Blogs related to nickel allergic contact dermatitis

Nickel Allergic Contact Dermatitis: Identification, Treatment, and Prevention

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Review and Synopsis by Jalal Maghfour, MD and Alina Goldenberg, MD of Original Peer-Reviewed Article:

Silverberg NB, Pelletier JL, Jacob SE, Schneider LC; SECTION ON DERMATOLOGY, SECTION ON ALLERGY AND IMMUNOLOGY. Nickel Allergic Contact Dermatitis: Identification, Treatment, and Prevention. Pediatrics. 2020;145(5):e20200628. doi:10.1542/peds.2020-0628

Nickel (Ni) remains one of the most common causes of allergic contact dermatitis (ACD), a type IV hypersensitivity reaction, since the publication of its first case in 1888 by Dr. George Henry Fox. This metal continues to be highly prevalent in every day goods within the US. Ni ACD is considered a public health issue and has been gaining international attention.

The impact of nickel on both adults and children has been increasingly reported in the literature. However, Ni ACD is primarily a disease of the young as it rarely affects elderly (> 60 years). In this synopsis, we provide a brief overview on an article written by Silverberg et al. in which the authors discussed epidemiology, clinical presentation, pathogenesis and management of Ni ACD among pediatric population.

With the discovery of Ni in the 18th century and advancement in the steel industry in early 19th century, Ni has become commonly utilized among manufacturers and is now considered the 5th most common metal in the world. Ni ACD may manifest as mild pruritus with ill-defined erythema to diffuse and pronounced redness with oozing and bullae. Classically, Ni ACD presents as an erythematous lichenified papule/plaque and matches the object touching the specific skin area. Any parts of the body can be affected by nickel.

Ni ACD has a multifactorial etiology with a combination of genetic and environmental factors. Contact with nickel is simply not enough for a reaction to occur. The following conditions must be met for both induction and elicitation phase to occur: 1) Contact with a metal containing corroded Ni, 2) degree of solubility of Ni (higher the solubility the higher ion leakage); 3) Ni ions being absorbed by the skin.

In case of a Ni ACD, the majority of diagnoses are clinical. However, when the cutaneous patterns are atypical, the diagnosis may be difficult in which cases patch testing can be performed. Patch testing is the criterion standard method to diagnose Ni ACD. While it is usually a localized reaction, the appearance of 3 large papules following Ni patch testing strongly suggests a systemic nickel hypersensitization.  

Ni ACD can be a diagnostic challenge in AD patients as the morphologic eruption may not match the triggering object. In addition, patients may also experience an exacerbation of their AD. In parallel, adults with psoriasis often experience flare of their disease during a Ni ACD episode. Although Ni ACD is primarily a type IV reaction, immediate hypersensitivity through IgE has been reported as a cause of Ni ACD.

For Ni ACD treatment, this review recommends the avoidance of the offending agent as the next best step in management, followed by the treatment of inflammation with the use of glucocorticoids (potency is based on the affected area). Finally, restoration of the skin barrier is essential. This can be performed with a generous application of emollients. 

As exemplified by Denmark and Finland, enacting a national policy to regulate the amount of Ni that a population is exposed to was proven efficacious in reducing the rate of Ni ACD and has increased awareness on the topic among adolescents. There is no such regulation within the US. Because Ni is primarily found in jewelry and ear piercings, it may be beneficial to regulate Ni found in other forms of jewelry, as well as children’s toys, metal protectors for phone which are now increasingly recognized to as a cause of Ni ACD.

Increased production and manufacturing regulations, specific diagnoses and focused avoidance strategies can make Ni ACD a preventable pediatric health issue.  As it was shown with European countries, the United States can benefit from limiting Ni exposure to its population.  Until then, individual awareness and knowledge of daily objects containing nickel should be encouraged as part of avoidance.

Free Article: IRRITABLE BOWEL SYNDROME-LIKE DISORDERS IN ENDOMETRIOSIS: PREVALENCE OF NICKEL SENSITIVITY AND EFFECTS OF A LOW-NICKEL DIET. AN OPEN-LABEL PILOT STUDY.

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Authors: Borghini R, Porpora MG, Casale R, Marino M, Palmieri E, Greco N, Donato G, Picarelli A

Journal: Nutrients. 2020 Jan 28;12(2). pii: E341. doi: 10.3390/nu12020341.

