Is Food-Triggered Atopic Dermatitis a Form of Systemic Contact Dermatitis?

Food allergy in atopic dermatitis is mediated by complex immune interactions between genetics, diet, environment, and the microbiome. When contact between inflamed skin and food antigens occurs, contact hypersensitivity can develop. Consequently, systemic contact dermatitis (SCD) can occur after ingestion of allergenic foods or food additives in the setting of a Th2 response with CLA-positive T cells, triggering dermatitis where skin resident memory lymphocytes reside. This phenomenon explains food-triggered dermatitis. Atopy patch tests (APTs) detect sensitization to food proteins responsible for SCD, which in turn can be confirmed by oral food challenge with delayed interpretation. We summarize the literature on using APTs to identify foods for oral challenge with dermatitis as an outcome. In dermatitis patients at risk for Th2 skewing based on a history of childhood-onset flexural dermatitis, shared decision-making should include a discussion of identifying and avoiding food and food additive triggers, as well as identifying and avoiding all contact allergens, prior to initiation of systemic therapy for dermatitis.

Stasis Dermatitis: The Burden of Disease, Diagnosis, and Treatment.

Stasis dermatitis (SD), an inflammatory dermatosis occurring on the lower extremities, is a cutaneous manifestation of chronic venous insufficiency (CVI). SD is associated with a significant burden of disease. Symptoms such as pain, swelling, and itching can be debilitating for patients, leading to poor sleep, loss of mobility, and the inability to perform daily activities, and can interfere with work and leisure activities. Moreover, SD is a progressive disease with serious secondary complications such as ulcerations, which increase the patients' morbidity, reduce their quality of life, and increase health care burden. Challenges in diagnosing patients may have both short- and long-term sequalae for the patients due to unnecessary treatment and management. In addition, misdiagnosis may result in hospitalizations, placing additional burden on health care professionals in terms of time and financial burden on the health care system. Compression therapy and leg elevation represent the mainstay of treatment for CVI; however, it is also difficult to self-manage, which places a substantial burden on patients and caregivers. Moreover, compression therapy may cause discomfort and exacerbate itching. Subsequent nonadherence may result in disease progression that places additional burden on the physicians who manage these patients and the health care system in terms of resources required and costs incurred. A large proportion of patients with SD develop allergic contact dermatitis because of innate immune signals and altered skin barrier predisposing to sensitization to topical prescriptions, over-the-counter medications, and compression devices used to treat SD. Other than topical corticosteroids, there are no approved pharmacological options to treat inflammation in SD.

Stasis Dermatitis: An Overview of Its Clinical Presentation, Pathogenesis, and Management.

Stasis dermatitis is a chronic inflammatory skin disease of the lower extremities. It typically occurs in older individuals and is the cutaneous manifestation of venous hypertension caused by venous reflux. Such retrograde venous blood flow is the result of incompetent venous valves, valve destruction, or venous obstruction. Stasis dermatitis is eczematous. The associated impairment of venous valves may cause swelling of the legs, leading to serious conditions including venous ulcerations. Diagnosis can be challenging because of its clinical resemblance to other skin conditions and poor clinical recognition by physicians. The cornerstones of stasis dermatitis treatment are compression therapy to ameliorate pain and swelling, topical treatments to alleviate secondary skin changes, and interventional treatment options to correct the underlying causes of venous reflux. Given the central role of inflammation of the lower extremities in driving the cutaneous changes characteristic of stasis dermatitis, new therapeutic approaches that target the inflammation are under clinical evaluation in patients with stasis dermatitis.

Stasis dermatitis is a skin disease that can affect a person for a long time. It affects the legs of older people who have a disease called chronic venous insufficiency. This is when a person's veins have difficulty sending blood from their limbs back to their heart. Stasis dermatitis is caused by increased pressure inside a person's veins. Its signs and symptoms are skin discoloration, itch, dryness, and scaling and can be similar to the signs and symptoms of cellulitis and allergic contact dermatitis. Cellulitis is a common skin infection caused by bacteria. Cellulitis causes redness, swelling, and pain. Allergic contact dermatitis is an itchy skin rash caused by contact with something that irritates the skin. Stasis dermatitis is usually diagnosed after a healthcare provider has looked at person's skin and their medical history. Treatment for stasis dermatitis should treat the chronic venous insufficiency that causes the disease. It should also treat the skin lesions caused by stasis dermatitis. One way to treat stasis dermatitis is to reduce pain and swelling. This is done by applying pressure with compression stockings or bandages. Minor surgery can treat the venous insufficiency that causes stasis dermatitis. No treatments have been approved for the skin symptoms associated with stasis dermatitis. New ways to treat such symptoms need to be developed.

