Collection of Blogs related to information about contact dermatitis

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Petrolatum Facts—150 years to today.

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Petrolatum was discovered in 1859 inadvertently by the oil rig drillers in Titusville, Pennsylvania. The thick “rod wax” caused the rigs to malfunction and had to scraped off, however the workers found it to help soothe and heal their skin cuts. Robert Chesebrough, a chemist, refined, distilled, patented, and named it Vaseline—from the German wasser (water) and the Greek elaion (olive oil).

Purified petrolatum is a highly useful moisturizer and skin protectant as it prevents up to 98% of transepidermal water loss, is triple-purified and devoid of any allergens. It is recommended by the National Eczema Association as safe treatment option. There have not been any evidence-based reports directly linking purified petrolatum to cancer.

However, unrefined, low grade petrolatum does contain carcinogens called polycyclic aromatic hydrocarbons. Although the US does not regulate petrolatum use in cosmetics, labels stating “white petrolatum” or “Petrolatum, USP” can be sure they are buying a purified high grade product.

Petrolatum itself has never been reported to cause allergic contact dermatitis. Some petrolatum-based products, however, may not use a purified form of petroleum and often have additional ingredients such as Lanolin or fragrances and should be carefully evaluated for their ingredients by patients with known sensitizations.  

SNAS and thyroid autoimmunity risk

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SNAS (Systemic nickel allergic syndrome may predispose susceptible individuals to developing chronic autoimmune thyroiditis (CAT)

 

Systemic nickel allergic syndrome as an immune-mediated disease with an increased risk for thyroid autoimmunity

Original Article:

Andrioli M, Trimboli P, Maio D, Persani L, Minelli M. Systemic nickel allergic syndrome as an immune-mediated disease with an increased risk for thyroid autoimmunity. Endocrine. 2015;50(3):807-810.

Go To Pubmed

Reviewed by Erin Wesner, BS, MSII & Jack Guccione, BS, MSIII. Loma Linda University School of Medicine

 

Keywords: Systemic nickel allergic syndrome, Nickel, Chronic autoimmune thyroiditis, Hashimoto

 

Key points:

  • Systemic nickel allergic syndrome (SNAS) may predispose susceptible individuals to developing chronic autoimmune thyroiditis (CAT)
  • Thyroid dysregulation is identified by elevated blood levels of thyroglobulin antibody and symptoms including fatigue, constipation, and weight gain.
  • Prior nickel sensitization with gastrointestinal and diffuse cutaneous symptoms and elevated thyroglobulin antibody may indicate SNAS-related thyroid disorder.
  • In over 200 patients studied, SNAS positive individuals showed a two-fold greater prevalence of CAT.

 

Introduction:

  • Chronic autoimmune thyroiditis (CAT) is the most common cause of hypothyroidism in areas with adequate iodine intake.1
    • CAT results from high circulating levels of anti-thyroid antigens and inflammatory mediators that cause gradual thyroid destruction.
    • Genetic, autoimmune and environmental factors (viruses, stress, hormones, pollution) have been identified as potential causes of CAT.2
  • Systemic nickel allergic syndrome (SNAS) is a chronic inflammatory disorder. It is characterized by a constellation of symptoms which can involve cutaneous, respiratory, gastrointestinal, and/or neurologic following systemic exposure to nickel (eg:  ingestion, implantation, inhalation) in individuals with prior nickel sensitization. (Table 1).1,3
    • This is in contrast to allergic contact dermatitis (ACD) wherein localized skin lesions erupt in response to direct contact with nickel (jewelry).
    • Approximately 20% of patients with a delayed allergy to nickel sulfate experience SNAS.1
    • SNAS is mediated through the release of cytokines by Th2 cells and Th1 cells, particularly IL-5 and IL-4.1,3
    • Intestinal biopsies taken from SNAS patients following nickel ingestion have shown increased amounts of CD4+ lymphocytes in the duodenal lamina propria and a decrease in the number of epithelial CD8+ lymphocytes due to apoptosis.3