Abstract

Alimentary nickel (Ni) may result in allergic contact mucositis (ACM), whose prevalence is >30% and may present with IBS-like and extra-intestinal symptoms. These symptoms are also frequent in endometriosis, and Ni allergic contact dermatitis has already been observed in endometriosis. Therefore, intestinal and extra-intestinal symptoms in endometriosis may depend on a Ni ACM, and a low-Ni diet could improve symptoms. We studied the prevalence of Ni ACM in endometriosis and focused on the effects of a low-Ni diet on gastrointestinal, extra-intestinal, and gynecological symptoms. We recruited 84 women with endometriosis, symptomatic for gastrointestinal disorders. Thirty-one out of 84 patients completed the study. They underwent Ni oral mucosa patch test (omPT), questionnaire for intestinal/extra-intestinal/gynecological symptoms, and a low-Ni diet. Clinical evaluation was performed at baseline (T0) and after three months (T1). Twenty-eight out 31 (90.3%) patients showed Ni omPT positive results, with Ni ACM diagnosis, whereas three out of 31 (9.7%) patients showed negative Ni omPT. After three months of low-Ni diet, all gastrointestinal, extra-intestinal and gynecological symptoms showed a statistically significant reduction. Ni ACM has a high prevalence in endometriosis and a low-Ni diet may be recommended in this condition to reduce gastrointestinal, extra-intestinal and gynecological symptoms.

Link to article: https://www.ncbi.nlm.nih.gov/pubmed/32012984

Nickel allergy is associated with wheezing and asthma in a cohort of young German adults: results from the SOLAR study.

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Article from University Hospital Munich – elucidating the details of nickel allergy by – Kolberg L1,2,3, Forster F1,3, Gerlich J1,3, Weinmayr G4, Genuneit J4,5, Windstetter D1, Vogelberg C6, von Mutius E3,7, Nowak D1,3, Drexler H8, Schäfer T9, Radon K1,3,10. ERJ Open Res. 2020 Feb 3;6(1). pii: 00178-2019. doi: 10.1183/23120541.00178-2019. eCollection 2020 Jan.

BACKGROUND: Nickel allergy is the most prevalent contact allergy. It belongs to a different hypersensitivity type to asthma and rhinoconjunctivitis. The aim of this analysis was to assess whether self-reported nickel allergy is associated with incident wheezing, asthma and rhinoconjunctivitis in young German adults, taking into account potential effect modification by sex.

METHODS: In total, 2051 (70.6%) participants aged 19-24 years took part in the second phase of SOLAR (Study on Occupational Allergy Risks), a follow-up study of ISAAC II (the second phase of the International Study of Asthma and Allergies in Childhood) in Germany. Self-reported nickel allergy, as well as having pierced ears, and the three outcomes incident wheezing, asthma and rhinoconjunctivitis, were analysed stratified for sex. Logistic regression adjusted for potential confounders was performed.

RESULTS: An association between self-reported nickel allergy and incident wheezing was observed for men and women, while only in males did pierced ears show a significant association with the outcome (adjusted OR 2.26, 95% CI 1.10-4.62). Also only in males, self-reported nickel allergy was associated with elevated odds for incident asthma (adjusted OR 4.34, 95% CI 1.22-15.41). Neither in men nor in women was a significant association observed for incident rhinoconjunctivitis.

CONCLUSION: Our results suggest that self-reported nickel allergy is associated with incident wheezing. Whether this association is due to environmental or genetic predisposition, or due to an overlap of the mechanisms of type I and type IV hypersensitivity, needs to be elucidated. https://www.ncbi.nlm.nih.gov/pubmed/32039258

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.

 

It’s True – Metals in a Tattoo – Systemic Contact Dermatitis

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Yes, indeed metals can be implanted in a tattoo… and systemically activated reactions can occur in those tattoos related to those metals…

“We recommend assessment of permanent tattoos for inflammation in all patients undergoing patch testing, for additional diagnostic correlation.”  [ 2008 Sep-Oct;19(5):E33-4]

 

Article 1 (came out yesterday) :de Cuyper C1, Lodewick E2, Schreiver I3, Hesse B4, Seim C5,6, Castillo-Michel H4, Laux P3, Luch A3.   2017 Aug 9. doi: 10.1111/cod.12862. [Epub ahead of print]  Are metals involved in tattoo-related hypersensitivity reactions? A case report.

“BACKGROUND:  Allergic reactions to tattoos are not uncommon. However, identification of the culprit allergen(s) remains challenging.

OBJECTIVES: We present a patient with papulo-nodular infiltration of 20-year-old tattoos associated with systemic symptoms that disappeared within a week after surgical removal of metal osteosynthesis implants from his spine. We aimed to explore the causal relationship between the metal implants and the patient’s clinical presentation.

