Lübbe Jann
Clinique et Policlinique de Dermatologie et Vénéréologie, Hôpital Cantonal Universitaire, Geneva, Switzerland.
Am J Clin Dermatol. 2003;4(9):641-54. doi: 10.2165/00128071-200304090-00006.
Clinicians have long since been aware that bacteria and other microorganisms play a role in the etiology of atopic dermatitis. Indeed, the immunological profile of atopy favors colonization by Staphylococcus aureus, and the bacteria are present in most patients with atopic dermatitis, even in the absence of skin lesions. Clinical signs of impetiginization, such as weeping and crusting, periauricular fissuration, or small superficial pustules are a sensitive indicator that the numbers of S. aureus may have increased and a clinical indication of secondary infected dermatitis. However, recent research that has focussed on the role of S. aureus in atopic dermatitis, offers a reversed perspective, by presenting evidence that the underlying pathology of atopic dermatitis, i.e. an alteration of the skin barrier and inflammation of the upper dermis, depends itself on the presence of an infectious process. In other words, secondary infection with S. aureus emerges as a cause of atopic dermatitis. Secondary infections due to fungi have, comparatively, received less attention, but there is evidence for a role for Malassezia spp. as a factor in dermatitis with a head and neck distribution pattern. Viral infections, such as herpes simplex virus, and mixed infections of intertriginous spaces, may complicate an underlying atopic dermatitis, but are not perceived as etiologic factors. Recent research has greatly contributed to our understanding of the pathophysiological potential of S.aureus superantigens in atopic dermatitis, suggesting that antibiotic therapy might be an important element in the therapeutic management of atopic dermatitis. At present, however, the clinical evidence is scarce with regards to demonstrating a clear advantage of combined anti-inflammatory and antibiotic treatment, compared with anti-inflammatory treatment alone. If there is a consensus that the presence of clinically infected lesions in atopic dermatitis warrants a course of specific antibiotic topical therapy, the clinical benefit of antibiotic agents in apparently uninfected atopic dermatitis, as present in the majority of patients, remains an open question.Moreover, the impact of adjuvant skin care on the cutaneous microflora needs to be quantified in order to properly assess the role of specific antibiotic therapy in clinically uninfected atopic dermatitis. In the meantime, secondary infections in atopic dermatitis remain a secondary problem in clinical atopic dermatitis management, and specific anti-infective therapy remains a method of fine-tuning for optimizing individual atopic dermatitis treatment.
长期以来，临床医生一直意识到细菌和其他微生物在特应性皮炎的病因中起作用。事实上，特应性的免疫特征有利于金黄色葡萄球菌的定植，并且在大多数特应性皮炎患者中都存在这种细菌，即使在没有皮肤病变的情况下也是如此。脓疱病化的临床体征，如渗液和结痂、耳周皲裂或小的浅表脓疱，是金黄色葡萄球菌数量可能增加的敏感指标，也是继发性感染性皮炎的临床指征。然而，最近聚焦于金黄色葡萄球菌在特应性皮炎中作用的研究提供了一个相反的观点，通过呈现证据表明特应性皮炎的潜在病理学，即皮肤屏障的改变和真皮上层的炎症，本身取决于感染过程的存在。换句话说，金黄色葡萄球菌的继发性感染成为特应性皮炎的一个病因。相对而言，真菌引起的继发性感染受到的关注较少，但有证据表明马拉色菌属作为头颈部分布模式的皮炎的一个因素发挥作用。病毒感染，如单纯疱疹病毒，以及间擦部位的混合感染，可能使潜在的特应性皮炎复杂化，但不被视为病因。最近的研究极大地促进了我们对金黄色葡萄球菌超抗原在特应性皮炎中的病理生理潜能的理解，表明抗生素治疗可能是特应性皮炎治疗管理中的一个重要因素。然而，目前关于证明联合抗炎和抗生素治疗相对于单独抗炎治疗有明显优势的临床证据很少。如果有共识认为特应性皮炎中临床感染性病变的存在需要一个特定的抗生素局部治疗疗程，那么抗生素在大多数患者中明显未感染的特应性皮炎中的临床益处仍然是一个悬而未决的问题。此外，辅助皮肤护理对皮肤微生物群的影响需要量化，以便正确评估特定抗生素治疗在临床未感染的特应性皮炎中的作用。与此同时，特应性皮炎中的继发性感染在临床特应性皮炎管理中仍然是一个次要问题，特定的抗感染治疗仍然是优化个体特应性皮炎治疗的一种微调方法。
