de Vallière Serge, Mary Charles, Joneberg Jeanna E, Rotman Samuel, Bullani Roberto, Greub Gilbert, Gillmore Julian D, Buffet Pierre A, Tarr Philip E
Infectious Diseases Service, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland.
Am J Trop Med Hyg. 2009 Aug;81(2):209-12.
AA-amyloidosis in the setting of chronic visceral leishmaniasis (VL) has been reported in animal models but documentation in humans is unavailable. Here, we report on a Portuguese man who in 1996 was diagnosed with both human immunodeficiency virus (HIV)-infection and VL. Antiretroviral treatment led to sustained suppression of HIV viremia but CD4+ lymphocytes rose from 8 to only 160 cells/mL. Several courses of antimony treatment did not prevent VL relapses. Renal failure developed in 2006 and renal biopsy revealed AA-amyloidosis. The patient had cryoglobulinemia and serum immune complexes containing antibodies directed against seven leishmanial antigens. Antimony plus amphotericin B, followed by oral miltefosine resulted in a sustained VL treatment response with elimination of circulating Leishmania infantum DNA and CD4+ recovery. The concomitant reduction of serum AA levels and disappearance of circulating leishmanial immune complexes suggests that prolonged VL may lead to AA-amyloidosis in immunocompromised humans.
在慢性内脏利什曼病（VL）背景下的AA型淀粉样变性已在动物模型中有报道，但在人类中的记录尚不可得。在此，我们报告一名葡萄牙男子，他于1996年被诊断出感染人类免疫缺陷病毒（HIV）和VL。抗逆转录病毒治疗导致HIV病毒血症持续受到抑制，但CD4 +淋巴细胞计数仅从8个细胞/毫升升至160个细胞/毫升。几个疗程的锑剂治疗未能预防VL复发。2006年出现肾衰竭，肾活检显示为AA型淀粉样变性。该患者有冷球蛋白血症，血清免疫复合物中含有针对七种利什曼原虫抗原的抗体。锑剂加两性霉素B，随后口服米替福新，使VL得到持续治疗缓解，循环中的婴儿利什曼原虫DNA消失，CD4 +细胞计数恢复。血清AA水平的同时降低以及循环中利什曼原虫免疫复合物的消失表明，长期的VL可能导致免疫功能低下的人类发生AA型淀粉样变性。