Andrioli et al Article Review:

  • Andrioli et. al evaluated 239 patients over a 12-month period who had presented with immune-mediated inflammatory disease at the Department of Immune-Mediated Inflammatory Diseases of the Padre Pio Hospital in Campi Salentina, Lecce, Italy.1
    • All subjects underwent thyroid function testing as well as thyroid gland ultrasonography to identify thyroid disease.1
    • Thyroglobulin antibody (TGAb) (a blood test for thyroid dysfunction) was used to identify CAT in the study participants.
    • The authors defined SNAS by cutaneous and systemic manifestations, positive Ni patch testing in conjunction with an oral Ni challenge test, and clinical improvement following 4 weeks of a low Ni diet.1
      • 136 subjects met the diagnostic criteria for SNAS.1
      • Out of the remaining 103 subjects (non-SNAS), 40 tested positive for non-SNAS hypersensitivities (gluten, idiopathic dermatitis, lactose intolerance, allergic sensitivity to aeroantigens).1
      • The authors reported positive CAT in 26.5% of the SNAS group versus 12.7% in the non-SNAS group.
        • Notably, the global prevalence of CAT is estimated to be 1-2% in Caucasian women, but elevated in individuals with immune-mediated inflammatory disease, although the precise mechanisms remain unknown.1,4,5
        • For example, individuals with type 1 diabetes, celiac disease, Sjogren’s syndrome, rheumatoid arthritis and systemic lupus erythematosus all carry increased risk of developing CAT. None of these diseases were specifically identified in the non-SNAS group studied in Andrioli et al.1,6-9
      • Of note, TGAb levels were two fold higher in the SNAS group when compared to the non-SNAS group (19.9% vs. 7.8%).1

 

Key Points:

  • Andrioli et al. recognized a statically significant association between CAT and SNAS.1
  • The authors reported a two-fold greater prevalence of CAT in patients with SNAS (26.5%) compared to patients with other non-SNAS immune-mediated inflammatory disorders (12.7%).1
  • Based on Andrioli et al’s findings and literature review, the authors suggest that metal induced allergic reactions from nickel may promote increased production of TGAb through an autoimmune-inflammatory mechanism resulting in the development of CAT.
    • SNAS is associated with elevated levels of IL-4, a stimulator of B lymphocyte activity and differentiation.This cytokine may play a role in the production of TGAb in susceptible individuals when systemically exposed to nickel.
  • Concordant with these findings, elevated T-cell mediated pro-inflammatory cytokines are present in nickel-sensitized individuals, placing those with SNAS at a higher risk of developing autoimmune disorders (CAT).10
    • Further studies are warranted to define the pathogenic mechanism and protocol for screening for CAT in patients with SNAS.1

 

Table 1: Common SNAS and CAT individual and shared symptoms in descending order of frequency*10,11

Symptoms of SNAS10 Symptoms of CAT11 Shared symptoms10,11
Urticaria/angioedema Cold intolerance Fatigue
Dermatitis Impaired memory Edema
Recurrent abdominal pain Hair loss Constipation
Diarrhea Slowed movements Headache
Dyspepsia Brady cardia <60/min Bloating
Gastro-esophageal reflux Dry, coarse skin  
Itching Weight gain  
     
*SNAS – systemic nickel allergy syndrome; CAT – chronic autoimmune thyroiditis

 

References:

