The Leishmaniasis Research Group, Sudan ; Institute of Endemic Diseases, University of Khartoum, P.O. Box 45235, 11111 Khartoum, Sudan ; The Central Laboratory, Ministry of Science & Communications, 7099 Khartoum, Sudan.
J Trop Med. 2013;2013:275253. doi: 10.1155/2013/275253. Epub 2013 Mar 24.
Visceral leishmaniasis (VL) is a parasitic disease characterized by immune suppression. Successful treatment is usually followed by immune reconstitution and a dermatosis called post-Kala-azar dermal leishmaniasis (PKDL). Recently, PKDL was described as one of the immune reconstitution syndromes (IRISs) in HIV/VL patients on HAART. This study aimed to present PKDL as a typical example of paradoxical IRIS in non-HIV/AIDS individuals. Published and new data on the pathogenesis and healing of PKDL was reviewed and presented. The data suggested that PKDL is a typical example of paradoxical IRIS, being a new disease entity that follows VL successful treatment and immune recovery. PKDL lesions are immune inflammatory in nature with granuloma, adequate response to immunochemotherapy, and an ensuing hypersensitivity reaction, the leishmanin skin test (LST). The data also suggested that the cytokine patterns of PKDL pathogenesis and healing are probably as follows: an active disease state dominated by IL-10 followed by spontaneous/treatment-induced IL-12 priming, IL-2 stimulation, and INF- γ production. INF- γ -activated macrophages eliminate the Leishmania parasites/antigen to be followed by LST conversion and healing. In conclusion, PKDL is a typical example of paradoxical IRIS in non-HIV/AIDS individuals with anti-inflammatory cytokine patterns that are superseded by treatment-induced proinflammatory cytokines and lesions healing.
内脏利什曼病（VL）是一种免疫抑制性寄生虫病。成功治疗后通常会出现免疫重建，并发一种称为“卡拉-阿扎尔后皮肤利什曼病”（PKDL）的皮肤病。最近，PKDL 被描述为接受高效抗逆转录病毒治疗（HAART）的 HIV/VL 患者免疫重建综合征（IRIS）之一。本研究旨在将 PKDL 作为非 HIV/AIDS 个体中典型的矛盾性 IRIS 进行介绍。对 PKDL 的发病机制和愈合的已发表数据和新数据进行了回顾和介绍。这些数据表明，PKDL 是矛盾性 IRIS 的一个典型例子，是一种成功治疗 VL 并恢复免疫后出现的新疾病实体。PKDL 病变本质上是免疫炎症性的，伴有肉芽肿，对免疫化学疗法有充分的反应，随后发生超敏反应，即利什曼菌素皮肤试验（LST）。这些数据还表明，PKDL 发病机制和愈合的细胞因子模式可能如下：以 IL-10 为主导的活跃疾病状态，随后是自发/治疗诱导的 IL-12 启动、IL-2 刺激和 INF-γ 产生。INF-γ 激活的巨噬细胞消灭利什曼原虫/抗原，随后进行 LST 转化和愈合。总之，PKDL 是一种非 HIV/AIDS 个体中典型的矛盾性 IRIS，其抗炎细胞因子模式被治疗诱导的促炎细胞因子和病变愈合所取代。