Cutaneous dysbiosis may amplify barrier dysfunction in patients with atopic dermatitis.

Atopic dermatitis (AD) is associated with cutaneous dysbiosis, barrier defects, and immune dysregulation, but the interplay between these factors needs further study. Early-onset barrier dysfunction may facilitate an innate immune response to commensal organisms and, consequently, the development of allergic sensitization. We aimed to compare the cutaneous microbiome in patients with active dermatitis with and without a history of childhood flexural dermatitis (atopic dermatitis). Next-gen Ion-Torrent deep-sequencing identified AD-associated changes in the skin bacterial microbiome ("bacteriome") and fungal microbiome ("mycobiome") of affected skin in swabs from areas of skin affected by dermatitis. Data were analyzed for diversity, abundance, and inter-kingdom correlations. Microbial interactions were assessed in biofilms using metabolic activity (XTT) assay and scanning electron microscopy (SEM), while host-pathogen interactions were determined in cultured primary keratinocytes exposed to biofilms. Increased richness and abundance of Staphylococcus, Lactococcus, and Alternaria were found in atopics. Staphylococcus and Alternaria formed robust mixed-species biofilms (based on XTT and SEM) that were resistant to antifungals/antimicrobials. Furthermore, their biofilm supernatant was capable of influencing keratinocytes biology (pro-inflammatory cytokines and structural proteins), suggesting an additive effect on AD-associated host response. In conclusion, microbial inter-kingdom and host-microbiome interactions may play a critical role in the modulation of atopic dermatitis to a greater extent than in non-atopic adults with allergic contact dermatitis.

Design and implementation of a health systems science curriculum at a large teaching hospital.

BACKGROUND: Physicians must increasingly lead change for improvement in the value of health care for individuals and populations. Leadership, stewardship, and population health competencies are not explicitly part of the Accreditation Council for Graduate Medical Education (ACGME) requirements and are best appreciated in the context of Health Systems Science (HSS). HSS education is best approached at the institutional level, yet almost all graduate medical education (GME) curriculum is at the program level. We describe the process of designing and implementing an institutional HSS GME curriculum in a hospital-based sponsoring institution. METHODS: A group of diverse stakeholders drafted a curriculum to build competencies in leadership, stewardship, and population health, which was further refined by our Graduate Medical Education Committee (GMEC) and Resident Forum in the academic years 2015-2017. The refined curriculum was implemented at the institutional level of a large urban teaching hospital with over 80 ACGME accredited programs in the 2017-2018 academic year, participation was tracked and impact surveys were conducted. RESULTS: All programs participate in at least parts of the curriculum with sustained use. Annual surveys show a progression in assessment of our target competencies and/or opportunities to reflect and provide feedback. The annual program review meeting and GMEC meetings are used to troubleshoot and identify new curricular opportunities. CONCLUSION: This innovative institutional curriculum has been sustained for over four years and we believe that other training institutions with similar goals will find our experience implementing an institutional curriculum translatable to their clinical learning environment.

American Contact Dermatitis Society Core Allergen Series: 2020 Update.

The American Contact Dermatitis Society Core Allergen series was introduced in 2013 and updated in 2017. Changes in our recommended allergens are again necessary, taking into account data from the American Contact Dermatitis Society's Contact Allergen Management Program top 100 allergens from 2018. For the updated series, we removed methyldibromoglutaronitrile and added new haptens: Lyral, Limonene, Linalool, carmine, benzyl salicylate, disperse yellow 3, jasmine, peppermint, pramoxine, shellac, and lauryl polyglucose (glucosides). These additional allergens should increase the yield of relevant positive reactions for our patients.

Allergic Contact Sensitization in Healthy Skin Differs from Sensitization in Chronic Dermatitis: Atopic, Occupational Wet Work, and Stasis Dermatitis.

The duration of cutaneous inflammation preceding sensitization influences the resulting allergic response; the innate immune system instructs the adaptive immune response. Potent allergens that function as their own irritant cause classic T helper cell type 1 skewed dermatitis. Examples include poison ivy, epoxy resin, and methylchloroisothiazolinone. Less potent allergens, such as food proteins and propylene glycol, sensitize skin affected by chronic dermatitis resulting in a T helper cell type 2 skewed response, sometimes with associated systemic contact dermatitis. Systemic contact dermatitis should therefore be suspected in patients with positive patch tests to ingested allergens in the setting of chronic dermatitis.

