Division of Parasitology, Central Drug Research Institute, Lucknow, UP, India.
Acta Trop. 2011 Aug;119(2-3):188-93. doi: 10.1016/j.actatropica.2011.05.017. Epub 2011 Jun 7.
Visceral leishmaniasis (VL) caused by the parasite Leishmania donovani, is a potentially fatal disease. It is characterized by prolonged fever, enlarged spleen and liver, substantial weight loss and progressive anemia. Available drugs are toxic, costly and require prolonged treatment duration viz; 28 days of oral treatment with miltefosine, 30 days infusion with Amphotericin B and 21 days intramascular with paromomycin sulfate. Drug combination for VL clinically proved to shorten the duration of treatment. The efficacy of drugs is also compromised due to suppression of immune function during the course of infection. To combat this situation leishmanicidal efficacy of already marketed standard antifungal drug, ketoconazole under the approach of 'therapeutic switching' in combination with standard antileishmanial drug, miltefosine and a potent immunomodulator agent, picroliv were evaluated in L. donovani/hamsters model. Animals treated with combination of ketoconazole (50 mg/kg, 5 days, po)+miltefosine (5 mg/kg, 5 days, po) showed augmentation in efficacy against leishmania parasite (72%) in comparison to those treated with ketoconazole (54.67%) and miltefosine (54.77%) separately. Co-administration of picroliv (10 mg/kg, 12 days, po) has further enhanced antileishmanial efficacy from 72% to 82%. Significant generation of ROS, RNS and H(2)O(2) and increased phagocytosis was observed in animals treated with ketoconazole+miltefosine; however, addition of picroliv to this combination did not alter the level of metabolites and phagocytosis due to its antioxidative and nonleishmanicidal characteristics, respectively. Significant rise in cell mediated immunity witnessed in this group reveals the role played by the immunomodulator, picroliv and justifies the significance of enhanced cell mediated immunity in the therapy. These findings suggest a new strategy for leishmanial chemotherapy at reduced cost and toxicity.
内脏利什曼病(VL)由寄生虫利什曼原虫引起,是一种潜在的致命疾病。其特征为长期发热、脾脏和肝脏肿大、体重显著减轻以及进行性贫血。现有的药物具有毒性、成本高且需要长时间治疗,例如米替福新的口服治疗 28 天、两性霉素 B 的输注治疗 30 天以及硫酸巴龙霉素的静脉内注射治疗 21 天。VL 的临床药物组合已被证明可以缩短治疗时间。由于在感染过程中免疫功能受到抑制,药物的疗效也受到影响。为了应对这种情况,已经上市的标准抗真菌药物酮康唑的杀利什曼原虫疗效,在“治疗转换”方法下与标准抗利什曼原虫药物米替福新和一种有效的免疫调节剂吡咯利凡联合,在利什曼原虫/仓鼠模型中进行了评估。与酮康唑(50mg/kg,5 天,po)+米替福新(5mg/kg,5 天,po)联合治疗的动物相比,酮康唑(54.67%)和米替福新(54.77%)单独治疗的寄生虫疗效增强(72%)。联合使用吡咯利凡(10mg/kg,12 天,po)可将抗利什曼原虫疗效从 72%进一步提高到 82%。与酮康唑+米替福新联合治疗的动物观察到 ROS、RNS 和 H2O2 的显著生成和吞噬作用增强;然而,由于其抗氧化和非杀利什曼原虫特性,向该组合中添加吡咯利凡并没有改变代谢物和吞噬作用的水平。该组中观察到细胞介导免疫的显著上升,表明免疫调节剂吡咯利凡发挥了作用,并证明增强细胞介导免疫在治疗中的重要性。这些发现为降低成本和毒性的利什曼病化学疗法提供了一种新策略。