Hyposensitization in nickel allergic contact dermatitis: clinical and immunologic monitoring. J Am Acad Dermatol
ABSTRACT In allergic contact dermatitis (ACD) previously sensitized T cells cause skin damage. If an ubiquitous allergen such as nickel is involved, no effective treatment is available. Down-regulation of this allergic response has been described after antigen presentation in the absence of adequate costimulatory signals. UV exposure can enhance such hyposensitization.
The aim of this study was to establish the capability of a hyposensitization procedure to induce antigen-specific tolerance.
Twenty-one patients with nickel ACD were randomly assigned to either a hyposensitized or control group. A schedule consisting of UVB treatment and subcutaneous nickel sulfate administration (hyposensitization) or UVB only (control) was applied. During the ensuing 2 years, several clinical and immunologic features were monitored.
During UVB treatment we observed a significant clinical improvement in both groups that persisted in the hyposensitized group. Except for increased slope variances of specific lymphocyte proliferation in time, no clear changes were seen in the immunologic findings.
Despite significant clinical improvement induced by UVB, hyposensitization did not induce significant changes in the immunologic findings in patients with nickel ACD.
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ABSTRACT: Nickel is an important metal in the automobile industry, in electronics, as a catalyst in chemical processes, in nickel-cadmium batteries and accumulators, in many household products, and in cheap jewelry. Almost everyone in the industrially developed countries may be in daily contact with nickel. Cutaneous nickel allergy (contact dermatitis) is very common, as typically 15% to 20% of the population have positive results in epicutaneous testing. Nickel sensitization may be avoided by restricting contact with objects that release nickel ions through sweat on skin. Because nickel is also carcinogenic to man, causing upper respiratory tract and lung malignancies, advanced control of exposure at workplaces is necessary. Control can be accomplished either by measuring the exposure in the occupational environment or through urinary nickel analysis by applying so-called biological monitoring. As covalent nickel adducts have not been found in DNA, the carcinogenic effect of nickel is probably related to its lipid-peroxidation properties, which induce DNA-strand gaps and breaks and DNA-protein crosslinks. The negative effect of nickel ions on glycoprotein metabolism may explain the nephrotoxic effects of excessive exposure.Reviews on environmental health 01/1996; 11(4):167-73. DOI:10.1515/REVEH.19188.8.131.52
- Clinics in Dermatology 07/1997; 15(4):547-55. DOI:10.1016/S0738-081X(97)00056-4 · 2.47 Impact Factor
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ABSTRACT: This study investigates the extent to which sunscreens protect humans from ultraviolet (UV)-radiation-induced immunosuppression. In the presence of solar-simulated UV, three sunscreens with differing UVA transmission were assessed for their ability to protect the contact hypersensitivity (CHS) response to nickel of 16 nickel-allergic subjects. The sunscreens contained 2-ethylhexyl para-methoxycinnamate (cinnamate), cinnamate with oxybenzone, or cinnamate with zinc oxide, respectively. All had sun protection factors of 10 and hence inhibited UV erythema to similar extents. Volunteers were irradiated on their backs with suberythemal UV daily for 5 d after application of the sunscreens and their base lotion to different sites. Nickel-containing patches were then applied to both UV-treated sites and adjacent, unirradiated control sites. Erythema caused by nickel CHS at each site was quantitated 72 h later with a reflectance erythema meter. In comparison of the nickel reactions of irradiated and unirradiated skin, there was 35% mean immunosuppression in unprotected UV-treated skin. Significant immunosuppression also occurred at sites irradiated through the narrow-spectrum cinnamate-only sunscreen but was prevented by the two broad-spectrum sunscreens. To determine whether UV-induced suppression of the nickel response is specific for cell-mediated immunity or reflects suppression of nonspecific inflammation, a further 16 subjects were patch-tested with a skin irritant, sodium lauryl sulfate (SLS), following a sunscreen and irradiation protocol identical to that of the nickel volunteers. UV had no significant effect on SLS responses. We conclude that nickel patch testing is a valid means of assessing UV-induced immunosuppression in humans and that even with suberythemal UV, immune protection was provided only by sunscreens filtering both UVA and UVB.Journal of Investigative Dermatology 09/1997; 109(2):146-51. DOI:10.1111/1523-1747.ep12319200 · 7.22 Impact Factor