids, and antihistamines, as well as systemic corticosteroids and immunosuppressants. Early and appropriate treatments are important to prevent further deterioration and persistence of the skin condition.

Allergic contact dermatitis (ACD) is one of the most common skin diseases, consisting of sensitization and elicitation phases. With the advancement of technology and the discovery of new types of immune cells, our knowledge of the immunological mechanisms of contact hypersensitivity (CHS) as a murine model of ACD has expanded significantly in the past decade. For example, by introducing regulatory T cells, CD4+ T-helper 17 cells, and Langerin-positive dermal dendritic cells, the initiation and termination mechanism of CHS has been revealed. In addition, the role of mast cells in CHS, long a matter of debate, has become apparent by developing conditional mast cell–deficient mice. Moreover, the role of the innate immunity system, such as that of Toll-like receptor signaling, has made a breakthrough in this field. In this review, we will integrate the recent advancement of immunological mechanisms of both the sensitization and elicitation phases of CHS into the classic view, and we will discuss updated mechanisms on its development and future directions.

Irritant contact dermatitis (ICD) and allergic contact dermatitis (ACD) are common skin disorders that are characterized by inflammation, oozing, crusting, and pruritus. Atopic dermatitis (AD) is an inflammatory skin disease characterized by immune and barrier abnormalities and is additionally a risk factor for acquiring ICD and ACD. New work on allergic sensitization to common allergens (e.g., nickel and fragrance) in human skin has shown that different allergens have distinct molecular fingerprinting. For example, nickel promotes strong Th1/Th17 polarization, whereas fragrance allergy causes Th2/Th22 skewing, which is similar to the phenotype of AD. While ACD has previously been considered to be constant across all allergens, largely based on mouse models involving strong sensitizers, these new data suggest that ACD differs mechanistically according to allergen. Further, ACD in the setting of concurrent AD shows a different and attenuated phenotype as compared to healthy individuals with ACD, which influences the way AD patients respond to vaccination and other treatment modalities. As in contact sensitization, skin challenged by food patch testing shows that common food allergens (e.g., peanut and barley) also cause distinct immune polarizations in the skin. Additionally, house dust mite reactions in human skin have been profiled to show unique Th2, Th9, and Th17/22 activation as compared to controls, which are similar to the phenotype of psoriasis and contact responses to nickel. Given this information, ACD patients should be treated based on their unique allergen polarity. Refined understanding of the molecular behavior of contact dermatitis and related diseases translates to improved methods of inducing tolerance in sensitized allergic patients, such as with targeted drug therapy and epicutaneous immunotherapy.

AbstractPurpose of ReviewOccupational hand dermatitis is a common work-related disorder of the skin. Prevention and management of this disease is critical to improving workers’ quality of life and for occupation-specific retention.Recent FindingsThis is a critical review of the current literature on occupational hand dermatitis. Occupational dermatitis continues to have a high prevalence among workers although the overall incidence may be slowly decreasing. Irritant contact dermatitis due to wet work exposure is the most common cause of occupational hand dermatitis. Healthcare workers, hairdressers, and metal workers are at particularly high risk for this disease. While some prevention programs have been ineffective in mitigating occupational hand dermatitis, other more resource-intensive initiatives may have benefit.SummaryContinued research is needed on ways to manage wet work exposures and on scalable, effective prevention programs for occupational hand dermatitis. The spectrum of culprit contact allergens continues to evolve, and vigilance for potential occupation-specific allergens remains important.

In two identical trials of treatment for psoriasis with the topical aryl hydrocarbon receptor–modulating agent tapinarof, clearance or near-clearance of lesions occurred in a larger proportion of patients who used tapinarof cream than of those who used placebo. Side effects included folliculitis, contact dermatitis, and headache.