METHODS: Metal implants and a skin biopsy of a reactive tattoo were analysed for elemental contents by inductively coupled plasma mass spectrometry and synchrotron-based X-ray fluorescence (XRF) spectroscopy.

RESULTS: Nickel (Ni) and chromium (Cr) as well as high levels of titanium (Ti) and aluminium were detected in both the skin biopsy and the implants. XRF analyses identified Cr(III), with Cr(VI) being absent. Patch testing gave negative results for Ni and Cr. However, patch tests with an extract of the implants and metallic Ti on the tattooed skin evoked flare-up of the symptoms.

CONCLUSION: The patient’s hypersensitivity reaction and its spontaneous remission after removal of the implants indicate that Ti, possibly along with some of the other metals detected, could have played a major role in this particular case of tattoo-related allergy.”

 

Article 2: Cobalt tattoo reaction:

2017 Jun 1;15(3):221-222. eCollection 2017.  Chemical Tattoo Treatment Leading to Systemic Cobalt Hypersensitivity.  Zajdel NJ1, Smith WA2, Taintor AR3, Jacob SE4, Olasz EB5.

“An otherwise healthy 36-year-old Caucasian woman, without prior history of atopic dermatitis or eczema, presented to an outside dermatologist with a generalized, severely pruritic eruption involving the entire body except the face. One month previously, she had used a 50% trichloroacetic acid tattoo removal solution on a blue-colored tattoo on the medial aspect of the left ankle. The patient’s eruption persisted for 7 months, and after several attempts to slowly taper her prednisone dose, she presented to our institution. On physical examination, there was a 3-cm erythematous, lichenified plaque surrounding the tattoo (Figure). On the trunk and upper regions of the arms, there were scattered, 1- to 2-cm, nummular patches and plaques. Biopsy of a truncal lesion revealed spongiotic pustules with a mixed dermal infiltrate and scattered eosinophils, consistent with subacute spongiotic dermatitis.”

 

Article 3:  Systemic Dermatitis following surgery — presenting as tattoo reaction

2017 Jul 19;3(4):348-350. doi: 10.1016/j.jdcr.2017.05.003. eCollection 2017 Jul.  Systemic contact dermatitis to a surgical implant presenting as red decorative tattoo reaction.
Cobb HK1, Shinohara MM2, Huss JT3, Welch MP2, Gardner JM2.
“The patient reported that within 2 weeks of surgery, the red-containing areas of her tattoos, which were previously flat and uninflamed, became raised and pruritic.”…
Read this article
Article 4: SCD to chromate in a tattoo triggered by patch testing
2008 Sep-Oct;19(5):E33-4.Inflammation in green (chromium) tattoos during patch testing.  Jacob SE1, Castanedo-Tardan MP, Blyumin ML.

“We report three patients with permanent tattoos and chronic dermatitis. During patch testing, the patients’ dermatitis worsened, and the previously quiescent green-colored portions of the tattoos became inflamed. All three patients were patch-tested and had positive reactions to potassium dichromate 0.25% in petrolatum. Avoidance led to the resolution of both the dermatitis and the tattooinflammation. We recommend assessment of permanent tattoos for inflammation in all patients undergoing patch testing, for additional diagnostic correlation.”

Article 5: 1962
1962 Aug-Sep;74:288-94.Green tattoo reactions associated with cement dermatitis.
CAIRNS RJ, CALNAN CD.
And … one of those reads that just makes you think… Article 6:
2004 Aug 21-27;364(9435):730.  A red tattoo and a swordfish supper.
Tsuruta D1, Sowa J, Higashi N, Kobayashi H, Ishii M.
Read more here
“Tsuruta et al. report- ed a case of a 40-year-old Japanese man with a red tattoo who developed a whole-body rash after eating 250 g of raw swordfish and alfonsino.”
Researchers are investigating metal allergic dermatitis and the role of piercing in nickel allergy.  Please pass along this survey.

Fiddler’s Neck and Nickel

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Review of: Fiddler’s neck: Chin rest-associated irritant contact dermatitis and allergic contact dermatitis in a violin player

Original Article: Caero, Jennifer E & Cohen, Philip R. (2012). Fiddler’s neck: Chin rest-associated irritant contact dermatitis and allergic contact dermatitis in a violin player. Dermatology Online Journal, 18(9).