  1. Andrioli M, Trimboli P, Maio D, Persani L, Minelli M. Systemic nickel allergic syndrome as an immune-mediated disease with an increased risk for thyroid autoimmunity. Endocrine. 2015;50(3):807-810.
  2. Duntas LH. Environmental factors and thyroid autoimmunity. Ann Endocrinol (Paris). 2011;72(2):108-113.
  3. Braga M, Quecchia C, Perotta C, et al. Systemic nickel allergy syndrome: nosologic framework and usefulness of diet regimen for diagnosis. Int J Immunopathol Pharmacol. 2013;26(3):707-716.
  4. Weetman AP. Non-thyroid autoantibodies in autoimmune thyroid disease. Best Pract Res Clin Endocrinol Metab. 2005;19(1):17-32.
  5. Fallahi P, Ferrari SM, Ruffilli I, Elia G, Biricotti M, Vita R, Benvenga S, Antonelli A. The association of other autoimmune diseases in patients with autoimmune thyroiditis: Review of the literature and report of a large series of patients. Autoimmun Rev. 2016; 15(12):1125-1128.
  6. Appenzeller S, Pallone AT, Natalin RA, Costallat LT. Prevalence of thyroid dysfunction in systemic lupus erythematosus. J Clin Rheumatol. 2009;15(3):117-119.
  7. Biro E, Szekanecz Z, Czirjak L, et al. Association of systemic and thyroid autoimmune diseases. Clin Rheumatol. 2006;25(2):240-245.
  8. Counsell CE, Taha A, Ruddell WS. Coeliac disease and autoimmune thyroid disease. Gut. 1994;35(6):844-846.
  9. Piatkowska E, Szalecki M. Autoimmune thyroiditis in children and adolescents with type 1 diabetes. Pediatr Endocrinol Diabetes Metab. 2011;17(4):173-177.
  10. Ricciardi L, Carni A, Loschiavo G, et al. Systemic nickel allergy: oral desensitization and possible role of cytokines interleukins 2 and 10. Int J Immunopathol Pharmacol. 2013;26(1):251-257.
  11. Kostoglou-Athanassiou I, Ntalles K. Hypothyroidism – new aspects of an old disease. Hippokratia. 2010;14(2):82-87.

 

Delayed-type hypersensitivity to metals in connective tissue diseases

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Delayed-type hypersensitivity to metals in connective tissue diseases and Fibromyalgia

 

Original article:

Bjørklund G, Dadar M, Aaseth J. Delayed-type hypersensitivity to metals in connective tissue diseases and fibromyalgia. Environmental Research. 2018;161:573-579. doi:10.1016/j.envres.2017.12.004

Reviewed by Jack Guccione, MS3 Loma Linda University School of Medicine.

Keywords: Fibromyalgia, Mixed connective tissue disease, Rheumatoid arthritis, Nickel, Mercury, Gold, Palladium, Metals, Allergy.

Abstract excerpt from: Delayed-type hypersensitivity to metals in connective tissue diseases

“Rheumatoid arthritis (RA) often involves the small joints of the hands in a symmetrical fashion that can lead to loss of joint function, and RA, as well as Sjögren’s syndrome (SS) and other rheumatic diseases, are often accompanied by sensitivity to metals… Metal-related DTH [delayed-type hypersensitivity] in these patients will induce an inflammatory response. Such inflammations are important factors in CTD [connective tissue disease] progress. It is hypothesized that metal-specific T cell reactivity can act as an etiological agent in the propagation and chronification of rheumatic inflammation. The key responses of metal delayed-type hypersensitivity in autoimmunity are precipitating as an appealing challenge for further investigations.”

Review:

