ABSTRACT
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ABSTRACT
Background@#Nickel is one of the leading causes of allergic contact dermatitis. Positive patch tests for nickel suggest the possibility of persistent dermatitis from nickel-plated item usage and nickel-containing food ingestion. Previous studies have suggested the clinical improvement of dermatitis in such patients after a nickel-restricted diet. @*Objective@#This retrospective study aimed to assess the efficacy of nickel-restricted diets in nickel-sensitized patients and evaluate their adherence to nickel-restricted diets. @*Methods@#A review of the records of nickel-sensitized patients from June 1, 2018 to April 30, 2020 with positive patch tests for nickel was conducted. Patients were interviewed in May 2020 to assess the current status of dermatitis and self-reported adherence. @*Results@#A total of 245 patients were identified, and 100 patients were contacted. The degree of nickel sensitivity between patients with localized skin lesions (n=44) and generalized skin lesions (n=56) did not show difference. Twenty-four of 29 patients (82.8%) with good compliance showed improvement, while only 32 of 71 patients (45.1%) with poor compliance showed improvement. The percentage of improved patients in the group with good compliance and that in the group with poor compliance showed a statistically significant difference (p=0.00086). Of the patients with good compliance, those with localized skin lesions showed statistically significant improvement (p=0.0074). @*Conclusion@#To improve patient compliance, revised, simplified, and interventional guidelines for nickel-restricted diet should be implemented along with dermatologists’ encouragement and reassurance of a diet modification.
ABSTRACT
OBJECTIVES: To determine the effects of exposure to hexavalent chromium, 93 male Sprague-Dawley rats were exposed to hexavalent chromium solution. METHODS: Rats were divided into 4 groups and exposed to 0.1 ml of 0 mM, 0.4 mM, 2.0 mM, and 10.0 mM potassium chromate in the first experiment, and to 0.1 ml of 0 mM, 20 mM, 40 mM, and 80 mM in the second for consecutive 3 days by tracheal instillation. Three and 10 rats were the controls for the first and the second experiments, respectively. Lung tissues were then removed to measure the 8-hydroxydeoxyguanosine (8-OH-dG) level using the HPLC-ECD method, superoxide dismutase (SOD) activity using the cytochrome C method, and 8-hydroxyguanine endonuclease activity using the oligonucleotide nicking assay. RESULTS: The results showed no significant linear relationship between chromium exposure level and 8-OH-dG level or 8-hydroxyguanine endonuclease activity. In the first experiment, 8-OH-dG level and 8-hydroxyguanine endonuclease activity increased in 0.4 mM group, and then decreased in 2.0 mM and 10.0 mM groups. The correlation coefficients between 8-OH-dG level and 8-hydroxyguanine endonuclease activity was statistically significant (P<0.01), and total SOD activity was elevated by chromium exposure in a dose-dependent manner (P<0.05). In contrast, there was no significant dose-response pattern or correlation in the second experiment. CONCLUSIONS: Based on the fact that there was no linear relationship between chromium dose and 8-OH-dG level or activity of the repair enzyme, it seems unlikely that 8-OH-dG formation is the major mechanism of chromium carcinogenesis.