Zijlstra E E, Musa A M, Khalil E A G, el-Hassan I M, el-Hassan A M
EEZ is at the Department of Medicine, College of Medicine, Malawi
Lancet Infect Dis. 2003 Feb;3(2):87-98. doi: 10.1016/s1473-3099(03)00517-6.
Post-kala-azar dermal leishmaniasis (PKDL) is a complication of visceral leishmaniasis (VL); it is characterised by a macular, maculopapular, and nodular rash in a patient who has recovered from VL and who is otherwise well. The rash usually starts around the mouth from where it spreads to other parts of the body depending on severity. It is mainly seen in Sudan and India where it follows treated VL in 50% and 5-10% of cases, respectively. Thus, it is largely restricted to areas where Leishmania donovani is the causative parasite. The interval at which PKDL follows VL is 0-6 months in Sudan and 2-3 years in India. PKDL probably has an important role in interepidemic periods of VL, acting as a reservoir for parasites. There is increasing evidence that the pathogenesis is largely immunologically mediated; high concentrations of interleukin 10 in the peripheral blood of VL patients predict the development of PKDL. During VL, interferon gamma is not produced by peripheral blood mononuclear cells (PBMC). After treatment of VL, PBMC start producing interferon gamma, which coincides with the appearance of PKDL lesions due to interferon-gamma-producing cells causing skin inflammation as a reaction to persisting parasites in the skin. Diagnosis is mainly clinical, but parasites can be seen by microscopy in smears with limited sensitivity. PCR and monoclonal antibodies may detect parasites in more than 80% of cases. Serological tests and the leishmanin skin test are of limited value. Treatment is always needed in Indian PKDL; in Sudan most cases will self cure but severe and chronic cases are treated. Sodium stibogluconate is given at 20 mg/kg for 2 months in Sudan and for 4 months in India. Liposomal amphotericine B seems effective; newer compounds such as miltefosine that can be administered orally or topically are of major potential interest. Although research has brought many new insights in pathogenesis and management of PKDL, several issues in particular in relation to control remain unsolved and deserve urgent attention.
黑热病后皮肤利什曼病（PKDL）是内脏利什曼病（VL）的一种并发症；其特征是在已从VL康复且其他方面状况良好的患者中出现斑疹、斑丘疹和结节性皮疹。皮疹通常从口腔周围开始，然后根据严重程度蔓延至身体其他部位。它主要见于苏丹和印度，在苏丹，50%接受治疗的VL患者会出现这种情况，在印度，这一比例为5% - 10%。因此，它主要局限于杜氏利什曼原虫为致病寄生虫的地区。在苏丹，PKDL在VL之后出现的间隔时间为0 - 6个月，在印度为2 - 3年。PKDL可能在VL的流行间期发挥重要作用，作为寄生虫的储存宿主。越来越多的证据表明，其发病机制主要由免疫介导；VL患者外周血中高浓度的白细胞介素10预示着PKDL的发展。在VL期间，外周血单个核细胞（PBMC）不产生干扰素γ。VL治疗后，PBMC开始产生干扰素γ，这与PKDL病变的出现同时发生，因为产生干扰素γ的细胞会引起皮肤炎症，作为对皮肤中持续存在的寄生虫的反应。诊断主要依靠临床，但通过显微镜检查涂片发现寄生虫的敏感性有限。PCR和单克隆抗体在超过80%的病例中可检测到寄生虫。血清学检测和利什曼原虫皮肤试验价值有限。印度的PKDL病例总是需要治疗；在苏丹，大多数病例会自愈，但严重和慢性病例需要治疗。在苏丹，葡萄糖酸锑钠的给药剂量为20mg/kg，持续2个月，在印度则为4个月。脂质体两性霉素B似乎有效；新型化合物如米替福新，可口服或局部给药，具有重大潜在意义。尽管研究在PKDL的发病机制和管理方面带来了许多新见解，但特别是与控制相关的几个问题仍未解决，值得紧急关注。
