Rees J, Friedmann P S, Matthews J N
Department of Dermatology, University of Newcastle-upon-Tyne, England.
Arch Dermatol. 1990 Sep;126(9):1173-5.
If there is a primary dysfunction of the immune system in atopic eczema it might be reflected in altered capacity to generate delayed-type hypersensitivity. Therefore, the dose-response relationships for contact sensitization were determined for 22 patients (10 men) with minimal atopic eczema and compared with those from 27 nonatopic, healthy control subjects (12 men). Sensitization was induced with 30 micrograms of dinitrochlorobenzene applied to the thigh. Four weeks later the subjects were challenged with three doses of dinitrochlorobenzene (8.8, 12.5, and 17.7 micrograms), and responses were quantified with calipers as change in skinfold thickness at 48 hours. Atopic patients were significantly less responsive with smaller reactions at all challenge doses and a flatter challenge dose-response curve than that for control subjects. Thus, proper quantitative comparisons have shown that subjects with minimal atopic eczema do not mount a normal contact hypersensitivity response. However, it is not clear whether this is a consequence of the atopic state per se or is related to the presence of even a minor degree of eczema.
如果特应性皮炎存在免疫系统的原发性功能障碍，那么它可能会反映在迟发型超敏反应产生能力的改变上。因此，对22例轻度特应性皮炎患者（10名男性）进行接触致敏的剂量反应关系测定，并与27名非特应性健康对照者（12名男性）进行比较。将30微克二硝基氯苯涂于大腿进行致敏。四周后，用三剂二硝基氯苯（8.8、12.5和17.7微克）对受试者进行激发，并用卡尺测量48小时时皮褶厚度的变化来量化反应。特应性患者在所有激发剂量下的反应明显较弱，反应较小，且激发剂量反应曲线比对照组更平缓。因此，适当的定量比较表明，轻度特应性皮炎患者不能产生正常的接触性超敏反应。然而，尚不清楚这是特应性状态本身的结果，还是与即使是轻微程度的湿疹的存在有关。