  • Connective Tissue Disease (CTD) refers to a group of autoimmune diseases including rheumatoid arthritis (joint pain, malformation), Sjogren’s syndrome (excess tears and saliva), dermatomyositis, and systemic lupus erythematosus (joint pain, swelling).3
  • Fibromyalgia (FM) is a chronic rheumatic disease with an unknown cause that presents with tenderness and pain at 11-18 “trigger points” on the body and a constellation of symptoms that include cognitive and sleep impairment and widespread musculoskeletal pain and stiffness.
    • It is found in up to 6.6% in the general population, affecting women 2x more than men.1,2
    • There is significant overlap in non-musculoskeletal symptoms with chronic fatigue syndrome.
    • Persistent symptoms can lead to social inability, depression, and poor overall quality of life.1
  • Bjorklund et al. reviewed more than 100 studies and two case reports which had found positive associations between metal allergies (see table 1) and CTD or FM1
    • One study in the review reported THAT over 50% of women who tested positive for FM also self-reported having prior positive skin testing to nickel (bracelets, earrings).5
    • This is a significantly higher sensitization rate than is estimated in the US general population to nickel of 17-20%.6Similarly, two reviewed case reports anecdotally showed removal of nickel-containing dental appliances (bridges, wires) resulted in resolution of fatigue and FM pain in the patients.8
    • Bjorklund reviewed Hart et al.’s paper which found exposures to silica, mineral oils, and traffic pollution containing detectable levels of nickel, mercury, and palladium to be a significant risk factor for the development of RA.7
    • Bjorklund et al.’s review of a larger study (N=111), showed up to 76% of patients reported improvement of their chronic fatigue when dental metals containing nickel were removed.9
      • This study documented removal of mercury tooth-fillings resulted in substantial “health improvements” in individuals with FM including reduced migraine, less joint pain in wrists, hands, and fingers, and reduced fatigue symptoms.9
    • Another review was of an environmental study from 2007 on a community subdivision located near a petroleum tank battery.
      • The primary researchers found a significantly higher incidence of confirmed diagnosed SLE in the exposed community, compared to an unexposed near-by community.4
      • In this same study, ambient air testing found higher levels of petroleum hydrocarbons as well as increased levels of mercury in the air, which are known to suppress the immune system and lead to SLE.4
      • One of Bjorklund’s reviewed studies described the use of the ‘Memory Lymphocyte Immunostimulation Assay (MELISA) that detected delayed T-cell reactivity to dental-metals in patients suffering from FM.9
        • In this study, all patient with a history for FM also tested positive for at least one of the metals in their dental materials with MELISA
        • A 5-year follow up from removing these metals showed that half the patients no longer fulfilled the American college of rheumatology 1990 criteria for FM.9
        • An explanation for this finding is that sensitization to nickel or mercury in dental amalgams can cause higher levels of pro-inflammatory cytokines such as interferon-gamma when compared to healthy individuals.
        • Though not reviewed by Bjorklund, studies have found changes in free radical/antioxidant balance, as well as low levels of glutathione, correlate with metal induced inflammation, thus putting certain individuals at higher risk for developing FM.10
          • This remarkable finding suggests metal-induced inflammation may be reversible and is an important risk factor in patients with FM.
        • Bjorklund also reviewed literature regarding the potential protective effects of micronutrients in apparently alleviating autoimmune diseases..
          • For example, selenium was reported to potentially inhibits the toxic effects of exposure to other metals.11
          • These authors proposed low selenium in our diet can result in higher levels of other metals (mercury) thereby aggravating muscle pains seen in FM.12

Conclusion:

  • The authors review compelling findings from a variety of published studies that show patients suffering from CTD or FM may benefit from reduced exposure to certain metals.
    • These benefits include reduced inflammation and potential partial reversal of symptoms, which can ultimately help restore the efficacy of conventional therapies.

 

Table 1: Summary of metals and their relation to CTD and FM compiled from various papers reviewed in Bjorklund et al.