Clinical Psoriasiform Dermatitis Following Dupilumab Use for Autoeczematization Secondary to Chronic Stasis Dermatitis.

T helper 2 (Th2) and T helper 1 (Th1) mediated immune processes lie on a spectrum. Autoeczematization secondary to chronic stasis dermatitis may fall on the Th2 side of the spectrum due to skin stretch and chronic barrier dysfunction, supporting a primary Th2 response to self-antigen. In our patient, we posited that dupilumab would benefit autoeczematization secondary to chronic stasis dermatitis given its efficacy in atopic dermatitis, a Th2-mediated immune process. We report a case of clinical psoriasiform dermatitis, suggesting a shift toward a Th1-mediated immune process developing during dupilumab treatment for autoeczematization secondary to chronic stasis dermatitis.

Relative Prevalence of Contact Allergens in North America in 2018.

BACKGROUND: The American Contact Dermatitis Society Contact Allergen Management Program (CAMP) database was developed to provide patients with safe alternative products free of selected contact allergens. However, the CAMP database also records valuable information including the frequency of contact allergen searches for patients. OBJECTIVES: The aim of the study was to determine the relative prevalence of contact allergens in North America. METHODS: Data from the CAMP database were analyzed from January 1, 2018, to January 1, 2019. The number of searches performed for each specific allergen served as a measure of the relative prevalence for each contact allergen. Results were then stratified by age, sex, atopic history, and patch screening tray used. RESULTS: The 2018 CAMP data show that many of the prevalent allergens are not currently on any contact allergy screening series. These data strongly indicate that testing only to an 80-item screening series will not provide adequate care for many patients with contact allergy. The most prevalent contact allergens seen were fragrance mix, nickel, balsam of Peru, methylchloroisothiazolinone/methylisothiazolinone, and cobalt. Some important differences are seen when stratifying CAMP data by age, sex, atopic history, and patch screening tray used. LIMITATIONS: Possible sources of data error exist because of lack of uniformity of patch test practices. CONCLUSIONS: The CAMP database can be used to determine the relative prevalence of contact allergens, to help develop North American core screening patch test series, and to document the medical necessity of more comprehensive patch testing for patients with recalcitrant contact allergy.

Art of prevention: Allergic sensitization through damaged skin: Atopic, occupational, and stasis dermatitis.

The prevention of allergic contact dermatitis hinges on maintaining the integrity of the skin barrier and responding appropriately when it is disturbed. Although intact skin is subject to sensitization via highly irritating allergens, such as poison ivy, acutely inflamed and chronically inflamed skin is subject to sensitization to allergens without inherent irritant potential. In the chronically inflamed state of atopic dermatitis, sensitization to proteins, such as food, also carries a risk for systemic contact dermatitis via ingestion of the allergen. Minimizing the development of irritant dermatitis is key to preventing sensitization. However, in patients with already chronically inflamed skin, reducing the use of products to the involved areas, recommending hypoallergenic products with caution, and taking measures to prevent biofilm formation are also integral to preventing sensitization to chemicals and proteins, such as food and commensal organisms.

Atopy patch tests may identify patients at risk for systemic contact dermatitis.

BACKGROUND: A subset of patients with positive patch tests demonstrates systemic contact dermatitis (SCD) upon ingestion or inhalation of the allergen. Concern has been raised about the use of patch tests for protein allergens (APTs) to detect SCD in atopic dermatitis (AD) patients. METHODS: We present atopy patch test (APT) data for 97 people. We reviewed APTs and tests for antigen-specific immunoglobulin E (IgE) to the same allergen in pediatric AD patients. We compared the frequency of APTs as a function of age in AD patients. To study the irritancy potential of APTs, we prospectively tested consenting non-AD dermatitis patients undergoing evaluation for allergic contact dermatitis and healthy controls to an APT panel. RESULTS: APT demonstrated fewer positive results than serum-specific IgE or skin prick tests to the same allergen. Positive APT to food was more common in children under 3 years, whereas positive APT to aeroallergens were more common in teens and adults. Only positive APTs to dust mite were significantly more common positive in subjects without AD. CONCLUSION: Our aggregate findings suggest that most APTs, but not dust mite, behave like conventional patch tests to low-potency allergens. They are more likely to be positive in patients with chronically inflamed skin and to identify allergens that cause SCD. The higher prevalence of APT positivity to foods in young children is consistent with food allergy as a trigger of AD (also known as SCD) being more common in children than adults. Positive APTs define patients who may have SCD; negative APTs may guide elimination diets.