Griffiths C E, Russman A N, Majmudar G, Singer R S, Hamilton T A, Voorhees J J
Department of Dermatology, University of Michigan Medical Center, Ann Arbor 48109-0314.
N Engl J Med. 1993 Aug 19;329(8):530-5. doi: 10.1056/NEJM199308193290803.
Topical tretinoin (retinoic acid) modifies fine wrinkles and certain other features of human skin damaged by exposure to the sun (photodamage), but histologic changes do not account for this improvement. In mice with photodamage induced by ultraviolet light, effacement of fine wrinkles by tretinoin is correlated with dermal collagen synthesis but not with histologic changes. We investigated whether collagen synthesis was reduced in photodamaged human skin and, if so, whether it could be restored by treatment with topical tretinoin.
Biopsies of photodamaged skin from the extensor aspect of the forearm and skin from the buttocks, which had been protected from the sun, were performed on 26 healthy subjects. In addition, 29 patients with photodamaged skin were treated for 10 to 12 months with a daily application of 0.1 percent tretinoin cream (15 patients) or vehicle cream (14 patients). Skin-biopsy specimens obtained at base line and after treatment were assessed immunohistologically for evidence of dermal collagen I formation (collagen synthesis).
Collagen I formation was 56 percent less in the papillary dermis of photodamaged skin than in skin protected from the sun (P < 0.001) and was correlated with the clinical severity of photodamage (r = -0.58, P = 0.002). Treatment of photodamaged skin with tretinoin produced an 80 percent increase in collagen I formation, as compared with a 14 percent decrease in collagen formation with the use of vehicle alone (P = 0.006).
The formation of collagen I is significantly decreased in photodamaged human skin, and this process is partly restored by treatment with tretinoin.
外用维甲酸(视黄酸)可改善因日晒(光损伤)而受损的人类皮肤的细纹及某些其他特征,但组织学变化并不能解释这种改善情况。在紫外线诱导光损伤的小鼠中,维甲酸消除细纹与真皮胶原合成相关,而非与组织学变化相关。我们研究了光损伤的人类皮肤中胶原合成是否减少,以及如果减少,外用维甲酸治疗能否使其恢复。
对26名健康受试者的前臂伸侧光损伤皮肤及臀部未受日晒的皮肤进行活检。此外,29名光损伤皮肤患者每日外用0.1%维甲酸乳膏(15例)或赋形剂乳膏(14例),治疗10至12个月。对基线时和治疗后获取的皮肤活检标本进行免疫组织学评估,以寻找真皮I型胶原形成(胶原合成)的证据。
光损伤皮肤乳头层真皮中的I型胶原形成比未受日晒的皮肤少56%(P<0.001),且与光损伤的临床严重程度相关(r=-0.58,P=0.002)。与单独使用赋形剂导致胶原形成减少14%相比,维甲酸治疗光损伤皮肤使I型胶原形成增加了80%(P=0.006)。
光损伤的人类皮肤中I型胶原的形成显著减少,维甲酸治疗可部分恢复这一过程。