Reviewed by: Jacqueline Chen, BA. MSII

  • String players such as violinists and violists can develop dermatitis (inflammatory skin disease), colloquially called ‘Fiddler’s Neck, which may occur on the submandibular region (just below the jaw) or the supraclavicular (on the neck) region.
    • Submandibular Fiddler’s neck, or Fiddler’s neck type 1, refers to the irritation caused by mechanical frictional that occurs following prolonged contact with the chinrest.
      • Submandibular Fiddler’s neck is often described as a lichenified (thickened) plaque that may be darker than the surrounding skin.
      • Four main factors contribute to Fiddler’s neck Type I: pressure of the fiddle, friction, hygiene, and the instrument position.
      • A barrier cushion and adjustment to more horizontal positioning of the instrument has been recommended between the chinrest and submandibular neck to avoid fiddler’s neck type 1
    • Supraclavicular Fiddler’s neck, or Fiddler’s neck Type II occurs from contact allergy to the materials in the chinrest apparatus on the instrument.
      • Supraclavicular dermatitis usually presents as a pruritic (itchy) and erythematous (red) eczematous plaques.
      • Allergic contact dermatitis (the allergic skin response) to the chinrest is most often caused by nickel sulfate in the bracket that holds the chinrest to the instrument, but can also be caused by allergens in the composite woods.
      • The diagnosis of Fiddler’s neck Type 2 is often made based on the patient history and through observing the musician playing his/her instrument to evaluate the contact point of the rash with the instrument.
      • A patch test is the diagnostic test to confirm allergic contact dermatitis
      • Notably, sweat can dissolve nickel, contributing to its corrosion and increasing nickel absorption by skin.
      • To confirm nickel release, the dimethylglyoxime (DMG) test can be used
      • https://www.youtube.com/watch?v=dJFcHo5fDbY
      • Treatment of supraclavicular Fiddler’s neck should be focused on avoidance of the component in the chinrest containing the allergenic material.

 

To read the article by Caero and Cohen please click here.

If you suffer from an allergy to your musical instrument, and would like to participate in a nickel allergy awareness survey, please click here.

Nickel allergy – immunologic inflammatory pathways

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Review of: Nickel sulfate promotes IL-17A producing CD4+ T-cells by an IL-23 dependent mechanism regulated by TLR4 and Jak-STAT pathways

Original article: Bechara, R, Antonios, D, Azouri, H, Pallardy, M, Nickel sulfate promotes IL-17A producing CD4+ T-cells by an IL-23 dependent mechanism regulated by TLR4 and Jak-STAT pathways. The Journal of Investigative Dermatology. 2017 Jun 17.

Reviewed by: Jacqueline Chen, BA. MSI & Brittanya A. Limone, MS, BS. MSIV

  • Allergic contact dermatitis (ACD) is classically described as a Type IV hypersensitivity reaction, however, the distinctive characteristics of a nickel-induced allergic contact dermatitis (Ni-ACD) lead to immunologic mechanisms that not only encompass a Th1 response but involve additional inflammatory cells, cytokines, and pathways.
  • In Ni-ACD, dendritic cells (antigen presenting [accessory] cells) play a critical role. Dendritic cells bind the antigenic nickel absorbed in the skin and then present it to T-cells at local lymph nodes, coordinating T-cell differentiation through cytokine messengers.
    • The two most crucial cytokine signals include:
      • IL-12p70 which promotes a T-helper Cell 1 type (Th1) response
      • IL-23 which stimulates the development of T-helper Cell 17 type (Th17) cells
    • Notably, the presence of IL-17A produced by Th17 cells correlates with the clinical reaction in nickel allergic patients. An injection of anti-IL-17 neutralizing antibodies may limit the severity of the contact hypersensitivity.
    • The IL-23/IL-12p70 balance determines the primary immunologic mechanism of the hypersensitivity reaction.
      • Increases in the IL-23/IL12p70 balance lead to a greater Th1 cell polarization
      • Decreases in the IL-23/IL-12p70 ratio produce a stronger Th17 cell response.
    • Brechara et al identified 5 specific modulators of T-cell differentiation that are important in the development of Ni-ACD through alterations in the IL-23/IL-12p70 balance.
      • IFN-γ
        • Produced by Th1 cells.
        • Greatly increases the IL-23 levels produced by nickel sulfate (NiSO4)-treated dendritic cells.
        • The increase in the IL-23/IL-12p70 ratio favors Th17 cell development.
      • Jak-STAT pathway
        • Inhibition of the Jak-STAT pathway increases IL-23.
        • Alternatively, activation of the pathway will increase IL-12p40 and IL-12p70 levels and decrease the IL-23/IL-12p70 balance.
        • This decrease in the IL-23/IL-12p70 balance favors a Th1 cell response.
      • TLR4, p38MAPK and NFkB pathways
        • Activation of these pathways is essential for nickel-induced production of IL-23, IL-12p40 and IL-12p70.
        • Since both IL-23 and IL-12 cytokines are produced, the IL-23/IL-12p70 balance remains high.
      • In summary, Ni-ACD is a complex immunologic disease involving not only a cell-mediated Th1 response but also Th17 cell development with alterations in IFN- γ levels and TLR4, Jak-STAT, p38MAPK, and NF-kβ immunologic pathways.