Metals and their relation to CTD and FM 1 What is it used for? What conditions or connective tissue disease is associated with it? What are the symptoms?
Gold 13 -Injectable Treatment for Rheumatoid arthritis14

 

-Jewelry, dental alloys, and orthopedic appliances 15

 

-chinaware16

 -Gold allergy seen in 50% of RA patients studied (n=399) after treatment with gold salts14 Eczematous skin reaction 15
Palladium 15 -Dental Crowns, toothbrushing may increase palladium release, 17 Jewelry -Cross-reaction with nickel resulting in dermatitis 18 -Oral diseases such as lichen planus or stomatitis 19
Titanium 20 -Dental implants20 -Chronic Fatigue Syndrome, Multiple chemical sensitivity20 -Joint pain, nerve pain, chronic fatigue syndrome, depression, acne-like inflammation 20
Chromium 21 -Dye, detergent, cosmetics, leather, wood preservative 21

-Cement production 15

 -Shoe contact dermatitis 22-Insulin dysregulation 23

 

 -Bronchial asthma, hepatotoxicity 24

 

References:

  1. Bjorklund G, Dadar M, Aaseth J. Delayed-type hypersensitivity to metals in connective tissue diseases and fibromyalgia. Environ Res. 2018;161:573-579.
  2. Salaffi F, Sarzi-Puttini P, Girolimetti R, Atzeni F, Gasparini S, Grassi W. Health-related quality of life in fibromyalgia patients: a comparison with rheumatoid arthritis patients and the general population using the SF-36 health survey. Clin Exp Rheumatol. 2009;27(5 Suppl 56):S67-74.
  3. Iaccarino L, Gatto M, Bettio S, et al. Overlap connective tissue disease syndromes. Autoimmun Rev. 2013;12(3):363-373.
  4. Dahlgren J, Takhar H, Anderson-Mahoney P, Kotlerman J, Tarr J, Warshaw R. Cluster of systemic lupus erythematosus (SLE) associated with an oil field waste site: a cross sectional study. Environ Health. 2007;6:8.
  5. Regland B, Zachrisson O, Stejskal V, Gottfries CG. Nickel Allergy is Found in a Majority of Women with Chronic Fatigue Syndrome and Muscle Pain—and may be Triggered by Cigarette Smoke and Dietary Nickel Intake. Journal of Chronic Fatigue Syndrome. 2001;8(1):57-65.
  6. Thyssen JP, Menne T. Metal allergy–a review on exposures, penetration, genetics, prevalence, and clinical implications. Chem Res Toxicol. 2010;23(2):309-318.
  7. Hart JE, Laden F, Puett RC, Costenbader KH, Karlson EW. Exposure to traffic pollution and increased risk of rheumatoid arthritis. Environ Health Perspect. 2009;117(7):1065-1069.
  8. Muris J, Feilzer AJ. Micro analysis of metals in dental restorations as part of a diagnostic approach in metal allergies. Neuro Endocrinol Lett. 2006;27 Suppl 1:49-52.
  9. Stejskal V, Ockert K, Bjorklund G. Metal-induced inflammation triggers fibromyalgia in metal-allergic patients. Neuro Endocrinol Lett. 2013;34(6):559-565.
  10. De Luca C, Scordo MG, Cesareo E, et al. Biological definition of multiple chemical sensitivity from redox state and cytokine profiling and not from polymorphisms of xenobiotic-metabolizing enzymes. Toxicol Appl Pharmacol. 2010;248(3):285-292.
  11. Turner RJ, Finch JM. Selenium and the immune response. Proc Nutr Soc. 1991;50(2):275-285.
  12. Stoffaneller R, Morse NL. A review of dietary selenium intake and selenium status in Europe and the Middle East. Nutrients. 2015;7(3):1494-1537.
  13. Moller H. Dental gold alloys and contact allergy. Contact Dermatitis. 2002;47(2):63-66.
  14. Burmester GR, Blanco R, Charles-Schoeman C, et al. Tofacitinib (CP-690,550) in combination with methotrexate in patients with active rheumatoid arthritis with an inadequate response to tumour necrosis factor inhibitors: a randomised phase 3 trial. Lancet. 2013;381(9865):451-460.
  15. Forte G, Petrucci F, Bocca B. Metal allergens of growing significance: epidemiology, immunotoxicology, strategies for testing and prevention. Inflamm Allergy Drug Targets. 2008;7(3):145-162.
  16. Eisler R. Mammalian sensitivity to elemental gold (Au degrees). Biol Trace Elem Res. 2004;100(1):1-18.
  17. Wataha JC, Lockwood PE, Frazier KB, Khajotia SS. Effect of toothbrushing on elemental release from dental casting alloys. J Prosthodont. 1999;8(4):245-251.
  18. Faurschou A, Menne T, Johansen JD, Thyssen JP. Metal allergen of the 21st century–a review on exposure, epidemiology and clinical manifestations of palladium allergy. Contact Dermatitis. 2011;64(4):185-195.
  19. Durosaro O, el-Azhary RA. A 10-year retrospective study on palladium sensitivity. Dermatitis. 2009;20(4):208-213.
  20. Muller K, Valentine-Thon E. Hypersensitivity to titanium: clinical and laboratory evidence. Neuro Endocrinol Lett. 2006;27 Suppl 1:31-35.
  21. Thyssen JP, Strandesen M, Poulsen PB, Menne T, Johansen JD. Chromium in leather footwear – risk assessment of chromium allergy and dermatitis. Contact Dermatitis. 2012;66(5):279-285.
  22. Mortz CG, Andersen KE. Allergic contact dermatitis in children and adolescents. Contact Dermatitis. 1999;41(3):121-130.
  23. Ryan GJ, Wanko NS, Redman AR, Cook CB. Chromium as adjunctive treatment for type 2 diabetes. Ann Pharmacother. 2003;37(6):876-885.
  24. Shrivastava R, Upreti RK, Seth PK, Chaturvedi UC. Effects of chromium on the immune system. FEMS Immunol Med Microbiol. 2002;34(1):1-7.

