Farr P M, Diffey B L
Department of Dermatology, Royal Victoria Infirmary, Newcastle upon Tyne, U.K.
Br J Dermatol. 1989 Mar;120(3):411-8. doi: 10.1111/j.1365-2133.1989.tb04169.x.
Five patients with actinic prurigo were treated twice weekly with PUVA. One area on the back was shielded from UVA throughout the 15-week treatment period. Before PUVA, all patients had increased erythemal sensitivity to UVA and showed abnormal augmentation of UVB erythema by topical indomethacin. After PUVA, all patients were free of photosensitive symptoms and skin that had been exposed to UVA showed normal erythemal responses. By contrast, the areas of skin that had been protected from UVA showed erythemal responses that were unchanged from pre-PUVA values. Augmentation of UVB erythema by topical indomethacin persisted, both on UVA exposed and UVA protected skin. These results show that, although PUVA is an effective treatment in actinic prurigo, it does not alter the underlying mechanism of photosensitivity. The protective effect is local and is due presumably to an increase in melanin pigmentation and epidermal thickness.
五名光化性痒疹患者每周接受两次补骨脂素加紫外线A(PUVA)治疗。在为期15周的治疗期间,背部的一个区域始终受到紫外线A(UVA)的遮挡。在接受PUVA治疗前,所有患者对UVA的红斑敏感性均增加,且外用吲哚美辛后紫外线B(UVB)红斑出现异常增强。接受PUVA治疗后,所有患者均无光敏症状,暴露于UVA的皮肤表现出正常的红斑反应。相比之下,未暴露于UVA的皮肤区域的红斑反应与PUVA治疗前的值无变化。外用吲哚美辛引起的UVB红斑增强在暴露于UVA和未暴露于UVA的皮肤上均持续存在。这些结果表明,虽然PUVA是治疗光化性痒疹的有效方法,但它并未改变光敏性的潜在机制。保护作用是局部的,可能是由于黑色素沉着增加和表皮厚度增加所致。