In vivo delayed-type hypersensitivity in 109 patients with vitiligo

Background Although the etiology of the depigmentation disorder vitiligo is still not completely understood, many investigators believe that an autoim mune reaction may play a major role. In this regard, T-lymphocyte-mediated immunity has been implicated frequently in the pathogenesis of the disease. Most studies have applied in vitro testing of cell-mediated immunity, howe ver, rather than in vivo measurements. Therefore, our study was undertaken to define the cutaneous delayed-type hypersensitivity (DTH) in vivo reactio n in association with the absence/presence of serum thyroid autoantibodies, which are a good representative marker for autoimmunity in patients with v itiligo, Methods DTH was evaluated in the normal pigmented skin of 109 vitiligo pati ents (29 men and 80 women) and in the depigmented skin of 27 of this group (5 men and 22 women) using the dermal application of seven common recall an tigens together with a negative control. Individuals were considered to be hypoergic if the DTH sum score was less than or equal to 5 mm in women or l ess than or equal to 10 mm in men, or ii they responded to only one or two antigens. Results The mean sum score was 10.2 +/- 8.4 with an average of 2.3 +/- 1.6 positive reactions in depigmented skin vs. a sum score of 12.4 +/- 9.0 with an average number of 2.6 +/- 1.6 positive reactions in normal pigmented sk in. There was no statistically significant difference between depigmented a nd normal pigmented skin using the paired t-test (P > 0.05). Further evalua tion of these data showed no significant correlation between the presence o f thyroid autoantibodies as well as selected clinical parameters and an abe rration in cutaneous DTH Conclusions In contrast to earlier reports, our in vivo studies of cutaneou s DTH reactions revealed no clinically significant aberrant cellular immuni ty in this patient group. These results indicate that the immune reaction i n vitiligo may be only a secondary event in the pathogenesis of the disease .