Br J Dermatol. 2021 Aug;185(2):e36-e67. doi: 10.1111/bjd.20528.
Linked Article: Vanden Oever et al. Br J Dermatol 2021; 185:380-390. Recessive dystrophic epidermolysis bullosa (RDEB) is a rare genetic disorder. Patients with RDEB experience severe painful blistering and skin fragility due to separation of two layers of the skin: the dermis and epidermis. This occurs because type VII collagen (C7) is deficient or absent in the skin. C7 is a major component responsible for tethering the epidermis to the dermis. The skin heals with disfiguring scarring, and patients are at risk of secondary infection and an aggressive form of squamous carcinoma, a type of skin cancer. There is currently no cure but there are encouraging results from some experimental treatments. One treatment is haematopoietic stem cell transplantion, where the engrafted cells appear to increase the amount of C7 (a process called deposition) over the long-term. Unfortunately, this treatment requires long term immunosuppression and this is particularly risky in patients with RDEB, who are prone to infections. The authors, based in Minneapolis, USA, explored whether any of the drugs used in chemotherapy treatment used before transplant might have an effect on C7 deposition. They found that fludarabine influences the production of C7 in affected cells in RDEB. They describe various mechanisms for this effect. They stress the need to determine how much the increased C7 deposition following haematopoietic stem cell transplantation is because of the engrafted cells, and how much is from the patient's own cells stimulated by drugs such as fludarabine. They caution that drugs may cause deposition of non-functional C7, which could be harmful. Unfortunately, fludarabine is generally too toxic to use in patients with RDEB, but there is the possibility of less toxic analogues that could have the same desirable effect on C7 deposition and have clinical benefit.
Vanden Oever 等人,《英国皮肤病学杂志》2021 年;185:380-390。隐性营养不良型大疱性表皮松解症(RDEB)是一种罕见的遗传性疾病。由于皮肤的真皮层和表皮层分离,患者会出现严重的疼痛性水疱和皮肤脆弱,这是由于 VII 型胶原(C7)在皮肤中缺失或缺乏所致。C7 是一种主要的组成部分,负责将表皮与真皮固定在一起。皮肤愈合后会留下瘢痕,而且患者存在继发感染和侵袭性鳞癌(一种皮肤癌)的风险。目前尚无治愈方法,但一些实验性治疗方法取得了令人鼓舞的结果。一种治疗方法是造血干细胞移植,其中植入的细胞似乎会随着时间的推移增加 C7 的量(称为沉积)。不幸的是,这种治疗需要长期免疫抑制,而这对于容易感染的 RDEB 患者来说尤其危险。美国明尼阿波利斯的作者们探讨了移植前化疗中使用的任何药物是否可能对 C7 的沉积产生影响。他们发现氟达拉滨会影响 RDEB 中受影响细胞中 C7 的产生。他们描述了这种影响的各种机制。他们强调需要确定造血干细胞移植后 C7 沉积的增加有多少是由于植入的细胞,有多少是由于药物(如氟达拉滨)刺激患者自身细胞所致。他们警告说,药物可能会导致无功能 C7 的沉积,这可能是有害的。不幸的是,氟达拉滨通常对 RDEB 患者毒性太大而无法使用,但有可能使用毒性较小的类似物,这些类似物可能对 C7 的沉积产生相同的理想效果,并具有临床益处。