Nickel skin patch testing

The most frequent causes of allergic contact dermatitis in the United States include plants (poison ivy, poison oak, and poison sumac), metallic salts, organic dyes, plastic resins, rubber additives, and germicides.74 The most common skin patch test allergens found to be positive in patients along with potential sources of exposure are shown in Table 32.1.75 In patients with occupational contact dermatitis who were skin patch tested, the common allergens included carba mix, thiuram mix, formaldehyde, epoxy resin, and nickel.76... 

IL-4 which is a strong inducer of a type 2 cytokine milieu itself is produced by early skin-infiltrating T cells but it may also be released from mast cells, basophils or eosinophils during the acute eczematous skin reaction. Of note, the high frequency of IL-4-producing T cells in the skin is not necessarily associated with atopy since mRNA for IL-4 and T cells expressing IL-4 are found in nickel-induced patch test reactions as well. 

If the excited skin syndrome phenomenon is hapten-related, this has not been elucidated. However, Andersen et al. employed adjacent nickel sulfate patch tests at different dilutions to study both the dose-response relationship for nickel sulfate among nickel-sensitive patients and the nickel-sulfate-related angry back phenomenon (Andersen et al. 1993). Strong reactions at high concentrations of nickel sulfate did not enhance the response to adjacent lower concentrations of nickel sulfate, and the spillover effect was not significant. 

Allenby CF, Basketter DA (1994) The effect of repeated open exposure to low levels of nickel on compromised hand skin of nickel-allergic subjects. Contact Dermatitis 30 135-138 Andersen KE, Liden C, Hansen J, Volund A (1993) Dose-response testing with nickel sulphate using the TRUE test in nickel-sensitive individuals. Multiple nickel sulphate patch-test reactions do not cause an angry back . Br J Dermatol 129 50-56... 

Nickel itch is a dermatitis resulting from sensitization to nickel the first symptom is usually pruritis, which occurs up to 7 days before skin eruption appears. The primary skin eruption is erythematous, or follicular it may be followed by superficial discrete ulcers that discharge and become crusted or by eczema. The eruptions may spread to areas related to the activity of the primary site such as the elbow flexure, eyelids, or sides of the neck and face. In the chronic stages, pigmented or depigmented plaques may be formed. Nickel sensitivity, once acquired, is apparently not lost of 100 patients with positive patch tests to nickel, all reacted to the metal when retested 10 years later. ... 

Although most patch testing is done with nickel sulfate because it is less irritating than nickel chloride, exposure of the skin to nickel alloys results in the release of nickel chloride from the influence of human sweat. Therefore, nickel chloride is the more relevant form of nickel for examining threshold concentrations (Menne 1994). Menne and Calvin (1993) examined skin reactions to various concentrations of nickel chloride in 51 sensitive and 16 nonsensitive individuals. Although inflammatory reactions in the sweat ducts and hair follicles were observed at 0.01% and lower, positive reactions to nickel were not observed. To be scored as a positive reaction, the test area had to have both redness and infiltration, while the appearance of vesicles and/or a bullous reaction were scored as a more severe reaction. At 0.1%, 4/51 and 1/51 tested positive with and without 4% sodium lauryl sulfate. Menne et al. (1987) examined the reactivity to different nickel alloys in 173 nickel-sensitive individuals. With one exception (Inconel 600), alloys that released nickel into synthetic sweat at a rate of <0.5 pg/cmVweek showed weak reactivity, while alloys that released nickel at a rate of >1 pg/cm /week produced strong reactions. 

Contact allergy to topically applied aluminium compounds is rare but skin sensitization has been described (54). In one case the use of a cream for acne and hyperpigmentation was followed by dermatitis, and patch tests were positive to both aluminium sulfate and aluminium chloride. A more typical antecedent of sensitization is the injection of aluminium-adsorbed vaccines, and such patients may present with a granulomatous nodule at the site. Mixed contact sensitivity to nickel and aluminium has been reported to respond to antihistamine therapy (55). 

A 32-year-old woman developed dermatitis on her left cheek and suggested that it might have been caused or worsened by her mobile phone. Patch tests showed only positive reaction to nickel sulfate. The dimethylglyox-ime test for nickel on the side of her phone was positive. The skin lesion resolved rapidly after she covered the phone with a plastic case. 

Skin In a cross-sectional patch test study in 1843 Danish women, the prevalence of nickel allergy was similar among women who reported cosmetic dermatitis from eye shadow or mascara and women who did not [8 ]. Cosmetic dermatitis was associated with self-reported atopic dermatitis and age. 

Skin A 23-year-old woman, who was allergic to penicilhn, developed erythematous, fissured, scaly, pruritic lesions on the backs of the fingers and both hands after working as a prosthodontist for 1 month [77" ]. Patch testing was positive only with manganese, which is used in the manufacture of dental prostheses as a nickel substitute. 

Fig. 6. Skin thickness (mm) and echogenicity (0-30 pixel) values expressing the intensity of the inflammatory response on forearm skin at nickel patch-test sites after pre-treatment with 5% sodium lauryl sulfate for 30 min in nickel-sensitive subjects with contact dermatitis (CD) and with atopic dermatitis (AD)...

Pustular reaction to contactant was first observed in patch-test reaction. The pustules are sterile and are transient. Fisher et al. (1959) reported that metallic salts, e.g., nickel, copper, arsenic and mercurial salts, may produce pustular reaction. Stone and Johnson explained that such reactions may represent an enhanced reaction of prior inflammation, rather than an irritant or allergic reaction, because such a reaction can be elicited in non-nickel-sensitive patients on skin sites previously injected with heat-killed Corynebacte-rial acne organisms (Stone and Johnson 1967). Hjorth reported that atopies are more predisposed to such reactions (Hjorth 1977). The significance of such reaction remains controversial. Wahlberg and Maibach believed that such pustular reactions are usually irritant in nature but may also be a manifestation of allergic reactions (Wahlberg and Maibach 1981). 

Fischer T (1989) Occupational nickel dermatitis. In Maibach HI, Menne T (eds) Nickel and the skin immunology and toxicology. CRC Press, Boca Raton, pp 117-132 Fischer T, Rystedt I (1990) Influence of topical metal binding substances, vehicles, and corticosteroid creams on the allergic patch test reactions in metal-sensitive patients. Dermatol Clin 8 27-31... 

A history of hand eczema was found in 36 of 39 individuals with reproducible patch tests to cobalt, while 21 of 23 individuals with a positive initial patch test, but negative retest using the serial dilution technique, had never had any skin problems. Patch testing with cobalt chloride and nickel sulfate often resulted in follicular erythematous reactions sometimes reproducible with serial dilution retests, but not reproducible as morphologically positive reactions. They were evaluated as irritant and were rarely associated with relevant hand eczema (Fischer and Rystedt 1985b). 

Respiratory A 25-year-old woman developed symptoms of rhinoconjunctivitis and asthma, attributed to an allergy to cyanoacrylate in a fingernail adhesive gel, which as a manicurist she had used for 6 months [41 ]. Skin prick tests were positive with dog and cat dander and grass pollens. Patch tests were positive with nickel, cadmium, and silver salts. An inhalation challenge with cyanoacrylate for 30 minutes elicited a late asthmatic response, with a 24% fall in FEVi, with rhinorrhea and asthma that worsened progressively until she received short-acting P2-adrenoceptor agonists. 

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