Contact dermatitis tremendously impacts the quality of life of suffering patients. Currently, diagnostic regimes rely on allergy testing, exposure specification, and follow-up visits; however, distinguishing the clinical phenotype of irritant and allergic contact dermatitis remains challenging. Employing integrative transcriptomic analysis and machine-learning approaches, we aimed to decipher disease-related signature genes to find suitable sets of biomarkers. A total of 89 positive patch-test reaction biopsies against four contact allergens and two irritants were analyzed via microarray. Coexpression network analysis and Random Forest classification were used to discover potential biomarkers and selected biomarker models were validated in an independent patient group. Differential gene-expression analysis identified major gene-expression changes depending on the stimulus. Random Forest classification identified CD47, BATF, FASLG, RGS16, SYNPO, SELE, PTPN7, WARS, PRC1, EXO1, RRM2, PBK, RAD54L, KIFC1, SPC25, PKMYT, HISTH1A, TPX2, DLGAP5, TPX2, CH25H, and IL37 as potential biomarkers to distinguish allergic and irritant contact dermatitis in human skin. Validation experiments and prediction performances on external testing datasets demonstrated potential applicability of the identified biomarker models in the clinic. Capitalizing on this knowledge, novel diagnostic tools can be developed to guide clinical diagnosis of contact allergies.

Systemic contact dermatitis (SCD) traditionally refers to a skin condition where an individual who is cutaneously sensitized to an allergen will subsequently react to that same allergen or a cross reacting allergen via a different route. It occurs to allergens including metals, medications, and foods. The exact pathophysiology underlying this disease remains unknown, although it appears to be mediated by type 4 hypersensitivity reactions and possibly type 3 hypersensitivity reactions. The p-I concept (pharmacologic interaction with immunoreceptors) hypothesized that drugs are able to bind directly to a T cell receptor without first being presented by MHC (major histocompatibility complex) molecules and without prior metabolism, which would help explain why SCD can be seen on first exposure to medications. Nomenclature remains a challenge as SCD can be subcategorized using terms such as ACDS (allergic contact dermatitis syndrome) and its four clinical stages, Baboon syndrome, and SDRIFE (symmetrical drug-related intertriginous and flexural exanthema), which share many overlapping features. Food allergens may be responsible for uncontrolled or persistent symptoms in patients with contact dermatitis who do not respond to topical avoidance. With medications, symptoms may be induced by topical application versus systemic administration. Patch testing (PT) may be beneficial in diagnosing SCD caused by metals and many topical medications including corticosteroids, antimicrobials (ampicillin, bacitracin, erythromycin, neomycin, nystatin), NSAIDs (diclofenac, ibuprofen), anesthetics, and antihistamines (chlorphenamine, piperazine). Current treatment options include topical steroids and oral antihistamines for symptom relief and dietary avoidance to causative foods or metals.

Contact dermatitis accounts for 95% of occupational skin disorders. Irritant contact dermatitis (ICD) is often caused by cumulative exposure to weak irritants, accounting for 80% of all cases of contact dermatitis. ICD can co-exist with atopic dermatitis (AD) and allergic contact dermatitis (ACD). Patients with AD and ACD may have a lower inflammatory threshold for developing ICD. Therefore, it needs to be distinguished from lesions of AD and ACD. ICD Patients report stinging and burning in excess of pruritus. Pruritus is classically reported by patients with AD and ACD. ICD lesions are typically well-demarcated unlike AD and ACD. ICD is diagnosed by exclusion. Patients undergo testing to rule out type I and type IV hypersensitivity. Negative results suggest a diagnosis of ICD. Management consists of irritant identification and avoidance with regular emollient use. Although ICD is more common in certain occupations, genetics and environment play significant roles in its development.

PurposeIrritant contact dermatitis (ICD) is a major cause of occupational disease. The aim was to review the relation between exposure to occupational irritants and ICD and the prognosis of ICD.MethodsThrough a systematic search, 1516 titles were identified, and 48 studies were included in the systematic review.ResultsWe found that the evidence for an association between ICD and occupational irritants was strong for wet work, moderate for detergents and non-alcoholic disinfectants, and strong for a combination. The highest quality studies provided limited evidence for an association with use of occlusive gloves without other exposures and moderate evidence with simultaneous exposure to other wet work irritants. The evidence for an association between minor ICD and exposure to metalworking fluids was moderate. Regarding mechanical exposures, the literature was scarce and the evidence limited. We found that the prognosis for complete healing of ICD is poor, but improves after decrease of exposure through change of occupation or work tasks. There was no substantial evidence for an influence of gender, age, or household exposures. Inclusion of atopic dermatitis in the analysis did not alter the risk of ICD. Studies were at risk of bias, mainly due to selection and misclassification of exposure and outcome. This may have attenuated the results.ConclusionThis review reports strong evidence for an association between ICD and a combination of exposure to wet work and non-alcoholic disinfectants, moderate for metalworking fluids, limited for mechanical and glove exposure, and a strong evidence for a poor prognosis of ICD.