Tsutomu Takashima

POTENTIAL EFFICACY OF LOW METAL DIETS AND DENTAL METAL ELIMINATION IN THE MANAGEMENT OF ATOPIC DERMATITIS: AN OPEN CLINICAL STUDY

We performed an open clinical study on the effects of low metal diets and/or dental metal elimination on 27 patients with moderate to severe atopic dermatitis (AD), who showed positive patch tests for metal allergens and/or clinical exacerbation by oral provocation tests with metal salts. All the patients were recommended to ingest low metal diets for 3 months and/or undergo dental metal elimination. Marked or moderate improvement was noted in 18 patients (67%); 7 patients (26%) showed marked improvement and 11 patients (41%), moderate improvement. Nine patients (33%) showed minimal improvement or no change. In the patients who showed marked or moderate improvement, we observed statistically significant decreases (p<0.05) in both peripheral blood eosinophil counts and serum LDH levels after 3 months of treatment. The present study suggests that restriction of ingested metal allergens to which patients have positive patch tests and/or oral challenge tests may be useful in the management of some patients with AD who have metal sensitivity.

Increased contact hypersensitivity response in mice by topical application of 1α,25-dihydroxyvitamin D3 to elicitation site

SummaryRecent evidence indicates that the biologically active metabolite of vitamin D3, 1α,25-dihydroxy-vitamin D3 [1α,25(OH)2D3], has an effect on the regulation of the immune response. We investigated whether topical treatment of mice with 1α,25(OH)2D3 influences the contact hypersensitivity (CHS) response to trinitrochlorobenzene (TNCB). 1α,25(OH)2D3 was applied to the dorsal trunk of A/J mice on days 0–3, and on day 4 topical application of 5% TNCB on the 1α,25(OH)2D3-treated site was performed. The mice were tested for CHS on day 10 by applying 1% TNCB to the ears. No effect on induction of CHS response to TNCB was observed in 1α,25(OH)2D3-treated mice compared with 24,25-dihydroxyvitamin D3[24,25-(OH)2D3]-treated mice as control. In a second experiment, the dorsal trunk of A/J mice was treated with 5% TNCB on day 0. The topical application of 1α,25(OH)2D3 on the ears was performed from days 2 to 5. On day 6, the mice were tested for CHS by applying 1% TNCB to the 1α,25(OH)2D3-treated ears. When 1α,25(OH)2D3 increased their response to TNCB by 40% compared with 24,25(OH)2D3-treated mice as 1α,25(OH)2D3 increased their response to TNCB by 40% compared with 24,25(OH)2D3-treated mice as control (P<0.01). There were no findings suggesting that the pretreatment of the challenge site with 1α,25(OH)2D3 induced an irritant dermatitis that was superimposed on a subsequent CHS reaction. The 1α,25(OH)2D3 modulation of CHS response to TNCB in mice suggests that the hormone may play a role in the regulation of the immune response in vivo.