Marsella Rosanna
Department of Small Animal Clinical Sciences, College of Veterinary Medicine, 2015 SW 16th Avenue, University of Florida, Gainesville, FL 32610, USA.
Vet Dermatol. 2013 Feb;24(1):73-6.e17-8. doi: 10.1111/j.1365-3164.2012.01073.x.
Skin barrier dysfunction exists in both human and canine atopic dermatitis, leading to increased water loss and potentially facilitating allergen penetration and sensitization. Both lipid (e.g. ceramides) and protein (e.g. filaggrin) abnormalities have been described. Some are genetically inherited (e.g. filaggrin mutations are one of the major risk factors in humans) and some are secondary and linked to inflammation. In humans, numerous studies have shown efficacy of emollients and moisturizers in barrier restoration, and this approach has been for years the mainstay of therapy. Recently, this strategy has shown promise as a preventative function. In veterinary medicine, evidence regarding skin barrier impairment is rapidly building. Decreased ceramides and filaggrin (in some subsets of dogs) have been described. Altered metabolism of ceramides has also been proposed. Despite these preliminary data and the availability of products marketed to improve the skin barrier, evidence regarding the clinical benefit of skin repair intervention is still limited. Preliminary studies have demonstrated that topical application of fatty acids and ceramides and systemic administration of fatty acids improve lipid deficiencies in the skin of dogs with atopic dermatitis, but limited clinical evidence exists. Disease remission in humans is paralleled by an improved skin barrier, both with calcineurin inhibitors and glucocorticoids. In veterinary medicine, a preliminary study on ciclosporin and prednisone failed to detect significant improvement of water loss, while successful immunotherapy correlated with an improved skin barrier. Controlled, large studies are needed to address the question of which skin repair approach is clinically most effective and whether this can be used as a preventative strategy.
人类和犬类特应性皮炎均存在皮肤屏障功能障碍，导致水分流失增加，并可能促进变应原渗透和致敏。脂质（如神经酰胺）和蛋白质（如丝聚合蛋白）异常均有相关描述。有些是遗传继承的（如丝聚合蛋白突变是人类的主要风险因素之一），有些是继发性的且与炎症相关。在人类中，大量研究表明润肤剂和保湿剂在修复屏障方面具有疗效，多年来这种方法一直是治疗的主要手段。最近，这种策略已显示出具有预防作用的前景。在兽医学中，关于皮肤屏障受损的证据正在迅速积累。已描述了神经酰胺和丝聚合蛋白减少（在某些犬类亚群中）。也有人提出神经酰胺代谢发生改变。尽管有这些初步数据以及市场上有旨在改善皮肤屏障的产品，但关于皮肤修复干预临床益处的证据仍然有限。初步研究表明，局部应用脂肪酸和神经酰胺以及全身给予脂肪酸可改善特应性皮炎犬皮肤中的脂质缺乏，但临床证据有限。在人类中，使用钙调神经磷酸酶抑制剂和糖皮质激素时，疾病缓解与皮肤屏障改善同时出现。在兽医学中，一项关于环孢素和泼尼松的初步研究未能检测到水分流失有显著改善，而成功的免疫疗法与皮肤屏障改善相关。需要进行对照的大型研究来解决哪种皮肤修复方法在临床上最有效以及这是否可作为预防策略的问题。
