Alford R H, Vire C G, Cartwright B B, King L E
Am J Med Sci. 1986 Feb;291(2):75-80. doi: 10.1097/00000441-198602000-00001.
Ketoconazole, an oral antifungal imidazole, has been effective in some refractory cases of psoriasis, particularly those with scalp involvement, perhaps because of suppression of Pityrosporum ovale. To assess an ancillary immunologically mediated role for ketoconazole, its effects were evaluated on psoriatic patients' lymphocyte function. Ketoconazole in vitro markedly inhibited Pityrosporum antigen-induced lymphocyte blastogenesis as indicated by impairment of cellular tritiated thymidine uptake. Ketoconazole likewise inhibited lymphocyte uptake of other pyrimidine nucleosides by both normal and psoriatic lymphocytes. Neither imidazole or an investigational triazole antifungal (Bay n7133) inhibited the uptake. Thus, ketoconazole potentially could affect psoriasis in seborrheic areas of skin by a direct antifungal action or indirectly by suppressing fungal antigen-induced lymphocyte-mediated immune responses affecting the skin.
酮康唑是一种口服抗真菌咪唑类药物,对一些难治性银屑病病例有效,尤其是那些累及头皮的病例,这可能是由于其对卵圆形糠秕孢子菌的抑制作用。为了评估酮康唑在免疫介导方面的辅助作用,研究人员对银屑病患者的淋巴细胞功能进行了评估。体外实验表明,酮康唑显著抑制了糠秕孢子菌抗原诱导的淋巴细胞增殖,这表现为细胞摄取氚标记胸腺嘧啶核苷的能力受损。酮康唑同样抑制了正常淋巴细胞和银屑病淋巴细胞对其他嘧啶核苷的摄取。咪唑或一种研究性三唑类抗真菌药物(Bay n7133)均未抑制这种摄取。因此,酮康唑可能通过直接抗真菌作用或间接抑制真菌抗原诱导的影响皮肤的淋巴细胞介导的免疫反应,从而对皮肤脂溢部位的银屑病产生影响。