 

Palladium allergic contact granuloma

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Discussion on Palladium granuloma

Title:Palladium-induced allergic contact granuloma in a child wearing an earring

Original article:

Gonzalez-Perez, R, Carrillo-Ruiz, G, & Soloeta, R. Sarcoid-type Allergic Contact Granuloma Caused by Earrings in a Boy. Actas Dermo-Sifiliográficas (English Edition). 2012;103(1):73-74. doi: 10.1016/j.adengl.2010.12.008

Reviewed by Jack Guccione, BS. MSIII & Brittanya Limone, MA, BS, MSIV. Loma Linda University School of Medicine

Case Description

  • A case of granulomatous allergic contact dermatitis (ACD) in an 11-year-old boy due to an earring containing palladium reported in Spain.
    • He complained of a firm, asymptomatic papule on his left earlobe that had been present since he began wearing an earring 3-years prior.
    • Surgical removal and pathology evaluation of the papule revealed a reactive “sarcoidal granulomatous infiltration with no evidence of refringent material”, suggesting that the papule did not form due to retention of a foreign body (metal fragment) present in the skin.
    • Skin patch testing determined that the boy was sensitized to palladium.
  • Palladium chloride skin patch testing resulted in a primary eczematous response.
  • Mass spectrometry of the patient’s earring identified palladium as the primary metal composing the earring.
  • Given the temporal association between the skin patch testing and confirmation of palladium in the earring, the diagnosis of granulomatous allergic contact dermatitis reaction (gACDr) due to palladium was made [aka palladium granuloma].
  • The boy stopped wearing his earring and there was complete resolution of the reaction, confirming the diagnosis of palladium granuloma.

 

Discussion:

  • Sarcoidal-type (non-caseating/non-necrotizing) granulomas are abnormal nodules composed of inflammatory immune cells and macrophages.
    • They develop in response to a perceived need of the skin to encase a ‘foreign’ substance it is unable to eliminate.
    • This type of granuloma suggests the lesion is not caused by an infection from Mycobacteria tuberculosis, Treponema pallidum (syphilis) or some fungi, all of which can cause the necrotizing (internally breaking down) type of granuloma.
  • Several metals have been reportedly to cause gACDr (See Table 1).