Article: link to publishers site

Researchers are investigating the role of piercings and the development of nickel allergy – please consider to take the Loma Linda University Nickel Allergy Survey:

Nickel allergy survey

 

 

Patch Testing in Hand Eczema – Free Article!

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REVIEW of: The Efficacy of the Patch Test in Diagnosing Hand Eczema

Original article: Vigneshkarthik, N, Ganguly, S, and Kuruvila, S. Patch Test as a Diagnostic Tool in Hand Eczema. Journal of Clinical Diagnostic and Research, 2016; 10(11): WC04–WC07. India

Reviewed by Jacqueline Chen, BA. MSI and Brittanya Limone, MA. MSIII, Loma Linda University.

  • Hand eczema is a frequently encountered dermatologic problem that may be secondary to an allergic contact dermatitis (ACD). Patch testing is a diagnostic tool that can confirm an ACD etiology and determine the necessary allergens to avoid to prevent future exacerbations.
  • Vigneshkarthik, Ganguly, and Krurvila’s cross-sectional study analyzed patch test results to determine common allergens associated with ACD in patients with hand eczema. The study included 54 individuals, 27 men and women. The authors discovered that:
    • Of the patients with hand eczema 37% had positive patch test results to 25 different allergens, confirming that ACD is a common cause of hand eczema
    • Specific occupations were more susceptible including housewives, agriculturists, students and masons
  • Nickel was the most common allergen associated with hand eczema, particularly amongst patients with a vesicular hand eczema, or pompholyx, morphology.
    • In patients with nickel allergy, high levels of nickel in the diet have been associated with this more severe form of hand eczema.
  • Risk factors thought to be associated with the development of nickel hand eczema:
    • Ear piercings and adornment with nickel jewelry.
    • Chores in wet environments
    • Use of nickel-containing utensils
  • Detergents were another important association with nickel allergy
    • Over one-third of patients with regular detergent exposure had a positive patch test result.
      • 54% of these positive patch test results were due to nickel, either alone or in combination with cobalt sensitivity.
      • The association of nickel and cobalt allergies was determined to be due to co-exposure to the metals from a common source.

PubMed Link:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5198439/   Adobe PDF Icon

Not all nickel allergy reactions are delayed

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Nickel allergy early reactions reported within 30 min of contact!

 Nickel allergy in a Danish population 25 years after the first nickel regulation.

 Ahlström MG1, Menné T1, Thyssen JP1, Johansen JD1.

Author information

 Contact Dermatitis. 2017 Apr 7. doi: 10.1111/cod.12782. [Epub ahead of print]

Abstract

BACKGROUND:

Nickel in metallic items has been regulated in Denmark since 1990; however, 10% of young Danish women are still sensitized to nickel. There is a need for continuous surveillance of the effect of regulation.

OBJECTIVES:

To identify current self-reported metallic exposures leading to dermatitis in nickel-allergic patients, and the minimum contact time needed for dermatitis to occur.

METHODS:

A questionnaire was sent to all patients who reacted positively to nickel sulfate 5% pet. within the last 5 years at the Department of Dermatology and Allergy, Gentofte Hospital.

RESULTS:

The response rate was 63.2%. Earrings were the foremost cause of dermatitis after the EU Nickel Directive had been implemented, followed by other jewellery, buttons on clothing, belt buckles, and wrist watches. Dermatitis reactions within 10 min of contact were reported by 21.4% of patients, and dermatitis reactions within 30 min of contact were reported by 30.7% of patients. [Noting nickel allergy early reactions]

CONCLUSIONS:

Nickel exposures that led to implementation of a nickel regulation seem to persist. The durations of contact with metallic items to fall under the current REACH regulation of nickel correspond well with the results of this study.

© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

KEYWORDS:

EU directive; allergic nickel dermatitis; metallic items; nickel; prolonged direct contact