 

Allergic contact granulomas are a less common presentation (variant) of allergic contact dermatitis.  The article was reviewed to acknowledge the spectrum of allergic dermatitis.

 

Table 1. Metals and Respective Sources Implicated in Granulomatous ACD

Metal Sources of Exposure
Palladium Earrings
Beryllium Mining

Fluorescent lighting tubes

Beryllium alloy production
Aluminum Vaccine & hypo-sensitization extract adjuvants

Deodorants

Tattoos
Zirconium Deodorants
Titanium Pacemakers
Mercury Tattoos
Chromium
Cobalt

 

References:

Gonzalez-Perez, R, Carrillo-Ruiz, G, & Soloeta, R. Sarcoid-type Allergic Contact Granuloma Caused by Earrings in a Boy. Actas Dermo-Sifiliográficas (English Edition). 2012;103(1):73-74. doi: 10.1016/j.adengl.2010.12.008

Lubeck, G., & Epstein, E. (1952). COMPLICATIONS OF TATTOOING. California Medicine, 76(2), 83–85.

New report on Nickel allergy

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Nickel allergy and EU nickel restriction workshop report from the Nickel Institute

NACD WS Report Brussels June 2017

See Report

THIS SKIN RASH IS SERIOUS!

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SKINSERIOUS – report your experience with Dermatitis, Evaluation, Impact of Patch Testing on your Diagnosis and Care.

This weekend marked a magnificent occasion… The revival of the American Contact Dermatitis Society Mid-Year meeting — more than a decade after the last such meeting. This meeting FRONTIERS in DERMATITIS was attended by dermatologists, allergists, scientists from all over the country. We heard from Past-Surgeon General and Dermatologist Boris Lushniak MD “Reflections from my time as Surgeon General” and interfaced with Linda Katz, MD/MPH from the FDA “FDA Update on Cosmetics”, and Past-president of the ACDS, Bruce Brod MD on the importance of representing Contact Dermatitis in the House of Medicine at the AMA.

We are supporting the American Academy of Dermatology’s campaign to share stories about skin conditions — PLEASE report your experience with Dermatitis, Evaluation, Impact of Patch Testing on your Diagnosis and Care:

SKINSERIOUS Link

or for ease – we placed it on the Dermatitis Academy patient resource page.

 

The Dermatologist – Features Regional Atlas on Contact Dermatitis

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“The Dermatologist is a print and digital brand that circulates to more than 14,798 dermatologists, dermatology residents, dermatology nurse practitioners, physician assistants and nurses, as well as other healthcare professionals. The Dermatologist is collaborating with numerous associations, including the National Psoriasis Foundation, the world’s leading patient advocacy organization dedicated to the 7.5 million Americans with psoriasis and psoriatic arthritis, to educate dermatologists on the latest research related to psoriasis through The Dermatologist print and digital brand. Others include The National Eczema Association, The National Rosacea Society, and The Skin Cancer Foundation.

The editorial mission of The Dermatologist  focuses on providing practical and clinical insight, industry news and peer perspectives into today’s general dermatology issues. This award-winning publication offers dermatologists reader-friendly, timely and informative articles that highlight clinical advances for treatment of cutaneous pathologies such as skin cancer, acne and psoriasis, as well as information on how to incorporate cosmetic procedures, such as Botox and laser skin resurfacing, into a dermatology practice. Practice management topics, such as managed care, Medicare regulations and marketing techniques that can easily be translated into current practice settings, are also featured.”

Check out the Regional Atlas of Contact Dermatitis!

The Dermatologist (formerly Skin and Aging) has had a column dedicated to allergic contact dermatitis (allergen focus) since January 2005!

Experimental T cell regulation in ACD – novel potential interventions

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Original Article: Balmert SC, Donahue C, Vu JR, Erdos G, Falo LD Jr, Little SR. In vivo induction of regulatory T cells promotes allergen tolerance and suppresses allergic contact dermatitis. J Control Release. 2017 Sep 10; 261:223-233.

Reviewer: Calvin T Sung, BS. MSIII, University of California Riverside School of Medicine

  • Allergic contact dermatitis (ACD) is a T-cell mediated inflammatory skin condition commonly treated with topical corticosteroids through nonspecific immunosuppression.
  • The underlying immune hypersensitivity dysfunction can be addressed through identification and avoidance of the causative agent.
  • Essentially, ACD results from an inbalance between immune suppressing T regulatory cells (Tregs) and the pro-inflammatory cells that are inappropriately responding to specific allergens.
  • Immunologial chemical messengers, aka cytokines, (IL-2 and TGF-b1) and the antibiotic rapamycin can promote the expansion of Tregs to suppress the over active immune function underlying ACD.
  • Microparticle polymers are notable large molecules that can carry and release IL-2, TGF-b1, and rapamycin.
    • Balmert et al demonstarted that a Poly(ethylene glycol)-poly(lactic-co-glycolic acid) microparticle (PEG-PLGA) had a faster release rate of IL-2, TGF-b1, and rapamycin compared to the original PLGA microparticle formulation previously described by Jhunjhunwala et al.1
    • The cytokine and antibiotic releasing microparticle treatment was formulated as a subcutaneous injection and delivered experimentally to mice two days prior to topical and microneedle delivered allergen exposure (to induce sensitization).
    • Microparticle treatment injections at the ear (where allergens were introduced) revealed the potential for increasing the number of local Tregs to dampen unwanted immune responses upon subsequent allergen exposure.
  • Experiments demonstrated that microparticle treatment injections must be delivered locally near the site of allergen exposure (ear), whereas distal treatment (abdomen) failed to proliferate Tregs at the ear.
  • Interestingly, abdominal microparticle treatments followed by allergen exposure is capable of eliciting a systemic hyporesponsiveness that significantly reduces ear swelling when exposed to subsequent allergen challenges without any local prophylaxis.
  • This experimental data in mice suggests that prophylactic treatment during exposure and sensitization to a particular allergen could significantly suppresses immune dysfunction upon subsequent exposures anywhere on the body.
  • Considering that PEG-PLGA microparticle treatments can induce specific Tregs to suppress specific allergen mediated response, this modality offers a promising translatable novel treatment concept that could be used to decrease immune reactivity to known allergens inducing dermatitis.

 

For original article please visit: https://www.ncbi.nlm.nih.gov/pubmed/28694031 or http://www.sciencedirect.com/science/article/pii/S0168365917307046?via%3Dihub

T.R.U.E. Test (patch test) receives pediatric indication

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T.R.U.E Pediatric indication: T.R.U.E. Test (patch test) receives approval letter from Food and Drug Administration (FDA) for children 6 and older. After 12 years of investigations, evidence and data indicating that the patch testing is safe and efficacious in children suffering from recalcitrant dermatitis – the FDA has approved T.R.U.E Pediatric indication – the use of TRUE test to aid in the diagnosis of ACD in children.

This is the first commercially available patch test to receive approval for use in children 6 and older.  The T.R.U.E. test has 36 components, one is a negative control.

To read more about patch testing in children:

Article on Pediatric Allergic Contact Dermatitis.

“August 25, 2017

Dear Ms. Sullivan:
SUPPLEMENT APPROVAL PMR FULFILLED
August 25, 2017
We have approved your request dated October 26, 2016, to supplement your Biologics License Application submitted under section 351(a) of the Public Health Service Act (42 U.S.C. 262) for Thin-layer Rapid Use Epicutaneous Patch Test (T.R.U.E. TEST), to use as an aid in the diagnosis of allergic contact dermatitis in persons 6 years of age and older whose history suggests sensitivity to one or more of the 35 substances included on the T.R.U.E. TEST panels.”

FDA indication
Approval letter